Cases reported "Placental Insufficiency"

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1/15. anesthesia for cesarean section in two patients with brain tumours.

    PURPOSE: To describe two patients with brain tumours where general anesthesia was used for cesarean sections under emergency and urgent conditions. CLINICAL FEATURES (CASE #1): The first patient presented at 38 wk gestation with an acute intracranial tumour herniation, requiring emergency craniotomy and simultaneous cesarean section. General anesthesia was induced with thiopental and vecuronium, maintained with enflurane 1% in O2 100%. Maternal P(ET)CO2 was maintained at 25 mmHg. After delivering a healthy infant, she was given syntocinon, mannitol and dexamethasone i.v. anesthesia was maintained with fentanyl, nitrous oxide 50% in O2 and isoflurane 1% during frontal-lobe tumour resection. CLINICAL FEATURES (CASE #2): The second patient presented at 37 wk gestation for urgent cesarean section because of placental insufficiency. She had had a brain tumour resection four years earlier. An increase in intracranial pressure necessitated craniotomy for decompression at 20 wk gestation. She was further treated with dexamethasone, carbamazepine and radiation for control of cerebral oedema at 34 wk. cesarean section was performed under general anesthesia; rapid-sequence-induction with thiopental and succinylcholine, followed by isoflurane 1% in O2 100%. Syntocinon, fentanyl and atracurium i.v. were administered after delivery of a healthy infant. Although neurosurgeons stood by, their intervention was unnecessary. CONCLUSION: General anesthesia remains safe and dependable for operative delivery in parturients with intracranial tumour. Tracheal intubation allows maternal hyperventilation thereby controlling raised intracranial pressure. Hemodynamic stability is readily achieved to maintain cerebral perfusion. However, a multidisciplinary-team approach is critical for successful patient management.
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keywords = placental insufficiency, insufficiency
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2/15. Small for gestational age infant in association with maternal prothrombin gene variant (nt 20210A).

    Most of disproportionate infants born small for gestational age (SGA) have an history of placental dysfunction with no explained cause. We report a case of an unexplained SGA infant with placental infarctions and thrombosis. Maternal thrombophilic disorder tests revealed that the patient was heterozygous for the A20210 prothrombin gene variant a newly identified thrombotic risk factor. It may be suggest that prothrombin gene variant, as factor v Leiden, could be a genetic risk factor for placental insufficiency.
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keywords = placental insufficiency, insufficiency
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3/15. Legionnaire's disease complicating pregnancy: a case report with intrauterine fetal demise.

    OBJECTIVE: Legionnaire's disease complicating pregnancy is an unusual event that can seriously compromise both the mother and the fetus. CASE REPORT: We describe one case of such association, with an unfavourable intrauterine fetal outcome, secondary to acute placental insufficiency, related to infection. DISCUSSION: It is important in these high risk pregnancies complicated by acute pneumonia to take into consideration the diagnosis, as early as possible, and the appropriate treatment or the careful monitoring of fetal wellbeing.
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keywords = placental insufficiency, insufficiency
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4/15. placental insufficiency and maternal death caused by advanced stage of breast cancer in third trimester.

    We describe a case with placental, and general metastases, resulting in transient intrauterine and general hypoxia, and with additionally clinical features similar to hellp syndrome. A patient in the third trimester with dyspnea at rest developed right heart failure during c-section. During emergency thoracotomy the patient went into generalized shock and died after intense CPR. placental insufficiency was based on a multilocal metastatic event, decreasing the utero-placental perfusion.
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ranking = 6.4542936382289E-5
keywords = insufficiency
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5/15. An endocrine model for the diagnosis of intrauterine growth retardation as demonstrated by the determination of total estrogen and pregnandiol 24-hour urinary excretion in 222 at risk pregnancies.

    A reliable method for surveillance of chronic impairment of nutritive placental function is described. The techniques are simple, tested for their reliability, without need for isotopes or special apparatus and hence inexpensive. Using 222 pregnancies at risk it is shown that the simultaneous determination of a fetal (estrogen) and a placental (pregnandiol) parameter makes the early diagnosis of intrauterine growth retardation possible. Estrogen diagnosis alone has a reliability of 90.1% with 1.8% falsely pathological and 8.1% falsely normal findings (Tab. I). Simultaneous pregnandiol determinations increase the number of falsely pathological findings to 8.1% but reduce that of falsely normal ones to 2.7%. No small for date (SGA) infants are found here. It consists of 5 cases of imminent (3 times actual) premature delivery and one postmature one. Hence our technique indicates the risk of intrauterine growth retardation in all cases but not the risk of premature or postmature delivery. early diagnosis (from week 20) indicates that impairment of placental function as indicated by decreased pregnandiol excretion, occurs weeks or months earlier than decreased estrogen excretion (Fig. 1). This can be explained only by assuming that the rate of estrogen excretion is usually not dependent on the placenta but on the capacity of the fetal adrenals and liver. Thus our results indirectly confirm those of others who claim that the fetus can synthetize estrogen precursors without the need for placental pregnenolon by using acetate. Thus it appears that the synthetic pathway is independent of the placenta at the beginning plays a quantitative role also. Since the placenta can form aromatic compounds even when its nutritive function is severely impaired, our finding is further proof that estrogen excretion reflects fetal and not fetoplacental well-being. It follows that pathological estrogen excretion indicates fetal injury that has already occurred. The requirement that a sensitive parameter of placental function be hence determined in time is met by pregnandiol assays. Low pregnandiol excretion often precedes low estrogen excretion which leads to a SGA infant, indicating that pregnandiol excretion is closely correlated to placental nutritive function. Synthetic reactions in the fetus require energy and hence depend on the placenta. Normal estrogen excretion frequently observed in the presence of prolonged decreased pregnandiol excretion must hence indicate that the fetus can compensate for placental insufficiency. In the placenta this can be demonstrated by hyperplasia of the capillaries. This is reflected in the undulating excretion of pregnandiol (Fig. 1), where compensation (new vessel formation) and depression (lesion of vessels) make these contradictory placental processes "visible". The functional unity of the fetus and the placenta is finally also demonstrated by the fact that each prolonged compensatory phase of the placenta is reponded to by the fetus with a clearly compensatory excretion of estrogen (Fig. 1)...
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keywords = placental insufficiency, insufficiency
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6/15. placental insufficiency as a possible cause of low maternal serum human chorionic gonadotropin and low maternal serum unconjugated estriol levels in triploidy.

    We report three cases in which triploidy (69,XXX) was detected by amniocentesis performed for very low maternal serum human chorionic gonadotropin levels. All three cases also had low maternal serum unconjugated estriol levels. We suggest placental insufficiency as the cause of the very low human chorionic gonadotropin because of histologic observations and because a known marker for placental insufficiency, estriol, was also very low.
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ranking = 2.0000516343491
keywords = placental insufficiency, insufficiency
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7/15. The dehydroepiandrosterone loading test. III. A possible placental function test.

    The dehydroepiandrosterone loading test (DLT) has been used in a small population of normal and high-risk obstetric patients, to date, in an attempt to develop a dynamic test of placental function. In spite of its limited applications, it has shown reliability in discriminating, with statistical significance, between high-risk pregnancies that result in normally grown, undistressed infants, and high-risk pregnancies that result in infants showing signs of placental insufficiency. The present report expands the study population by presenting our data on 40 loading tests performed in 37 high-risk and normal obstetric patients. Results of 19 of these DLT's have been previously reported and are included herein for statistical analysis. The DLT utilizes an excess substrate load of dehydroepiandrosterone to assess the maximum capability of the placenta to convert it to estrogen. Although our previous report did not show false positive or negative results in the conversion rates, the present results (40 DLT's) found two (2 out of 17) false positives (12%) and two (2 out of 19) false negatives (11%). The highly significant correlation between DLT result and pregnancy outcome seen previously was preserved. In addition, the data of another five DLT's in four patients are presented. This group includes a pregnancy with a fetus with multiple congenital malformations, two patients with intrauterine fetal death, and a nonpregnant woman. The results are not included in the statistical analysis, but discussion of these results has interesting pathophysiologic implications.
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ranking = 1
keywords = placental insufficiency, insufficiency
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8/15. Intrauterine growth retardation associated with chromosomal aneuploidy confined to the placenta. Three observations: triple trisomy 6,21,22; trisomy 16; and trisomy 18.

    cytogenetic analysis in three pregnancies revealed chromosomal mosaicism confined to chorionic villi. They were ascertained in the third trimester by intrauterine growth retardation (IUGR) in otherwise normal fetuses. In case of triple trisomy 6,21,22 and trisomy 16, it was obvious that these findings were most likely restricted to the placenta. These trisomies act as early lethal factors when they occur in the embryo itself. With trisomy 18, however, the interpretation of the cytogenetic finding remains ambiguous. The question arises as to whether an abnormal karyotype may be the cause of placenta insufficiency or is just coincidentally associated.
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ranking = 1.2908587276458E-5
keywords = insufficiency
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9/15. Pregnancy in a patient with Raynaud's disease.

    We report a patient who, at the time of her third pregnancy at the age of 35, had had Raynaud's disease for 18 years. Her first pregnancy (during which she took Marcumar, an anticoagulant) ended in a miscarriage at three months gestation. The second pregnancy ended in fetal death due to placental insufficiency. The third pregnancy was also complicated by placental insufficiency which became evident during the second trimester. The patient was observed carefully and allowed to continue to 37 weeks gestation when a Caesarean section was done for late fetal heart rate decelerations during early labour of spontaneous onset. The baby had a low birth weight but developed normally. The placenta showed certain abnormalities which are described.
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ranking = 2
keywords = placental insufficiency, insufficiency
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10/15. Incorrect diagnosis of placental insufficiency in a patient with pre-eclampsia.

    A case of pre-eclampsia is described where suspicion of placental insufficiency arose due to low estriol levels and a positive oxytocin challenge test (OCT). The cause, however, of these findings was later proven to be strictly fetal. It is concluded that low estriol levels and a positive OCT may be caused by a decreased placental capacity but specific tests of placental function, as for instance estimations of HPL in plasma and/or a DHAS-test, should be used to verify or rule out a suspicion of placental insufficiency.
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ranking = 6
keywords = placental insufficiency, insufficiency
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