In-vitro fertilisation-embryo-transfer complicates the antenatal diagnosis of placenta accreta spectrum using MRI: a retrospective analysis.

AIM: To evaluate the diagnostic accuracy of magnetic resonance imaging (MRI) for the antenatal diagnosis of placenta accreta spectrum (PAS). MATERIALS AND METHODS: Data from 95 patients with placenta previa or low-lying placenta who underwent MRI at Osaka University Hospital for the antenatal diagnosis of PAS between January 2013 and December 2018 were reviewed retrospectively. The antenatal MRI signs suggesting PAS were assessed. Patients were divided into two groups depending on whether they were diagnosed with PAS. Factors that affected PAS diagnosis were identified using multivariate analysis. RESULTS: The diagnostic accuracy of MRI for detecting PAS was as follows: 71.4% sensitivity, 96.4% specificity, and area under the curve (AUC) of 0.839 (95% confidence interval [CI]: 0.73-0.91). The diagnostic accuracy was lower in patients with in-vitro fertilisation with embryo transfer (IVF-ET): 22.2% sensitivity, 93.3% specificity, and AUC=0.578 (95% CI: 0.417-0.724). On multivariate analysis, only IVF-ET showed a significant association with false-positive or -negative MRI diagnosis of PAS (adjusted odds ratio: 26.5; 95% CI: 2.42-289.4; p=0.007). CONCLUSION: IVF-ET affects the antenatal diagnosis of PAS using MRI.

Placenta accreta following laparoscopic adenomyomectomy: a case report.

BACKGROUND: The influence of adenomyomectomy on subsequent pregnancy is unknown. Placenta accreta is most often associated with placenta previa in women with multiple previous cesarean sections. CASE: A 41-year-old woman became pregnant six years after a laparoscopic uterine posterior adenomyomectomy. She was diagnosed with complete placenta previa and considered at a low risk for placenta accreta by ultrasonography. Cesarean section and subsequent hysterectomy were required, and histopathological analysis revealed a posterior placenta accreta. DISCUSSION: The authors discuss the association of adenomyomectomy and placenta accreta on subsequent pregnancy and conclude that previous adenomyomectomy may increase the risk of abnormal placentation. Therefore, careful treatment is required during the pregnancies of patients with previous adenomyomectomy.

Imbalance of angiogenic factors and avascular edematous cystic villi in a trisomy 13 pregnancy: a case report.

The incidence of pre-eclampsia is significantly higher in trisomy 13 pregnancies than in normal pregnancies. Soluble fms-like tyrosine kinase-1 (sFlt-1), located on chromosome 13, is an anti-angiogenic molecule derived from the placenta and contributes to the pathogenesis of pre-eclampsia. Elevated sFlt-1 and reduced placental growth factor (PlGF) are associated with trisomy 13 pregnancies and may play a pathogenic role in the subsequent development of pre-eclampsia. Here we present a case of a trisomy 13 pregnancy without any signs of pre-eclampsia that showed alterations in circulating angiogenic factors and abnormal placental appearance. The placenta developed edematous changes and contained multiple small cysts. Histology of the placenta confirmed avascular edematous cystic villi and did not show the typical appearance of a partial mole or mesenchymal dysplasia. The sFlt-1/PlGF ratio in maternal serum (134) was much higher than that in gestational age-matched women who were normotensive (2.9-7.2; mean, 5.0). Immunostaining for Flt-1 and endoglin was more intense in our case compared with gestational age-matched controls, and at a similar level to a case of pre-eclampsia. Placental findings that showed avascular edematous cystic villi in our case may be associated with angiogenic imbalance involved in the pathogenesis of pre-eclampsia in trisomy 13 pregnancies.

Maternal arterial stiffness in normotensive pregnant women who subsequently deliver babies that are small for gestational age.

OBJECTIVE: To assess the association between maternal arterial stiffness and delivery of a baby that is small for gestational age (SGA) in normotensive pregnant women. STUDY DESIGN: Pulse wave analyses were performed to assess maternal arterial stiffness at 26-33 weeks of gestation in 40 normotensive women who subsequently delivered SGA babies (SGA group) and 111 normotensive women who delivered babies with normal growth (control group). RESULTS: Central systolic pressure (CSP), augmentation index (AIx) and AIx at a heart rate of 75 beats/min (AIx-75) were significantly higher in the SGA group compared with the control group, but this was not the case for brachial systolic pressure, brachial diastolic pressure or brachial pulse pressure. Birth weight was significantly correlated with CSP (r=-0.26, p<0.01), AIx (r=-0.33, p<0.01) and AIx-75 (r=-0.27, p<0.01), but not with brachial systolic pressure, brachial diastolic pressure or brachial pulse pressure. CONCLUSION: Increased arterial stiffness may be involved, in part, in the pathogenesis of SGA in normotensive women, suggesting an association between fetal growth and maternal endothelial function. Pulse wave analysis may be a clinically applicable method for assessment of maternal arterial stiffness, and may be more relevant to intrauterine fetal growth than conventional brachial blood pressure.

Surgical repair of pelvic-floor prolapse: lessons learned from longitudinal follow-up of quality-of-life survey.

BACKGROUND: Scant evidence has been reported on the evaluation of quality-of-life (QOL) in patients who had undergone surgical treatment due to pelvic floor prolapse including cystocele. The aim of this study is to evaluate the impact of surgical intervention on patients' QOL before and after surgery. METHODS: Between 1997 and 2007, 135 patients (median age: 66.6 years) with pelvic floor prolapse including cystocele underwent bladder neck suspension with anterior/posterior colporrhaphy. The follow-up period was 39.6 months. Seventy-two patients (53 %) had urinary incontinence. The cystocele was graded as mild (grade 2), moderate (grade 3), and severe (grade 4) in 35, 60, and 40, respectively, according to the Baden-Walker classification. A urodynamic study was performed in 69 patients (51 %) who had obstructive symptoms with 100 ml or more of postvoid residual urine. Postoperative QOL was longitudinally assessed in 114 patients by scoring three disease-specific items (sensation of vaginal bulging, obstructive symptoms, urinary incontinence), and one overall health-related QOL (HR-QOL), and compared with corresponding baseline scores. RESULTS: A longitudinal study demonstrated that a significant improvement in these symptoms was sustained at a median follow-up of 62.2 months. HR-QOL was significantly associated with vitality assessed by SF 36 (p = 0.036). Multivariate analysis revealed that update urinary incontinence, pre-operative HR-QOL was independent prognostic factors for predicting postoperative patient's satisfaction. CONCLUSIONS: Although surgical repair of pelvic floor prolapse can achieve acceptable results with intermediate-term durability as well as improving the QOL, preoperative patients' HR-QOL may be considered in the decision making process for treatment.

Oxidative stress-induced S100B protein from placenta and amnion affects soluble Endoglin release from endothelial cells.

Oxidative stress with elevated intracellular Ca(2+) concentration as well as endothelial dysfunction is a component of pre-eclampsia. Our aim was to investigate the oxidative stress-dependent expression of Endoglin and Ca(2+)-binding S100B protein from villous and amniotic tissue cultures, and to assess sEng expression from S100B protein-stimulated endothelial cells. We initially examined Endoglin and Hydroxy-nonenal-(HNE)-modified proteins in the placentas and amnion obtained from women with pre-eclampsia (n = 8), and healthy controls (n = 8) by immunohistochemistry. To examine oxidative stress and the S100B protein effect on sEng expression from endothelial cells, normal villous and amniotic tissue cultures were stimulated by 4-HNE, sodium fluoride and xanthine/xanthine oxidase, whereas human umbilical vein endothelial cell cultures were treated with S100B protein in a dose- and time-dependent manner at 37 degrees C in an environment of 95% air and 5% of CO(2). Culture supernatants were assessed using ELISA. Cell viability was determined using MTS assay. The concentrations of sEng and S100B protein were significantly increased in the villous and amniotic tissue culture supernatants under oxidative stress. S100B protein-stimulated endothelial cells released sEng into conditioned media with a significantly higher expression levels at a concentration of 200 pM-20 nM S100B by 2 h, whereas treated with 200 nM of S100B endothelial cells significantly expressed sEng by 12 h and stimulated the cell proliferation by the same period of time. Our findings show that oxidative stress affects sEng and S100B protein expression from villous and amniotic tissues, and picomolar and low nanomolar concentrations of S100B protein significantly up-regulate sEng release from endothelial cells leading to endothelial dysfunction.

Spinal subarachnoid hematoma following spinal anesthesia in a patient with HELLP syndrome.

A case of subarachnoid hematoma following spinal anesthesia for cesarean section in a patient with HELLP syndrome is reported. A 39-year-old woman underwent cesarean section under spinal anesthesia for worsening preeclampsia with HELLP syndrome. Despite full recovery from the spinal anesthetic, on the second postoperative day she felt numbness on the posterior aspect of her right leg, noticed she was insensitive to bladder fullness and had mild flaccid paraparesis. Magnetic resonance imaging revealed a spinal subarachnoid hematoma with cauda equina compression. With conservative management she made an almost complete recovery within three months. Serial magnetic resonance imaging showed spontaneous regression of the hematoma. The risk of spinal subarachnoid hematoma following obstetric regional anesthesia is exceedingly small even in a patient with coagulopathy and, to our knowledge, this is only the second reported case following obstetric regional anesthesia. Anesthesia for HELLP syndrome in patients with an adequate platelet count but without disseminated intravascular coagulation is controversial. It is therefore important for clinicians to recognize the symptoms and signs of spinal subarachnoid hematoma to avoid delay in treatment that might result in severe neurological deficit.

Amniotic fluid 'sludge' detected in patients with subchorionic hematoma: a report of two cases.

Amniotic fluid 'sludge' is defined as the presence of dense aggregates of particulate matter in close proximity to the internal cervical os. It is of clinical significance in asymptomatic patients at high risk for spontaneous delivery, and in patients with preterm labor and intact membranes. Subchorionic hematoma is another ultrasound finding that is associated with a higher incidence of threatened miscarriage and preterm delivery. We report two cases of occurrence of amniotic fluid sludge in patients with previously detected large subchorionic hematoma. In the first case subchorionic hematoma and amniotic fluid sludge were detected by ultrasonography at 13 + 1 and 18 + 6 weeks' gestation, respectively, followed by preterm premature rupture of membranes, placental abruption and emergency Cesarean section. In the second case subchorionic hematoma and amniotic fluid sludge were detected by ultrasound at 11 + 3 and 15 + 5 weeks' gestation, respectively, followed by miscarriage with histological chorioamnionitis. The coincidence of subchorionic hematoma and amniotic fluid sludge in these cases points to a possible connection between these two significant ultrasound findings.

The human tumor-associated antigen RCAS1 in pregnancies complicated by pre-eclampsia.

The human tumor-associated antigen RCAS1 (receptor-binding cancer antigen expressed on SiSo cells) is considered to play a role in the escape of tumor cells from immune surveillance and, at the same time, participates in the inhibition of the maternal immune response during pregnancy. The aim of our study was to investigate the expression of tumor-associated RCAS1 protein in the placenta and amniotic membranes and to assess and compare its concentration in amniotic fluid, maternal and cord blood sera in pregnancies complicated by pre-eclampsia. Samples were obtained from women with pre-eclampsia (N=9), pre-eclampsia with IUGR (N=4), normotensive IUGR (N=7) and healthy term controls (N=25) after delivery. Placentas were studied by immunohistochemistry, Western blot analysis and real-time (RT)-PCR. For assessment of RCAS1 protein concentrations in biological fluids, ELISA was performed. RCAS1 mRNA expression in the placentas of pre-eclamptic patients was significantly lower than in controls (p<0.01). The maternal blood serum RCAS1 protein concentration in the pre-eclampsia cases was also significantly lower than in controls (p=0.0207). The other study groups did not differ significantly. This study reveals the possible role of the RCAS1 protein in the development of pre-eclampsia through an immunological pathway.

Effects of non-steroidal anti-inflammatory drugs on the methotrexate transport in rat small intestine.

BACKGROUND: Methotrexate (MTX) is used in the treatment of rheumatic disease, sometimes along with non-steroidal anti-inflammatory drugs (NSAIDs), and is actively co-transported with H+ in the small intestine, mediated by a reduced folate carrier (RFC). The co-administration of NSAIDs with MTX might cause a decrease in MTX absorption through the small intestine, since some NSAIDs are uncouplers of oxidative phosphorylation. The present study investigates whether flufenamic acid, diclofenac and indomethacin, NSAIDs, decrease the ATP content of small intestinal epithelial cells and affect MTX transport (the secondary active transport) in the small intestine. METHODS: MTX transport was examined in the presence and absence of the NSAIDs, using the everted intestine technique and brush border membrane vesicles (BBMVs) from the rat small intestine. The change in physical properties of the membrane was studied in BBMVs using the fluorescence techniques. RESULTS: MTX absorption in the small intestine with H+ gradient (mucosal side, pH 6.0; serosal side, pH 7.4) decreased in the presence of the NSAIDs, but absorption without H+ gradient (both sides, pH 7.4) was unaffected. The intestinal mucosal ATP content decreased in the presence of the NSAIDs. The uptake of MTX in BBMVs was unaffected by the NSAIDs. The activity of intestinal Na+-K+-ATPase was enhanced in the presence of the NSAIDs. The fluorescence measurements showed that membrane fluidity, membrane potential and membrane hydrophobicity of BBMVs were unaffected by the NSAIDs. CONCLUSIONS: NSAIDs decreased the H+/MTX absorption in the small intestine, but not the passive transport. The uncoupling effect of the NSAIDs decreased the ATP content in the small intestine, resulting in inhibition of the secondary active transport.

Expression of apoptosis in placentae from mice lacking the prostaglandin F receptor.

This study aimed to investigate the changes in apoptosis in the placenta and decidua of pregnant mice lacking the prostaglandin F receptor. Mouse placentae were removed from fetuses on days 10-23 of pregnancy. Apoptotic cells were examined by a DNA fragmentation assay and the terminal deoxynucleotidyl transferase-mediated dUDP nick end-labelling (TUNEL) technique. The placenta and decidual weight increased before day 18 and 14 of pregnancy, and then decreased with gestational day. After day 19, the fetuses gradually died in the uterus. All fetuses died in the uterus on day 23 of pregnancy. The number of apoptosis was not significantly different between wild type and FP-deficient mice before day 18 of pregnancy by DNA fragmentation and TUNEL staining. The DNA fragmentation was always more pronounced in decidual tissue on each day of pregnancy. DNA laddering on placentae was more extensive on day 22 than day 18. In placenta, most TUNEL-positive cells were detected in trophoblast and stromal cells. A higher intensity of apoptotic cells was in the decidual basalis. The main area was the centre of the decidual basalis, and was in decrease toward to margin of placenta. The index of TUNEL positive cells increased as gestation progressed toward termination. Especially, it was prominent in the placentae on day 22 compared with that day 18 of pregnancy. The increased TUNEL-positive staining in syncytiotrophoblast surface was found in placenta at post-term, compared with those at term. Apoptosis may provide insights into both normal placental development and placental dysfunction during an abnormal pregnancy from post-term pregnancy.

Effects of hypothermia on neonatal hypoxic-ischemic brain injury in the rat: phosphorylation of Akt, activation of caspase-3-like protease.

Neuroprotective mechanisms of hypothermia have not been clearly established especially in the immature brain. To investigate the effect of hypothermia on cell death and cell survival signal pathways, we studied caspase-3-like activity and activation of Akt in a rat model of neonatal hypoxic-ischemic (H-I) brain injury. Seven-day-old rats underwent a combination of left common carotid artery ligation and exposure to 8% O(2) for 1-h (n=32). During recovery, the body temperature was reduced to 30 degrees C for 24 h in 16 animals, but was kept at 37 degrees C in 16 animals. Post-ischemic hypothermia was shown to diminish the caspase-3-like activity compared to normothermia at 6 and 24 h after H-I. Phospho-Akt was increased during the early reperfusion period after H-I in the normothermia group, but hypothermia rather decreased this enhanced phosphorylation of Akt following H-I. These results indicated that hypothermia may have some depressant effects on both cell death and cell survival signal pathways, and that Akt conceivably may not play a major role in the neuroprotective effect of hypothermia in the immature brain.

Characteristics of transport of fluoresceinated methotrexate in rat small intestine.

The small intestinal damage induced by the methotrexate (MTX) treatment results in malabsorption and diarrhea. The fluoresceinated methotrexate (F-MTX) may possibly be useful to study such effects of MTX on the small intestine. The purpose of this study is to characterize the transport of F-MTX in the small intestine in order to use it as a membrane transport and cellular marker of MTX. The transport of F-MTX in the rat small intestine (jejunum) was examined in the in vitro everted segments of the intestine. The uptake was pH-dependent and showed a maximal effect at pH 6.0, which was the same as the results of MTX previously reported. Further, it was temperature-dependent and was inhibited by metabolic inhibitors, dinitrophenol and sodium azide, and by MTX. The transport kinetics at pH 6.0 in the mucosal solution and at pH 7.4 in the serosal solution was saturable with Km of 0.48 +/- 0.23 microM and Vmax of 0.66 +/- 0.24 pmol/cm/min and in addition, the passive diffusion was observed there. These results suggested that the transport of F-MTX was energy-dependent and was mediated by the same transporter as that of MTX, although, in addition to it, other transport mechanism might contribute to the F-MTX transport. Therefore F-MTX will be of great use to investigate the MTX transport system in the normal and diseased states of small intestine, using various fluorescence techniques like visualization of membrane-associated transport proteins.

Post-ischemic hypothermia blocks caspase-3 activation in the newborn rat brain after hypoxia-ischemia.

The effects of hypothermia on caspase-3 activation were investigated in the newborn rat brain after hypoxia-ischemia (HI). Intense caspase-3 activation was observed in the control brains after HI, but this activation was significantly reduced by postischemic hypothermia. These findings suggest that the inhibition of caspase-3 activation may be an interventional point underlying the neuroprotective effect of hypothermia in neonates.

Increased Na(+)-dependent D-glucose transport in small intestine of retinyl palmitate treated rats.

The administration of retinyl palmitate (RP) to rats enhanced Na(+)-dependent D-glucose transport in the small intestine. Effects of RP on Na(+)-dependent D-glucose cotransporter (SGLT1) in rat small intestine were investigated in this study. RP was orally administered (1000 IU/kg/day) to rats for 3 days. The uptake of [3H]D-glucose into the brush-border membrane vesicles (BBMV) of the RP-treated rats, was 1.7-fold larger than that of the control rats. The western blot analysis of SGLT1 protein in BBMV indicated that the amount of SGLT1 was unaffected by the RP treatment. Scatchard analysis of phlorizin binding to both BBMV also showed that the dissociation constant (Kd) and number of phlorizin binding site (Bmax) were unchanged by the RP treatment. The fluidity of the brush-border membrane (BBM) was examined by measuring the fluorescence anisotropy of BBM labeled with 1, 6-diphenyl-1, 3, 5-hexatriene (DPH). The membrane fluidity decreased in the RP-treated rats compared with that of the control rats. In conclusion, the RP treatment increased the glucose transport in BBMV. This enhancement of glucose transport is unlikely due to the change in the amount of SGLT1 protein in BBM. The decrease of the BBM fluidity may contribute to the enhancement of glucose transport in BBM of the RP-treated rats by changing the affinity of SGLT1 for glucose and/or the turnover rate of SGLT1.

A comparative study of intraplacental villous arteries by latex cast model in vitro and color Doppler flow imaging in vivo.

OBJECTIVE: The purpose of this study was to determine whether color Doppler sonogram can accurately depict the placental vascular structures using a latex cast model of the placental vessels, and to make a nomogram of several blood flow parameters according to the vascular structures. METHODS: First, we made 9 latex cast models of placental arteries and performed morphologic observation and measurement. Second, the comparative anatomical observation of placental vessels by color flow mapping was performed for all 9 patients from whom the latex models were made. Third, a total of 102 uncomplicated pregnant women between 18 and 40 weeks gestation were examined by color Doppler imaging. The resistance indices (RI) and peak systolic velocity (PSV) were measured. RESULTS: In the latex cast model of placentas, cotyledons could be differentiated by the presence of independent vascular structure units. First, second, third and fourth branches were noted in one cotyledon. Cotyledons were easily identified and counted by color Doppler imaging. Each cotyledon contained only one first branch of the intraplacental villous artery (IPVA). The number of IPVA-1 on color Doppler imaging was equal to the number of the cotyledon calculated from the latex model. RI exhibited a negative, and PSV a positive correlation with gestational age (p < 0.05 in both cases). At any given gestational age, both RI and PSV in the peripheral arteries were significantly lower (p < 0.01) than those in the upstream arteries. CONCLUSIONS: Color Doppler flow sonography is a valuable tool for detecting the blood flow of intraplacental villous arteries in vivo and the images agree with the vascular anatomy of placenta in vitro. These results may also provide the basic parameters for future studies of some complicated pregnancies.

Enhanced absorption of 3-O-methyl-D-glucose through the small intestine of rats administered retinyl palmitate.

All-trans retinyl palmitate (RP) (1000 IU/kg body weight) was orally administered to rats for three days. The absorption of 3-O-methyl-D-glucose (3-OMG), which is actively transported by Na+-dependent D-glucose co-transporter (SGLT1), in the small intestine of the control and RP-treated rats was investigated by the in vito everted sac and in situ closed loop of intestine techniques. The absorption of [3H]3-OMG in both experiments of the in vito everted sac and in situ closed loop of intestine significantly increased in the RP-treated rats. AUC(0-120min) obtained from the [3H]3-OMG plasma concentration vs. time curve in the RP-treated rats was significantly larger than that in the control rats. On the other hand, the activity of Na+-K+-adenosinetriphosphatase (ATPase) and the transport rate of D-glucose mediated by Na+-independent facilitative glucose transporter (GLUT2) on the basolateral membrane (BLM) were similar between the control and RP-treated rats. Thus it is suggested that RP treatment of rats enhance the small intestinal absorption of glucose mediated by SGLT1.

Autocrine inhibition of leptin production by tumor necrosis factor-alpha (TNF-alpha) through TNF-alpha type-I receptor in vitro.

The aim of this study was to find factors which regulate m-leptin secretion during pregnancy. Mouse parametrial adipocytes from day 13 of pregnancy were cultured with or without mouse placental lactogen (mPL)-I, mPL-II, or mouse tumor necrosis factor-alpha (mTNF-alpha) and mouse-leptin (m-leptin) concentration in the medium was assessed by RIA. Up to four days of mPL-I or mPL-II treatment did not affect m-leptin secretion. However, mTNF-alpha, which is produced by adipocytes, significantly inhibited m-leptin secretion in a dose- and time-dependent manner. Antibody to mTNF-alpha completely blocked the inhibitory effect of mTNF-alpha on m-leptin secretion. mTNF-alpha significantly inhibited the expression of m-leptin messenger RNA. Agonistic polyclonal antibody directed against the mTNF-type-I receptor (mTNF-RI) significantly inhibited m-leptin secretion, but the anti-mTNF-RII antibody did not change m-leptin secretion. Moreover, human TNF-alpha (h-TNF-alpha) also inhibited human-leptin (h-leptin) secretion by cultured human adipocytes collected from the subcutaneous fat of pregnant women. These results suggest that TNF-alpha, which is secreted by adipocytes, inhibits m-leptin secretion through mTNF-RI and suggest the presence of an autocrine or paracrine regulation of leptin secretion in human and mouse adipose tissue in vivo.

Increase of mouse leptin production by adipose tissue after midpregnancy: gestational profile of serum leptin concentration.

The serum concentration of leptin in 10 week old virgin ICR mice assessed by RIA was 1.70 +/- 0.08 ng/ml. The serum leptin concentration in the pregnant mice mated at 10 weeks of age significantly increased from day 11 of pregnancy and reached a peak on day 17 of pregnancy (42.2 +/- 4.8 ng/ml). AFter the delivery, the serum leptin concentration rapidly decreased and reached the level of the virgin mouse on the seventh day in the puerperium. Tissue contents of leptin in the placenta, the decidua, the uterus, and the adipose tissue were between 40 to 130 ng/g wet tissue. However, leptin mRNA was expressed only in the adipose tissue and the level of leptin mRNA on days 13 and 17 of pregnancy increased 3- to 5-fold compared with that of virgin mouse. Tissue content of leptin in the adipose tissue significantly increased from day 17 of pregnancy compared with that of the virgin mouse. The m-leptin secretion from the adipose tissue also significantly increased in vitro. These results suggest that leptin, which was secreted by adipose tissue, may play important roles in mouse reproduction after midpregnancy.

Infarcted intestinal volvulus detected by prenatal ultrasonography.

This article describes a prenatal ultrasonographic finding of an infarcted intestinal volvulus. Ultrasonography showed polyhydramnios, multiple dilated intestinal loops, increased transverse abdominal area, and ascites. After cesarean section due to premature rupture of membranes and fetal distress, derotation of the infarcted volvulus caused postoperative thrombocytopenia, hyperkalemia, and acidosis and a subsequent resection was required. A high output of intestinal juice from the jejunostomy caused severe hypovolemia and electrolyte imbalance with resultant death. Increased transverse abdominal area caused by marked intestinal dilatation, ascites, fetal distress, and hydrops fetalis may suggest an infarcted intestinal volvulus.