Home About us Contact | |||
Fetal Infection (fetal + infection)
Selected AbstractsSinusoidal heart rate pattern: Reappraisal of its definition and clinical significanceJOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 3 2004Houchang D. Modanlou Abstract Objectives: To address the clinical significance of sinusoidal heart rate (SHR) pattern and review its occurrence, define its characteristics, and explain its physiopathology. Background: In 1972, Manseau et al. and Kubli et al. described an undulating wave form alternating with a flat or smooth baseline fetal heart rate (FHR) in severely affected, Rh-sensitized and dying fetuses. This FHR pattern was called ,sinusoidal' because of its sine waveform. Subsequently, Modanlou et al. described SHR pattern associated with fetal to maternal hemorrhage causing severe fetal anemia and hydrops fetalis. Both Manseau et al. and Kubli et al. stated that this particular FHR pattern, whatever its pathogenesis, was an extremely significant finding that implied severe fetal jeopardy and impending fetal death. Undulating FHR pattern: Undulating FHR pattern may be due to the following: (1) true SHR pattern; (2) drugs; (3) pre-mortem FHR pattern; (4) pseudo-SHR pattern; and (5) equivocal FHR patterns. Fetal conditions associated with SHR pattern: SHR pattern has been reported with the following fetal conditions: (1) severe fetal anemia of several etiologies; (2) effects of drugs, particularly narcotics; (3) fetal asphyxia/hypoxia; (4) fetal infection; (5) fetal cardiac anomalies; (6) fetal sleep cycles; and (7) sucking and rhythmic movements of fetal mouth. Definition of true SHR pattern: Modanlou and Freeman proposed the following definition for the interpretation of true SHR pattern: (a) stable baseline FHR of 120,160 bpm; (b) amplitude of 5,15 bpm, rarely greater; (c) frequency of 2,5 cycles per minute; (d) fixed or flat short-term variability; (e) oscillation of the sinusoidal wave from above and below a baseline; and (f) no areas of normal FHR variability or reactivity. Physiopathology: Since its early recognition, the physiopathology of SHR became a matter of debate. Murata et al. noted a rise of arginine vasopressin levels in the blood of posthemorrhagic/anemic fetal lamb. Further works by the same authors revealed that with chemical or surgical vagotomy, arginine vasopressin infusion produced SHR pattern, thus providing the role of autonomic nervous system dysfunction combined with the increase in arginine vasopressin as the etiology. Conclusion: SHR is a rare occurrence. A true SHR is an ominous sign of fetal jeopardy needing immediate intervention. The correct diagnosis of true SHR pattern should also include fetal biophysical profile and the absence of drugs such as narcotics. [source] Fetal Endothelial Cells Express Vascular Cell Adhesion Molecule in the Setting of ChorioamnionitisAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2000CATHERINE M. CRAVEN PROBLEM: In intrauterine infection, inflammatory mediators may be released into the fetal circulation prior to fetal infection. We hypothesize that, in chorioamnionitis, inflammation alters fetal blood vessels. To test this, fetal endothelial cells were examined for vascular cell adhesion molecule (VCAM). METHOD OF STUDY: Umbilical cords (n=9) from placentas with chorioamnionitis were immunostained for VCAM. Controls from preterm preeclamptic pregnancies (n=7) without histologic inflammation were selected, and matched for gestational age and method of delivery. VCAM sections were reviewed by a pathologist blinded to clinical diagnoses. RESULTS: All endothelial cells from each of the nine cords from placentas with chorioamnionitis had strong VCAM staining. Two of nine samples also had acute cord vasculitis. No cord endothelial cells from preeclamptic placentas demonstrated similar VCAM staining (p<0.01). CONCLUSION: Histologic chorioamnionitis was associated with VCAM expression of the umbilical cord vessels. In chorioamnionitis, inflammatory mediators may have entered the fetal circulation to activate endothelial cells. Intrauterine inflammation was not restricted to the chorioamnion, but also involved the fetal circulation. [source] Recombinant proteins in the diagnosis of toxoplasmosisAPMIS, Issue 8 2010DUPADAHALLI KOTRESHA Kotresha D, Rahmah N. Recombinant proteins in the diagnosis of toxoplasmosis. APMIS 2010; 118: 529,42. Toxoplasma gondii is an important human pathogen with a worldwide distribution. It is primarily of medical importance for pregnant women and immunocompromised patients. Primary infection of the former is often associated with fetal infection, which can lead to abortion or severe neonatal malformation. Immunocompromised patients are at risk of contracting the severe form of the disease that may be fatal. Thus, detection of T. gondii infection with high sensitivity and specificity is crucial in the management of the disease. Toxoplasmosis is generally diagnosed by demonstrating specific immunoglobulin M (IgM) and IgG antibodies to toxoplasma antigens in the patient's serum sample. Most of the commercially available tests use T. gondii native antigens and display wide variations in test accuracy. Recombinant antigens have great potential as diagnostic reagents for use in assays to detect toxoplasmosis. Thus in this review, we address recent advances in the use of Toxoplasma recombinant proteins for serodiagnosis of toxoplasmosis. [source] Fetal extrasystole may predict poor neonatal outcomeAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 4 2009Jake A. BROWN Extrasystoles particularly premature atrial contractions noted during labour on the fetal heart rate monitoring strip are usually thought to be benign. In pregnancies complicated by fetal infection and/or the fetal inflammatory response syndrome, there are some data that extrasystoles noted during the intrapartum period may be related to neonatal sepsis and eventual poor neonatal outcome including death or neonatal encephalopathy. Additional observations are needed to substantiate this hypothesis. [source] |