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Kohli, S., et al. “Maternal Extracellular Vesicles and Platelets Promote Preeclampsia via Inflammasome Activation in Trophoblasts.” Blood, vol. 128, no. 17, Feb. 2016, pp. 2153-2164.

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Article

Unusual Case of Acute Pulmonary Edema as a Manifestation of Postpartum Preeclampsia: A Case Report

1Department of Internal Medicine, Cone Health Teaching Affiliate UNC Chapel Hill Medical Center


American Journal of Medical Case Reports. 2020, Vol. 8 No. 7, 185-186
DOI: 10.12691/ajmcr-8-7-6
Copyright © 2020 Science and Education Publishing

Cite this paper:
Obed Agyei, James Granfortuna, Lawrence Klima. Unusual Case of Acute Pulmonary Edema as a Manifestation of Postpartum Preeclampsia: A Case Report. American Journal of Medical Case Reports. 2020; 8(7):185-186. doi: 10.12691/ajmcr-8-7-6.

Correspondence to: Obed  Agyei, Department of Internal Medicine, Cone Health Teaching Affiliate UNC Chapel Hill Medical Center. Email: okagyei33@gmail.com

Abstract

Background: Hypertensive disease of pregnancy remains a leading cause of maternal morbidity and mortality. Four subcategories of hypertensive disorders of pregnancy are recognized by the international society for the study of hypertension in pregnancy: chronic hypertension; gestational hypertension, pre-eclampsia, & white coat hypertension. Pre-eclampsia is defined as systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 on two occasions at least 4 hours apart after 20 weeks of gestation with accompanying signs of end organ damage in a woman with previously normal blood pressure. The majority of cases present ante-partum or immediately post-partum. I review the case of a woman diagnosed with pre-eclampsia at 2 weeks post-partum. Case presentation: A 38-year-old woman presented with increasing dyspnea, orthopnea, intermittent palpitations, and central chest pain 2 weeks after an uncomplicated vaginal delivery. On arrival, she was hypertensive at 168/117, spO2 of 100% on BiPAP. Exam was notable for diffuse rales, a regular rhythm, no JVD, and 1+ peripheral edema. Urine was positive for hemoglobin and protein and the liver panel revealed transaminitis (AST=50 ALT=53), Chest X-ray demonstrated increased pulmonary vasculature congestion, confirmed on CT angiography which was negative for venous thromboembolism. Echocardiography found a preserved ejection fraction without diastolic dysfunction or valvular abnormalities. She was managed with a nitroglycerin infusion and parenteral diuresis with resolution of her pulmonary edema. Conclusion: Pre-eclampsia affects 4-9% of all pregnancies and confers a high risk for both fetal and maternal morbidity and mortality. The definitive treatment for preeclampsia is delivery of fetus and placenta but there is limited information to guide the management of post-partum pre-eclampsia. It has been hypothesized that activation of maternal platelets in the placental bed play a role in preeclampsia through activation of inflammasomes such as sFlt-1. Yes, further research is needed to explore the benefit of suppressing these inflammasomes. Although peri-partum cardiomyopathy and venous thromboembolism usually come to mind in women with cardio-pulmonary complaints post-partum. In the appropriate setting, post-partum pre-eclampsia should also be entertained in the differential.

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