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Our understanding of the pathophysiologic processes leading to preterm premature rupture of membranes (PPROM) has grown tremendously in recent years. Evidence suggests that there may be a genetic susceptibility to PPROM and that genetic and environmental elements are important cofactors in its development. A number of risk-based protocols have been proposed in an attempt to identify those women at highest risk for PPROM. While we have made advances in the area of predicting PPROM, treatments based on current risk-based systems have failed to distinguish a specific, effective preventive therapy for PPROM. The concept that genetic factors increase susceptibility or decrease resistance to disease has stimulated new work in the field of PPROM. Several maternal and fetal gene polymorphisms have been identified that are associated with an increased risk for PPROM. Patients with 'susceptible' genotypes may also have clinical risk factors for PPROM resulting in a synergistic increase in the risk for PPROM, a so-called gene-environment interaction. The concept that these gene-environment interactions represent new targets for our efforts to prevent PPROM is explored.

Objective We sought to determine whether vitamins C and E could be delivered to the fetal-placental unit through maternal oral supplementation. Study design In a randomized, double-blind study, 20 women received a daily prenatal vitamin with or without 400 IU of vitamin E and 500 mg of vitamin C, starting at 35 weeks' gestation. At randomization, a nutritional questionnaire, plasma vitamin C and E and red blood cell (RBC) vitamin E levels were determined. At delivery, concentrations of maternal and fetal plasma vitamin C and E, maternal and fetal RBC vitamin E, amniotic fluid vitamin C, and chorioamnion vitamin E and tensile strength were determined. Results Maternal plasma vitamin E levels increased in the supplemented women but not in the control subjects. No changes in maternal vitamin C levels were noted. Maternal plasma vitamin C concentrations at delivery correlated closely with amniotic fluid vitamin C levels. Similarly, maternal plasma vitamin E levels at delivery correlated with the chorioamnion concentration of vitamin E. Conclusions Maternal plasma vitamin E levels are increased by oral supplementation. Maternal plasma vitamin C and E concentrations correlate with the concentration of vitamin C in the amniotic fluid and vitamin E in the chorioamnion, respectively.

This study was conducted to compare maternal and fetal plasma, amniotic fluid, and chorioamnion levels of vitamins C and E in term (38 weeks' gestation) subjects undergoing elective repeat cesarean section (CS) without labor with values of subjects of similar gestational age and dietary intake undergoing labor and vaginal delivery (VD).Healthy women undergoing elective repeat CS (n = 5) or uncomplicated VD (n = 5) at term (38 weeks' gestation) were studied. For CS patients, maternal and fetal (cord) blood, amniotic fluid, and chorioamnion samples were collected at time of surgery. For VD patients, maternal blood and amniotic fluid were obtained at 5 cm cervical dilation and fetal cord blood and chorioamnion were collected at delivery. Each patient completed a nutritional questionnaire. Plasma and membrane vitamin E concentrations were determined by reversed-phase high-performance liquid chromatography and standardized to cholesterol or membrane protein, respectively. Vitamin C was determined with the use of the 2,4-DNPH method.Dietary intakes for vitamins C and E as well as maternal and fetal vitamin E plasma concentrations were similar for CS and VD patients. In both groups, maternal levels were higher than fetal levels(P.05). Chorioamnion membrane vitamin E measurements in both groups were similar. Vitamin C concentrations in CS and VD patients were highest in amniotic fluid, lower in fetal plasma, and lowest in maternal plasma. However, mean vitamin C concentrations in maternal plasma, amniotic fluid, and fetal plasma of VD patients were significantly lower, being only 20% +/- 6%, 29% +/- 11%, and 22% +/- 2% of values obtained from CS patients.During labor in healthy women at term, uterine contractile activity may generate reactive oxygen species (ROS) through the process of repetitive ischemia and reperfusion. With the significant depletion of vitamin C during labor, we speculate that water-soluble vitamin C scavenges ROS in the aqueous phase and recycles lipid-soluble vitamin E to combat ROS-induced tissue damage.

Objective: Our purpose was to assess the tensile strength of the chorioamnion at various gestational ages. Study Design: Segments of chorioamnion were obtained from 35 patients delivered at gestational ages ranging from 17 to 41 weeks. Clinical information including gestational age, chorioamnionitis, premature rupture of membranes, and onset of labor was recorded. Tensile strength (grams to burst and deflection at rupture) was measured on 2 to 16 specimens per patient. Tensile strength of several commercial products was used for comparison. Results: Tensile strength increases up to 20 weeks of gestation and then plateaus until 39 weeks of gestation, when it falls dramatically. Clinical chorioamnionitis alone did not affect tensile strength, but gross membrane inflammation resulted in reduced tensile strength. Conclusions: Tensile strength of the chorioamnion varies with gestational age. This baseline information will be useful in assessing the effects of various conditions and therapies on membrane strength and may provide insight into spontaneous rupture of membranes. (Am J Obstet Gynecol 2002;187:672-5.)

Our objective was to assess the perinatal management and neonatal outcomes of premature, severely intrauterine growth-restricted (IUGR) neonates. A cohort of neonates1000 grams,or = first percentile for weight, and37 weeks' gestation was identified and matched 2:1 to two control sets of premature, appropriate-for-gestational age (AGA) infants-one with similar gestational age (AGA-GA group) and the other with similar birth weight (AGA-BW group) to determine the effect of IUGR on the outcome of the premature infant. The IUGR group was then examined in detail for descriptive statistics. Data were analyzed by t-tests and Chi-square analyses where appropriate. The IUGR infants had worse outcomes than AGA-GA controls but had somewhat better results than the AGA-BW controls. In the IUGR group, a birth weight less than 550 grams was significantly associated with neonatal death (p0.001). However, increasing gestational age was not associated with neonatal survival (p = 0.661) if birthweight remained below 550 grams. Classical cesarean delivery was associated with neonatal death (p = 0.003). Neonatal variables associated with poor outcome included patent ductus arteriosus (p = 0.034), feeding intolerance (p = 0.046), and failure to thrive (p = 0.05). Overall, neonatal survival was 73%. Of the surviving neonates, 69% had evidence of neurodevelopmental delay when tested at 6 and 12 months. Premature, growth-restricted neonates with birth weights of550 grams versus those of550 grams have dismal outcomes despite a gestational age that is compatible with survival.

We propose that generation of reactive oxygen species may be a potentially reversible pathophysiologic pathway leading to preterm premature rupture of the membranes. Reactive oxygen species generated by the body's response to diverse insults such as infection, cigarette smoking, bleeding, or cocaine use can activate collagenolytic enzymes and impair fetal membrane integrity. Vitamin E, a lipid-soluble antioxidant, inhibits membrane-damaging effects of reactive oxygen species-induced lipid peroxidation. Vitamin C, a water-soluble antioxidant in plasma, stimulates and protects collagen synthesis while recycling vitamin E. Prior evidence shows that (1) damage by reactive oxygen species can impair fetal membrane integrity, (2) reduced midgestation levels of vitamin C are associated with preterm premature rupture of membranes, and (3) these vitamins can be safely and effectively absorbed and delivered to gestational tissues. Current prenatal vitamin preparations contain vitamins C and E in concentrations that are less than 1/3 and 1/10, respectively; these levels have been suggested for effective antioxidant protection. We hypothesize that increased dietary consumption or supplementation of vitamins C and E during pregnancy may reduce physiologically the risks of that portion of preterm premature rupture of membranes that is mediated by excessive or undamped peroxidation of fetal membranes. This hypothesis, if confirmed, should stimulate initiation of therapeutic trials to test the efficacy of enhanced supplementation with vitamins C and E during pregnancy to prevent preterm premature rupture of membranes.

Objective: Preterm premature rupture of fetal membranes has been associated with infection, cigarette smoking, and bleeding. Hypochlorous acid (a reactive oxygen species) is central to the body’s response to infection, yet it may damage surrounding tissue while destroying pathogens. We examined in vitro the tissue-damaging actions of hypochlorous acid on the amnion-chorion and the protective role provided by pretreatment with vitamins C and E. Study Design: Amnion-chorion samples were obtained from 4 term pregnancies, cut into segments, and divided into 6 exposure groups. Half were treated in advance with vitamins C and E (Trolox C) and half were treated with buffer solution alone. After rinsing, amnion-chorion samples were exposed to hypochlorous acid at 1 or 10 mmol/L for 4 hours. Histologic and immunocytochemical evaluations were conducted with antibodies for collagen I and IV. Results: Extensive damage to amniotic epithelium and collagen I but not collagen IV resulted from hypochlorous acid exposure and was dose related. Pretreatment with vitamins C and E prevented this damage in all cases. Conclusion: Hypochlorous acid damages the amniotic epithelium and collagen I in the amnion-chorion. The protection against hypochlorous acid–induced damage provided by antioxidant therapy (vitamins C and E) is of therapeutic significance. (Am J Obstet Gynecol 2000;183:979-85.)

There is a growing body of information relating diverse diseases and the consequences of injury to generation and toxicity of reactive oxygen species (ROS). Recently, it has been shown that the fetus and its membranes are also vulnerable to this toxicity, suggesting that a number of obstetric diseases may result from exposure to ROS, which are ubiquitous in aerobic organisms. Endogenous antioxidants, including superoxide dismutase, catalase, and glutathione peroxidase are essential for defense against ROS. It is significant that all antioxidants appear to be down-regulated in the fetus and membranes, suggesting the possibility that any process that further depresses their activities or increases the burden of ROS may compromise fetal development or maternal health. When permitted to accumulate, ROS can damage all classes of macromolecules, including lipids, proteins, and nucleic acids. Toxicity includes mutation, protein degradation, and lipid peroxidation, which can severely disturb membrane permeability and alter intracellular calcium and pH. An understanding of the generation and toxicity of ROS should help to define their potential roles in obstetric disease and lead to innovative preventive and therapeutic approaches.

Cocaine's cardiotoxicity was reported in our laboratory to be augmented by progesterone. This study was designed to replicate these findings and determine the mechanism. Rats were pretreated with progesterone (study) or vehicle (control). Papillary muscles were attached to transducers in Krebs' baths. Paced contractility parameters were measured while increasing concentrations of cocaine, norepinephrine, or tetrodotoxin were added. In nine baths, yohimbine was added before the cocaine. Twelve rats were pretreated with reserpine, and cocaine added to the baths. In muscles from nonreserpinized control rats, there was a small positive inotropic effect (8.6% above baseline) at 10(-6) M cocaine, not seen in study muscles. There were no differences between study and control muscles in cocaine concentrations at which muscles became acontractile, nor in responses to norepinephrine, tetrodotoxin, or to cocaine after the addition of yohimbine or following reserpine pretreatment. We could not replicate cocaine's previously reported increased negative inotropic effect in progesterone-treated rats, nor was there evidence supporting possible mechanisms for this reported effect.

Progesterone increases cocaine's cardiovascular toxicity in sheep and rats. To determine whether progesterone enhances the lethality of cocaine, nonpregnant female rats were treated with either IM progesterone (P4) or vehicle, and pregnant rats (Preg) were untreated. The rats received one IP injection of cocaine at a dose between 25-75 mg/kg and were observed for seizures and/or death. All 62 rats that died did so within 17 min, preceded by seizures in 90.3%. Mean times-to-seizure and times-to-death, and mean lethal serum cocaine concentrations did not differ among groups. Serum progesterone levels (ng/ml +/- SEM) at the time of death were different among groups: 24 +/- 1.7 (C), 102 +/- 6.4 (P4), and 139 +/- 5.2 (Preg). Logistic regression dose/fatality curves, LD50s, and LD10s for the pregnant, progesterone, and control groups were not significantly different from one another. Though progesterone has enhanced cocaine's cardiac toxicity in some studies, it does not increase the risk of death from acute cocaine exposure in rats.

Although malignant transformation of fetal cervical teratoma is extremely rare, perinatal morbidity is high and usually related to the size of the tumour, which may compromise fetal swallowing and subsequently lead to upper airway obstruction. We present a case in which mid-trimester serial sonography demonstrated markedly rapid early growth of a lesion of this type between 17 and 19 weeks' gestation indicating the aggressive nature of this tumour, assisting parental decision to terminate the pregnancy. Histopathology confirmed grade 3 immaturity of the lesion.

Objective To evaluate in vivo the anatomy and physiology of the normal early uteroplacental circulation. Design Forty-six women were included, all of whom continued their pregnancy into the second trimester. Color Doppler was used to identify peritrophoblastic flow, and spectral Doppler was used to analyze waveforms obtained from the different segments of the uteroplacental circulation. Results Flow was detected in the spiral arteries of the peritrophoblastic region in all patients. Flow was detected within the intervillous space in only one case. Conclusions This study demonstrated that color Doppler imaging can be employed as an in vivo means of studying the uteroplacental circulation. The study confirmed the in vitro findings that trophoblastic invasion of the decidual spiral arteries occurs at 5 to 6 weeks' gestation. The study also confirmed the fact that there is no noticeable blood flow within the intervillous space during most of the first trimester of a normal pregnancy. Both of these findings may serve to protect the early gestation from the forces of arterial blood flow.

Unusual sonographic visualization of the interlobar fissure of the herniated fetal liver in a case of right congenital diaphragmatic hernia was misinterpreted as the right diaphragm leading to misdiagnosis of this fetal anomaly.

Our purpose was to establish a nomogram of fetal sacral length throughout gestation and to assess its value in cases of abnormal fetal growth.A prospective cross-sectional study of 506 singleton fetuses with normal growth between 15 and 41 weeks' gestation was performed. Regression analyses were performed on sacral length, gestational age, biparietal diameter, head circumference, and femur length. The sacral length in 80 singleton gestations with abnormal growth (4090th percentile and 4010th percentile for gestational age) were compared with the nomogram.Linear relationships between gestational age and sacral length, biparietal diameter, head circumference, and femur length were demonstrated. Sacral length (centimeters) as a function of gestational age (weeks) was expressed by the regression equation: Sacral length = -0.108 + 0.102 Gestational age, with a Pearson correlation coefficient of R2 = 0.959. The sacral length of all 80 fetuses with abnormal growth demonstrated the same relationship to gestational age as did the 506 normal controls.This study defines the normal limits of sacral length; demonstrates a high correlation between sacral length, gestational age, and other standard measurements of fetal growth; and indicates that sacral length can predict gestational age, irrespective of fetal nutritional status.

Objective Elevated interleukin-6 (IL-6) level in midtrimester amniotic fluid is associated with preterm delivery. We hypothesized that, in patients with elevated IL-6, vitamin C and alpha-fetoprotein may provide protection from spontaneous preterm delivery through antioxidant functions. Study Design Antioxidant potential of alpha-fetoprotein was assessed in vitro. Amniotic fluid was collected from a prospective cohort of patients who underwent midtrimester amniocentesis. In patients with IL-6 >600 pg/mL, alpha-fetoprotein, vitamin C, tumor necrosis factor–alpha, tumor necrosis factor receptors, and antioxidant capacity were compared between subjects with spontaneous preterm and term deliveries. Results Alpha-fetoprotein demonstrated 75% the antioxidant capacity of albumin in vitro. Of 388 subjects, 73 women had elevated IL-6 levels. Among these subjects, alpha-fetoprotein, but not vitamin C, was significantly lower in 9 women with preterm birth. Antioxidant capacity correlated with vitamin C and tumor necrosis factor receptors, but not with alpha-fetoprotein or pregnancy outcome. Conclusion Amniotic fluid alpha-fetoprotein, but not vitamin C, may protect against preterm birth in patients with elevated midtrimester IL-6 levels.

A prospective study of 98 pairs of nonstress tests (NSTs) was obtained simultaneously from members of 30 twin gestations. Fifty-five percent of the total fetal heart rate (FHR) accelerations of both twins were associated with each other and occurred within 15 seconds of each other. There were 8.46% synchronous FHR accelerations of both twins, possibly reflecting evoked fetal movements. Statistical analysis failed to reveal evidence of a dominant twin in utero, with one twin initiating the majority of coinciding fetal movements with statistical significance in only three gestations. Examination of combinations of the 30 separate individual significance tests using techniques of meta-analysis demonstrated a p value of 0.81, indicating lack of dominance in any of the 30 pairs of twins. The probability plot, consistent with the large p value for the combination test statistic, suggested that fetal movements in two gestations are related, strengthening the hypothesis of in utero tactile communication between twins. We conclude that the existence of a "dominant twin" in utero cannot be detected by electronic FHR monitoring methods.

Contraction dynamics of isolated papillary heart muscles from nonpregnant, pregnant, and progesterone-treated nonpregnant Long Evans rats were studied during exposure to cocaine. With increasing cocaine concentrations from 10−16 to 10−4 m , papillary muscles from nonpregnant rats demonstrated a biphasic pattern of positive, then negative, inotropy. Only negative inotropy with increasing cocaine concentrations was observed in papillary muscles from pregnant and progesterone-treated nonpregnant rats. Papillary muscles from pregnant and progesterone-treated nonpregnant rats became nonfunctional at cocaine concentrations 1–4 orders of magnitude lower than those for nonpregnant rats. These findings demonstrate that pregnancy and progesterone treatment alter cocaine effects upon cardiac papillary muscle function and response patterns and shift the cocaine dose-function curve to the left when compared to the nonpregnant group. We conclude that pregnancy increases the direct cardiotoxicity to cocaine, and progesterone may be responsible for this enhanced cocaine toxicity.

We present a case that describes a partial fetal response to external vibratory acoustic stimulation in that, although no fetal movements were elicited, a blunted, brief positive cardioacceleratory response was noted. This fetus exhibited features of the Pena-Shokeir syndrome, characterized by skeletal neurogenic atrophy, yet with a normal auditory system at autopsy. This observation may suggest that the prolonged increase in the basal fetal heart noted after fetal vibratory acoustic stimulation is sustained by active fetal movements, absent in this fetus due to joint contractures.

The Roberts-SC phocomelia syndrome (pseudothalidomide syndrome) is a rare, usually lethal condition involving short limbs and occasional hydrocephalus. Presented is a case in which prenatal sonographic findings were highly suggestive of this syndrome, although not definite. In this fetus, findings of hydrocephalus, short limbs, and probable pulmonary hypoplasia changed the intrapartum management. The findings, correlated with the postmortem radiography, led to diagnosis of probable Roberts-SC syndrome.

Cocaine produces a greater hypertensive response in pregnant ewes than in nonpregnant ewes. To determine whether pregnancy-related progesterone levels augmented this cocaine response, six nonpregnant ewes were surgically oophorectomized, implanted with femoral artery and vein catheters, and later administered progesterone 10 mg/kg intramuscularly for 3 days. Consistent responses in blood pressure and heart rate to intravenous norepinephrine 0.4 and 0.6 wg/kg, before and during progesterone treatment, indicated that progesterone did not increase a-adrenergic receptor sensitivity to exogenous norepinephrine. In contrast, intravenous cocaine at either 1.0 or 2.0 mg/kg produced approximately twofold greater increases in blood pressure and threefold greater increases in heart rate during each day of progesterone treatment when compared with responses to the same dose of cocaine before progesterone treatment. These results indicate that progesterone enhances the cardiovascular response to cocaine and does not involve an increase in «-adrenergic receptor sensitivity. (AM J OBsTET GVNECOL 1990;163:1659-64.)

Estimated fetal weights from 1684 cases with singleton, live infants born within 7 days of an ultrasonographic examinations were compared with their birth weights, which ranged from 520 to 5920 gm. Estimated weight calculated from Shepard's equation produced a linear relationship of birth weight against estimated weight with an intercept and slope of 209.5 gm and 0.929. Overall, 75% of the estimated weights were within 15% of the actual weight. A separate regression model that used the same variables from Shepard's equation failed to improve the comparison between estimated and actual weights. All cases were reevaluated with multiple regression modeling. Various examination-to-birth intervals were analyzed; intervals less than or equal to 3 days appeared optimal. The best equation increased the percent of cases that were within 15% of the actual birth weight to 80%. The plot of birth weight against estimated weight had an intercept and slope of 33.1 gm and 0.994. Unlike Shepard's equation, the best equation was not statistically different from the ideal one-to-one relationship between estimated and actual weight. When the new equation was applied to an additional 339 new cases, equally accurate results were obtained. Customizing a laboratory's ultrasonographic weight estimation equations may be necessary to obtain the best estimate of fetal weight.

The effects of intravenous cocaine on heart rate and blood pressure were studied in pregnant and oophorectomized nonpregnant ewes. In response to intravenous cocaine doses of 1.0 and 2.0 mg/kg, both pregnant and nonpregnant ewes demonstrated dose-dependent increases in systolic, diastolic, mean arterial, and pulse pressures with return to baseline by 30 to 60 minutes after cocaine administration. However, at both doses (1.0 and 2.0 mg/kg) pregnant ewes demonstrated greater increases in mean arterial pressure (+29.6%, +48.7%) than nonpregnant ewes (+15.6%, +27.7%) during the first 5 minutes after cocaine administration. Thereafter the responses were similar. Thus pregnancy increases the cardiovascular toxicity to cocaine.

Aim: To discuss the role of oxidant stress in preterm, premature rupture of the membranes (PPROM). Results: There is evidence to suggest that preterm, premature rupture of the membranes occurs secondary to focal collagen damage in the fetal membranes. Conclusion: Oxidant stress caused by increased ROS formation and/or antioxidant depletion may disrupt collagen and cause premature membrane rupture. We propose that supplementation with vitamins C and E may synergistically protect the fetal membranes, and decrease the risks of PPROM.

Congenital intracranial teratomas are rare and usually fatal. We present prenatal diagnosis of such a case associated with scalp, facial, and body skin edema, hepatomegaly, extramedullary hematopoiesis, polyhydramnios, and a hydropic placenta. These manifestations of high-output cardiac failure were thought to be the result of the large cardiac output required by massive intracranial tumor arteriovenous shunting.

Preterm premature rupture of membranes (PPROM) results initially from damage to collagen in the chorioamnion leading to a tear in the membrane. Tissue-damaging molecules called reactive oxygen species (ROS) are capable of damaging collagen in the chorioamnion that could lead to PPROM. This hypothesis is supported by epidemiological studies linking clinical conditions known to produce ROS or reduce antioxidant protection to PPROM, by in-vitro studies in which membrane segments exposed to ROS exhibited tissue alterations consistent with PPROM, and by clinical studies showing that chorioamnion and amniotic fluid samples obtained from PPROM patients exhibit excessive collagen degradation. The role of antioxidants to protect the chorioamnion from ROS damage has been demonstrated in one in-vitro study. A prospective, randomized blinded trial of antioxidant therapy during pregnancy is needed to evaluate this approach for the prevention of PPROM.

Infant survival with ever-decreasing birthweights is attainable with recent advances in maternal-fetal medicine and enhanced neonatal intensive care. We report a gestation complicated by severe chronic hypertension and fetal distress necessitating delivery at 26 1/7 weeks. The growth-retarded newborn weighed 345 g (12 oz) and survived with minimal sequelae despite a protracted and complicated neonatal course.

Type III congenital cystic malformation of the lung with nonimmune hydrops and oligohydramnios was diagnosed at 17 weeks by ultrasonography. Massive fetal cardiac compression with probable associated left- and right-sided failure causing both the oligohydramnios and the ascites, respectively, was thought to be the underlying pathophysiologic mechanism of this unusual clinical presentation. Pathologic examination after termination of the pregnancy confirmed the prenatal diagnosis.

Recurrent bilateral renal agenesis in siblings is very rare. Presented is a case diagnosed with sonographically aided amnioinfusion at 18 weeks in a woman with an infant affected with the same condition in a previous pregnancy.

Although beta-sympathomimetic tocolytic therapy has been associated with transient subendocardial ischemia, magnesium sulfate has rarely been noted to cause acute chest pain and is, in fact, known to improve myocardial perfusion in patients with variant angina. We believe this report represents the first case in which intravenous magnesium sulfate administered as a tocolytic agent caused acute chest pain accompanied by transient electrocardiographic evidence of subendocardial ischemia.

Fetal ultrasound examination at 29 weeks' gestation revealed a severely symmetrically growth-retarded fetus with microcephaly, hypertelorism, and hypoplastic genitalia with a two-vessel umbilical cord. G-banding analysis on amniotic cell cultures revealed a 46, XY,r(4)(p15-q35) karyotype in each of the colonies analyzed. This prenatal diagnosis, to our knowledge the first reported, assisted clinical management of this pregnancy.

Despite tremendous progress in medicine generally and in obstetrics specifically, neonatal death, stillbirth, and early pregnancy losses still occur. Although technology has given us the advantage of sophisticated measures of fetal health, these technologies are at times inadequate. For families who depend on modern techniques for prenatal genetic testing, the information gained from this same technology may lead to heart-wrenching decisions about continuing or terminating the pregnancy.

This study was performed to assess the association of lack of mandibular movement as manifested by absent fetal swallowing and micrognathia in a nonrestrictive intrauterine environment. Over a 5-year period, 14 fetuses with sonographic findings of polyhydramnios (amniotic fluid index [AFI] more than 20 cm), absent mandibular movement, and a nonvisualized fetal stomach, all consistent with absent fetal swallowing, were followed. A group of 14 fetuses, each with polyhydramnios (AFI more than 20 cm), yet with sonographic detection of fetal swallowing, served as controls. All gravidas in both groups were normoglycemic throughout gestation. Subsequent mandibular development was assessed at delivery or autopsy. Analysis of the data revealed that in the study group, 12 of these infants were liveborn, and two were stillborn. Eleven of the liveborn infants had an early neonatal death. All 14 infants of the study group demonstrated micrognathia. None of the control infants (all of whom survived) had micrognathia. In conclusion, this study supports the concept that normal mandibular growth may depend on the presence of mandibular movement during intrauterine development.

We report a case of a patient who received nalbuphine during labor. The fetus was in an awake state, but when exposed to intravenous nalbuphine manifested quiet sleep. This suggest a physiological response and not a sign of fetal compromise.

Placenta percreta is a severe condition associated with maternal morbidity and mortality even when surgery is performed electively. Methotrexate has been suggested as a possible treatment modality for adherent placenta to avoid catastrophic surgery. The purpose of this report is to present a case where the placenta was left in situ to avoid cystectomy at the time of cesarean section, with subsequent failure of treatment with methotrexate.

Objective: Cocaine and metabolites can be found in the amniotic fluid after maternal use, presumably as a result of fetal urination. The fetus may be repeatedly exposed to the effects of these drugs through contact with amniotic fluid that contains these substances. The purpose of this study was to determine whether the naive fetal lamb generates detectable fetal blood levels of cocaine and metabolites when cocaine is placed directly into the amniotic fluid and, if so, whether fetal swallowing accounts for these findings. Study Design: Six pregnant ewes with singleton fetuses of 120 to 125 days' gestation were chronically catheterized for daily sampling of cocaine and metabolite levels in maternal venous plasma, fetal venous plasma, and amniotic fluid over a 7-day period. Esophageal ligation was performed in three additional animals similarly instrumented to evaluate the role of fetal swallowing in the distribution of amniotic fluid cocaine and its metabolites. In each case, at the time of surgery, an Alzet osmotic pump delivering cocaine at 0.5 mg/kg estimated fetal weight per hour into the amniotic fluid was secured to the fetal back. Cocaine and metabolites (benzoylecgonine, ecgonine methyl ester, and norcocaine) were measured daily in material and fetal plasma, amniotic fluid, and meconium by solid-phase extraction and derivatization and quantified by high-performance gas chromatographic techniques. Results: The concentrations of ecgonine methyl ester were highest in the amniotic fluid followed by cocaine and benzoylecgonine. In the normal and esophagus-ligated groups, cocaine, benzoylecgonine, and norcocaine were found in fetal plasma in concentrations of approximately 3% that of amniotic fluid. Ecgonine methyl ester was not detected in fetal plasma from either group. Meconium samples from sheep with and without esophageal ligation demonstrated high levels of norcocaine. Conclusion: We conclude that cocaine and metabolites in amniotic fluid enter the fetal circulation to produce detectable plasma levels through routes other than swallowing. Moreover, the results of meconium analyses in the two groups of fetuses suggest that fetal swallowing is not the primary mechanism by which cocaine and metabolites enter the intestine.

The purpose of this study was to examine the predictability of intrapair percentage differences of ultrasonic fetal biometric parameters in detecting twin discordancy. Fetal biometric parameters obtained in 90 twin gestations within 7 days of delivery were analyzed. Intrapair differences of 5% and 10% were used for biparietal diameter (BPD), head circumference (HC), abdominal circumference (AC), femur length, and HC/AC to assess their predictive value. Statistical analysis was performed using chi 2 test and Fisher's exact test. Receiver operator characteristic (ROC) analysis was done to determine if there was a difference between absolute and intrapair differences. Intrapair AC and HC differences of 5% were found to have significantly higher true positive rates in detecting discordancy. At an intrapair difference of 10%, AC and BPD were found to have high sensitivity rates in detecting discordancy. ROC analysis did not show any difference between use of absolute and intrapair difference in predicting discordancy (P = 0.0001). We conclude that fetal AC is the most significant sonographic parameter in detecting discordancy in twins.

Prospective analysis of 75 pairs of nonstress tests (NSTs) obtained simultaneously from both members of 35 twin gestations was performed to quantitatively assess the incidence of simultaneous periods of fetal heart rate (FHR) reactivity and nonreactivity of twins. Comparative analysis of the paired NSTs was used to compute rates of simultaneous fetal heart rate reactivity and nonreactivity. Statistical analysis involved comparison of weighted averages of these rates, using sequence lengths as weights. Weighted standard deviations were used to describe variability between sets of NSTs. Trend analysis was performed using weighted linear regression to calculate slopes for pairs of twins with three or more repeat NSTs. Groups of twins were compared by performing a variance stabilizing transformation on the appropriate rates, and using a two sample t test to compare the means of transformed data. Analysis of this data revealed that twins exhibited similar in utero fetal heart reactivity and nonreactivity as indicated by simultaneous electronic fetal monitoring during 79.90% +/- 1.62 (SD) of the time monitored. The incidence of periods of simultaneously reactive FHR and simultaneously nonreactive FHR were 11.79% +/- 1.02 and 68.10% +/- 2.17, respectively, irrespective of gestational age. These data confirm the hypothesis that periods of FHR reactivity and nonreactivity of twins are strongly associated with each other.

Invasive hemodynamic monitoring has become an integral part of intensive care management. Whereas the pulmonary artery catheter is the mainstay for determination of the hemodynamic profile and differentiation between cardiogenic and noncardiogenic forms of pulmonary edema, immediate central venous access in itself is of importance in rapid volume replacement in cases complicated by severe hypovolemia. Central venous catheters are also the preferred route of administration of total parenteral nutrition to patients with cancer. We present our experience with real-time ultrasonographic guidance during subclavian vein catheterization in critical care obstetrics and gynecologic oncology.

The outcomes of 41 patients with prolonged, premature rupture of membranes in the midtrimester (19.5 to 26 weeks) managed conservatively were retrospectively analyzed. The maternal obstetric history was notable for a high incidence of second trimester bleeding and a prior history of preterm delivery. The mean duration of ruptured membranes before delivery was 10.6 days and was unrelated to gestational age. Delivery occurred within 2 weeks in 75% of the cases. The major indication for delivery was chorioamnionitis in 71% of patients. The only major maternal morbidity was chorioamnionitis. The overall perinatal survival was 47%, but in infants exceeding 24 weeks' gestation or 500 gm weight, the survival increased to 75%. No significant limb abnormalities, facial anomalies, growth retardation, or pulmonary hypoplasia occurred in the study population. Long-term follow-up demonstrated that 28% of infants exhibited major neurologic or developmental deficits.

Our purpose was to assess the value of the cheek-to-cheek diameter and the cheek-to-cheek diameter/biparietal diameter ratio in the ultrasonographic detection of abnormal fetal growth.The cheek-to-cheek diameter and cheek-to-cheek diameter/biparietal diameter ratio were examined in 21 small-for-gestational-age (10th percentile for estimated weight) and 87 large-for-gestational-age (90th percentile) fetuses. Statistical analysis consisted of Student's t test comparison between means and analysis of covariance for comparison of regression lines slope between these 108 fetuses and previously published nomograms of appropriate-for-gestational-age fetuses.The mean cheek-to-cheek diameters in small-for-gestational-age fetuses were significantly smaller than in appropriate-for-gestational-age fetuses (p0.0001). In large-for-gestational-age fetuses the mean cheek-to-cheek diameters were significantly larger (p0.005). Although large-for-gestational-age fetuses of diabetic mothers exhibited higher cheek-to-cheek diameter/biparietal diameter ratios than did appropriate-for-gestational-age fetuses (p0.0001), in fetuses of nondiabetic mothers this ratio was only minimally larger (p0.05).The cheek-to-cheek diameter and cheek-to-cheek diameter/biparietal diameter ratio are innovative ultrasonographic parameters for detecting abnormal fetal growth. Furthermore, the cheek-to-cheek diameter/biparietal diameter ratio permits insight into the possible underlying pathophysiologic mechanisms of fetal macrosomia.

A woman presented at 29 weeks' gestation with previously undiagnosed severe mitral stenosis. She did not respond to medical therapy, and underwent successful percutaneous balloon mitral valvulopiasty with complete resolution of her symptoms. The remainder of her pregnancy was uncomplicated, and she delivered a healthy infant at 40 weeks' gestation. Percutaneous balloon yalvuloplasty offers an innovative alternative to standard surgical therapy it medical management is unsuccessful.

Twin-twin transfusion syndrome is a serious complication of monozygotic twin pregnancies and is associated with high rates of perinatal morbidity and mortality. Unfortunately, therapies to disrupt the arteriovenous anastomoses are limited, and the success rates of these therapeutic modalities are poor. We present a case of severe twin-twin transfusion syndrome at 23 weeks' gestation in which selective feticide of the recipient hydropic twin by intracardiac injection of potassium chloride was followed by rapid development of hydrops in the donor twin.

As should be evident from the case reports, epidemiology studies, and animal data, the primary mode of cocaine action is vasoconstriction, whether it occurs on the maternal side or the fetal side of the placenta. Attempts to characterize the fetal effects of cocaine exposure during pregnancy in order to formulate a "fetal cocaine syndrome" has revealed a wide spectrum of fetal effects. Therefore, a well-defined "fetal cocaine syndrome" does not exist. In fact, most fetal defects may be related to vasoconstriction, hypertension, and infarcts at any time during gestation and in any structure. Even the issues of SIDS and seizures may be the result of clinically undetectable vasospasm or hemorrhages. Traditional dogma dictates that a teratogen interferes with normal development of a structure such that the structure is missing, malformed, or dysfunctional. Moreover, since individual structures are formed at specific times during development, these structures are vulnerable to injury at these "time windows." Classical teratogens exert their damaging effects during the organogenesis period. For cocaine, however, exposure during any period in gestation may place any organ or structure at potential risk for damage. While repeated exposures during pregnancy may increase the risk of cocaine-induced damage, it appears that even a single exposure may produce infarction, edema, and tissue necrosis. The site of damage may be related to the tissue level of cocaine and the weakness of the blood vessels at that site. Subsequent loss of vascular supply and tissue necrosis produce fetal damage that is beyond capacity for repair.