Postpartum pre-eclampsia

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Özet

Pre-eclampsia occurs only in humans during the second half of pregnancy or the postpartum period. It is known to be featured by the development of arterial hypertension and multiple organ failure. The main role of the placental lesions in the pathogenetic scenario was shown. The high level of perinatal pathology is a reason for the continual search in the field. Almost a third of eclampsia occurs in the postpartum period. The pre-eclamptic patients require thorough monitoring of blood pressure and administration of antihypertensive drugs in the puerperium. The pathogenesis and the management of the developed de novo postpartum pre-eclampsia have not been sufficiently studied. The greatest risk of brain stroke after delivery remains for 10 days. It is very important to start the antihypertensives in time. "First-line" drugs should be used not later than 30-60 minutes from the time of severe pre-eclampsia diagnosing to prevent intracranial hemorrhage. Labetalol or hydralazine should be used to reduce blood pressure. Sublingual administration of nifedipine may also be considered as "first-line" therapy. The use of magnesium sulfate is necessary for the prevention of seizures in patients with severe pre-eclampsia. In the case of eclampsia, a solution of magnesium sulfate is being administered intravenously at a loading dose of 4-5g for 15-20 minutes and then the infusion is being continued at a dose of 1 g per hour throughout the day. Uterine curettage is also a possible intervention for reducing blood pressure in women with preeclampsia. The clinical case of a systemic inflammatory response syndrome that occurred in a postpartum woman with mild pre-eclampsia is given. Postpartum endometritis, which was caused by group B streptococcus, should have played a triggering role in the progression of preeclampsia. The problem of poly chemical resistance has led to the inability of traditional antimicrobial agents to prevent the dissemination of infection after curettage. The systemic inflammatory response syndrome has contributed to the increased severity of preeclampsia and the development of multiple organ failure. © 2021 Nova Science Publishers, Inc.

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AlanDeğerDil
dc.contributor.authorLakhno, Igor
dc.contributor.authorUzel, Kemine
dc.date.accessioned2026-10-18T20:28:02.198068392Z
dc.date.available2026-10-18T20:28:02.198068392Z
dc.date.issued2021
dc.description.abstractPre-eclampsia occurs only in humans during the second half of pregnancy or the postpartum period. It is known to be featured by the development of arterial hypertension and multiple organ failure. The main role of the placental lesions in the pathogenetic scenario was shown. The high level of perinatal pathology is a reason for the continual search in the field. Almost a third of eclampsia occurs in the postpartum period. The pre-eclamptic patients require thorough monitoring of blood pressure and administration of antihypertensive drugs in the puerperium. The pathogenesis and the management of the developed de novo postpartum pre-eclampsia have not been sufficiently studied. The greatest risk of brain stroke after delivery remains for 10 days. It is very important to start the antihypertensives in time. "First-line" drugs should be used not later than 30-60 minutes from the time of severe pre-eclampsia diagnosing to prevent intracranial hemorrhage. Labetalol or hydralazine should be used to reduce blood pressure. Sublingual administration of nifedipine may also be considered as "first-line" therapy. The use of magnesium sulfate is necessary for the prevention of seizures in patients with severe pre-eclampsia. In the case of eclampsia, a solution of magnesium sulfate is being administered intravenously at a loading dose of 4-5g for 15-20 minutes and then the infusion is being continued at a dose of 1 g per hour throughout the day. Uterine curettage is also a possible intervention for reducing blood pressure in women with preeclampsia. The clinical case of a systemic inflammatory response syndrome that occurred in a postpartum woman with mild pre-eclampsia is given. Postpartum endometritis, which was caused by group B streptococcus, should have played a triggering role in the progression of preeclampsia. The problem of poly chemical resistance has led to the inability of traditional antimicrobial agents to prevent the dissemination of infection after curettage. The systemic inflammatory response syndrome has contributed to the increased severity of preeclampsia and the development of multiple organ failure. © 2021 Nova Science Publishers, Inc.
dc.identifier.endpage127
dc.identifier.isbn978-153619674-0; 978-153619574-3
dc.identifier.scopus2-s2.0-85109466813
dc.identifier.startpage115
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/13196
dc.language.isoen
dc.publisherNova Science Publishers, Inc.
dc.relation.ispartofEclampsia: Prevalence, Risk Factors and Complications
dc.rightsinfo:eu-repo/semantics/openAccess
dc.titlePostpartum pre-eclampsia
dc.typeBook Chapter
dspace.entity.typePublication
rdl.citation.scopus0
rdl.source.indexSCOPUS