Placenta and maternal endothelium during preeclampsia: Disruption of the glycocalyx explains increased inositol phosphoglycans and angiogenic factors in maternal blood.

The etiology of the pregnancy syndrome preeclampsia is still unclear, while most hypotheses center on the placenta as the major contributor of the syndrome. Especially changes of the placental metabolism, including the use of glucose to produce energy, are important features. As an example, inositol phosphoglycan P-type molecules, second messengers involved in the glucose metabolism of all cells, can be retrieved from maternal urine of preeclamptic women, even before the onset of clinical symptoms. Alterations in the placental metabolism may subsequently lead to negative effects on the plasma membrane of the placental syncytiotrophoblast. This in turn may have deleterious effects on the glycocalyx of this layer and a disruption of this layer in all types of preeclampsia. The interruption of the glycocalyx in preeclampsia may result in changes of inositol phosphoglycan P-type signaling pathways and the release of these molecules as well as the release of soluble receptors such as sFlt-1 and sEndoglin. The release of placental factors later affects the maternal endothelium and disrupts the endothelial glycocalyx as well. This in turn may pave the way for edema, endothelial dysfunction, coagulation, all typical symptoms of preeclampsia.

Practical approach to transfusion management of post-partum haemorrhage.

OBJECTIVES: To describe transfusion management during post-partum haemorrhage (PPH) and the usefulness of standard or point-of-care (POC) laboratory tests for guiding haemostatic management. BACKGROUND: PPH is the leading cause of maternal mortality and severe maternal morbidity worldwide. Despite the efforts made in recent years, PPH is often burdened by preventable death. Recent data from the active Italian Obstetric Surveillance System (ItOSS) highlighted the following main critical issues: inadequate communication between healthcare professionals, inability to correctly and promptly assess the severity of haemorrhage, delays in diagnosis and treatment, failure to request blood promptly and inappropriate monitoring post-partum. MATERIALS AND METHODS: Data in the literature have been compared with the rotational thromboelastometry (ROTEM)- and the thromboelastography (TEG)-guided algorithms applied in the authors' departments. RESULTS: PPH transfusion therapy may have an empirical approach based on the standard use of blood products or a targeted approach based on coagulation monitoring by laboratory or POC tests. Here, the authors describe how they manage PPH in their departments, according to the Italian guidelines, along with the addition of a ROTEM- and a TEG-guided algorithms developed by themselves. CONCLUSION: Although the proposed algorithms have not been validated by trials or observational studies conducted in our departments, we believe that these indications could be useful for supporting clinical practice. Furthermore, we deem it appropriate to emphasise the importance of a multidisciplinary approach and the need for standardised and shared protocols to support the decisions of healthcare professionals.