Cases reported "placental insufficiency"

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1/25. 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. ( info)

2/25. 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. ( info)

3/25. 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. ( info)

4/25. Clinical experience with the oxytocin challenge test. II. An ominous atypical pattern.

    Three cases have been observed over the past 3 years at los angeles County-USC Medical Center, women's Hospital, which have shown an unusual fetal heart rate response to induced uterine contractions during the antepartum period. All 3 cases resulted in perinatal death apparently due to asphyxia. This report describes this unusual pattern and presents a discussion of its possible significance. ( info)

5/25. 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. ( info)

6/25. Rapid onset of severe twin-twin transfusion syndrome caused by placental venous thrombosis.

    We report a case of rapid onset of severe twin-twin transfusion syndrome (TTTS) at 25 weeks gestation in a monochorionic twin pregnancy that was uneventful before that time. Thrombosis of a main venous branch draining several arteriovenous (AV) anastomoses to the donor changed the previous hemodynamic balance that existed between multiple bidirectional AV anastomoses. The opposing AVs became hemodynamically uncompensated and, despite amnioreductions, severe TTTS developed. At 27 weeks a cesarean section was performed because of worsening cardiotocography parameters of both fetuses. Birth weights were 750 and 1840 g, and initial hemoglobin concentrations were 9.2 and 13.4 mmol/liter for donor and recipient, respectively. The recipient twin died 5 months later of an ischemic, necrotic, and perforated small intestine due to a thrombosed superior mesenteric artery. The donor is well at 2.5 years. No abnormalities in several factors associated with thrombophilia, including factor v Leiden mutations, were found in the parents. ( info)

7/25. 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)... ( info)

8/25. thrombophilia, preeclampsia, and fetal demise: a case report.

    A patient with thrombophilia, preeclampsia, and fetal demise who was taking low molecular weight heparin, was managed with epidural analgesia for labor and delivery of the fetus. The anesthetic considerations and medical concerns in such patients are discussed. ( info)

9/25. oxytocin challenge test in high-risk pregnancy.

    Seven hundred sixty-seven oxytocin challenge tests (OCT) were performed on 333 high-risk maternity patients. All of the patients had pregnancies complicated by diabetes mellitus, suspected postmaturity, preeclampsia, intrauterine growth retardation, hypertension and other disorders. In conjunction with OCT, 24-hour urinary estriol determinations were performed. Negative OCT's were reassuring for fetal well-being. There were 26 positive OCT's on 24 patients. A positive test was significant in identifying endangered fetuses existing in a markedly unfavorable environment. In our experience, we found the OCT more reliable and more predictable than urinary estriol determination. The oxytocin challenge test proved to be significant in the successful management of these 333 high-risk patients. ( info)

10/25. Fetal and neonatal neurologic case histories: assessment of brain disorders in the context of fetal-maternal-placental disease. Part 1: Fetal neurologic consultations in the context of antepartum events and prenatal brain development.

    The pediatric neurologist can contribute to a fetal diagnostic service that includes the maternal-fetal specialist as well as placental and pediatric pathologists, neonatologists, neurosurgeons, geneticists, and other pediatric subspecialists. Selected case histories of patients who presented to our fetal neurology service illustrate the wide spectrum of disease entities that are highly dependent on the time during gestation, location of brain injury, and the direct as well as indirect effects of fetal/maternal/placental disease processes on brain maturation. The pediatric neurologist has the opportunity to provide an important consultative role, bridging prenatal to neonatal life and integrating medical and ethical concerns for the child in the context of the family. ( info)
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