PubMed · 6756754
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J Lawson. 1982. Eclampsia.. https://pubmed.ncbi.nlm.nih.gov/6756754/
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We report a case of splenic rupture after cesarean delivery for abruptio placentae. The diagnosis was not suspected until a laparotomy was performed. Diagnosis and management were complicated by disseminated intravascular coagulation and renal failure. The importance of early diagnosis and management modalities are discussed.
OBJECTIVE: Our purpose was to study the incidence and location of histologic evidence of intrauterine bleeding in preterm and term placentas. STUDY DESIGN: A total of 462 consecutive placentas delivered at < 32 weeks' gestation, from which cases of placenta previa, stillbirth, and multiple gestation were excluded, were compared with 108 consecutive term placentas (with similar exclusion criteria) in regard to the presence of hemosiderin in decidua of basal plate or placental membranes. Of the 462 preterm cases, 448 charts made specific reference to the presence or absence of vaginal bleeding. Bloody show alone was not considered bleeding. The blinded scoring of lesions (including acute ascending infection, uteroplacental vascular pathologic processes and related ischemic damage, chronic inflammation, and coagulation related lesions) was analyzed by contingency tables (p < 0.05 significant). RESULTS: A total of 196 of 462 (43%) preterm placentas had any decidual hemosiderin compared with one of 108 (0.8%) at term (p < 0.00001). Among the preterm cases, hemosiderin was significantly more common in preeclampsia (45/76, 60%) and in cases clinically diagnosed as nonhypertensive abruptio placentae (21/33, 64%) than in premature membrane rupture (72/192, 37.5%) and preterm labor (58/161, 36%, p < 0.003). The incidence of placental lesions in preterm cases with extraplacental membrane hemosiderin was not different than it was in cases without hemosiderin. Placental lesions related to basal-plate decidual hemosiderin in the preterm cases were villous infarct (p < 0.0001), uteroplacental vessels with absence of physiologic change (p < 0.003) and increased numbers of circulating nucleated erythrocytes (p < 0.0007), uteroplacental thrombosis (p < 0.0001), and villous fibrosis (p < 0.0001) and hypovascularity (p < 0.0001). Among the preterm cases, 23 of 48 (48%) with first-trimester bleeding, 33 of 66 (50%) with second-trimester bleeding, and 31 of 64 (48%) with multiple episodes of bleeding had decidual hemosiderin (p < 0.0001). A clinical history of gestational bleeding was significantly less common in cases of preterm preeclampsia with histologic evidence of bleeding (four of 73, 5.5%) than in nonhypertensive abruptio placentae (18/31, 58%), premature rupture of membranes (52/183, 28%), or preterm labor (31/161, 19%, p < 0.0001). Hemosiderin was not related to clinical bleeding < 72 hours of delivery (p > 0.20). CONCLUSIONS: Decidual bleeding is common in all clinical types of preterm birth and is most common in preterm preeclampsia and nonhypertensive abruption placentae. A clinical history of bleeding is not correlated with the presence of decidual hemosiderin. Bleeding in the basal plate is related to histologic evidence of chronic uteroplacental vascular pathologic processes, which in cases of spontaneous prematurity (premature rupture of membranes, preterm labor, nonhypertensive abruptio placentae) may be associated with decidual bleeding which occasionally may be clinically manifested as gestational bleeding.
Retinal detachment is a rare complication of preeclampsia, eclampsia and abruptio placentae. We report a case of bilateral retinal detachment in association with severe preeclampsia complicated with abruptio placentae, intrauterine fetal death and disseminated intravascular coagulation. In obstetric complications, placental thromboplastin may release into maternal circulation and activate the extrinsic coagulation system with resultant disseminated intravascular coagulation. This may be responsible for choroidal ischemia and consequent serous retinal detachment.