Maternal morbidity in postpartum severe preeclampsia by obstetric delivery volume.

BACKGROUND: Pre-eclampsia is a leading cause of maternal morbidity and mortality in the United States. Emerging data suggests that postpartum pre-eclampsia may be associated with a higher incidence of maternal morbidity compared to hypertensive disorders of pregnancy (HDP) diagnosed antenatally. Understanding postpartum maternal risk across facilities with a spectrum of obstetric services is critical with the rising rates of pre-eclampsia in all healthcare settings. OBJECTIVES: We investigated the relationship between facility delivery volume and rates of non-transfusion severe maternal morbidity (SMM) among patients readmitted postpartum for pre-eclampsia with severe features. STUDY DESIGN: This is a retrospective cohort study using the Nationwide Readmissions Database (2015-2019) of postpartum patients readmitted for pre-eclampsia with severe features. Our primary outcome was non-transfusion SMM during readmission, defined per U.S. Centers for Disease Control and Prevention criteria. We also evaluated SMM, cardiac SMM, and individual morbidities. The exposure variable was the number of annual deliveries at the readmitting facility. Restricted cubic splines with 4 knots were used to assess the functional form of the relationship between obstetric delivery volume and non-transfusion SMM; a linear relationship was identified as optimal. Logistic regression was used to estimate adjusted odds ratios (aOR) which controlled for maternal age, non-transfusion SMM at delivery, expanded obstetric comorbidity index, and HDP during delivery. RESULTS: The cohort included 29,472 patients readmitted with postpartum pre-eclampsia with severe features. The primary payer was 55% private and 42% governmental. Median age was 31.4 years. Most patients did not have prior HDP (65%) or chronic hypertension (86%) diagnosis antenatally. The median interval from delivery hospitalization to readmission was 3.9 days (25th percentile-75th percentile: 2.2-6.5). Non-transfusion SMM occurred in 7% of patients readmitted to facilities with >2,000 deliveries compared to 9% with 1-2,000 deliveries, and 52% without any delivery hospitalizations. The most common SMM was pulmonary edema and heart failure, observed in 4% of readmissions. We observed that for every increase in 1,000 deliveries, the odds of a non-transfusion SMM at readmission decreased by 3.5% (aOR: 0.965; 95% confidence interval: 0.94, 0.99) CONCLUSIONS: Non-transfusion SMM for postpartum readmissions with pre-eclampsia with severe features was inversely associated with readmitting hospital delivery volume. This information may guide risk-reducing initiatives for identifying strategies to optimize postpartum care at facilities with lower or no delivery volume.

Risk factors for readmission with preeclampsia: a call for more preventative surveillance and counseling.

BACKGROUND: Postpartum readmission for preeclampsia is a difficult predicament for patients which creates financial, psychosocial, and physical stress. It is often a challenge to predict postpartum preeclampsia and therefore identify patients that may be at risk prior to discharge. This study aims to identify risk factors in patients that are at high risk for readmission due to preeclampsia. The identification of these risk factors may also lead to enhanced education and counseling prior to discharge. METHODS: Researchers conducted a case-control study using a data set collected from 2015 to 2022 looking at obstetric readmissions within 6 weeks of delivery and then stratified these patients for preeclampsia diagnosis. A control set was created within the healthcare system's electronic medical record's search tools for patients diagnosed with preeclampsia who were not readmitted to the hospital. This study evaluates 78 patients who were readmitted with a diagnosis of preeclampsia and compared to 77 patients who were diagnosed with preeclampsia who were not readmitted. Again, the aim of this study was to investigate risk factors for readmission among patients with preeclampsia. RESULTS: A multivariable logistic regression model was used to assess predictors which revealed that older age (OR 1.13, CI 1.03-1.24), no history of preeclampsia with or without severe features within pregnancy before delivery (OR 15.29, CI 5.56-41.98 and 13.58, CI 4.46-12.85), no aspirin use in pregnancy (OR 4.38, CI 2.02-9.48), and number of triage visits related to hypertension during prenatal care were all significant predictors for readmission due to preeclampsia. CONCLUSION: With these risk factors in mind, better counseling and preventative surveillance can be provided to patients. Future studies are needed to evaluate the effectiveness of predictive models developed using these found risk factors.

Predictive biomarkers and initial analysis of maternal immune alterations in postpartum preeclampsia reveal an immune-driven pathology.

Introduction: Postpartum preeclampsia (PPPE) is an under-diagnosed condition, developing within 48 hours to 6 weeks following an uncomplicated pregnancy. The etiology of PPPE is still unknown, leaving patients vulnerable and making the identification and treatment of patients requiring postpartum care an unmet need. We aimed to understand the immune contribution to PPPE at the time of diagnosis, as well as uncover the predictive potential of perinatal biomarkers for the early postnatal identification of high-risk patients. Methods: Placentas were collected at delivery from uncomplicated pregnancies (CTL) and PPPE patients for immunohistochemistry analysis. In this initial study, blood samples in PPPE patients were collected at the time of PPPE diagnosis (48h-25 days postpartum; mean 7.4 days) and compared to CTL blood samples taken 24h after delivery. Single-cell transcriptomics, flow cytometry, intracellular cytokine staining, and the circulating levels of inflammatory mediators were evaluated in the blood. Results: Placental CD163+ cells and 1st trimester blood pressures can be valuable non-invasive and predictive biomarkers of PPPE with strong clinical application prospects. Furthermore, changes in immune cell populations, as well as cytokine production by CD14+, CD4+, and CD8+ cells, suggested a dampened response with an exhausted phenotype including decreased IL1ß, IL12, and IFNγ as well as elevated IL10. Discussion: Understanding maternal immune changes at the time of diagnosis and prenatally within the placenta in our sizable cohort will serve as groundwork for pre-clinical and clinical research, as well as guiding clinical practice for example in the development of immune-targeted therapies, and early postnatal identification of patients who would benefit from more thorough follow-ups and risk education in the weeks following an uncomplicated pregnancy.

Clinical Analysis of Postpartum Preeclampsia After an Uncomplicated Pregnancy.

Preeclampsia is a rare complication of pregnancy and can cause maternal death. This case report serves to increase awareness of the range and severity of symptoms in postpartum preeclampsia and highlights a stepwise approach to provide prompt management. The cause of preeclampsia is not fully understood but is correlated with many placental and maternal factors. Preeclampsia typically resolves with delivery, and it is uncommon to have symptoms in the postpartum period. Due to the rarity of the disease, it is not typically at the top of a differential list for postpartum women. A 35-year-old first-time mother presents with shortness of breath, tightness in her chest, and mild pulmonary edema. A series of chest X-rays, computed tomographic angiogram of the chest, and serial labs reveal she has postpartum preeclampsia. Many pre-eclamptic symptoms are common to a variety of conditions leading to an extensive list of differential diagnoses. Used in a stepwise fashion, clinical analysis allows physicians to accurately diagnose postpartum preeclampsia and provide lifesaving treatment for these mothers. This study highlights the need for vigilance in symptom analysis and diagnostic testing.

Posterior Reversible Encephalopathy Syndrome in a Late Postpartum Patient With a Rare Complication of Subarachnoid Hemorrhage.

Posterior reversible encephalopathy syndrome (PRES) is considered a neuroclinical syndrome of headache, confusion, visual changes, and seizures associated with neuroimaging findings of posterior cerebral white matter edema. Although the incidence of the syndrome is largely unknown, this condition is becoming increasingly recognized. The prognosis is generally good with most symptoms resolving within one week and lesions on imaging resolving in two weeks. Death and significant neurological disability have been reported but are relatively rare. In this report, we present a 10-day postpartum patient with an atypical history of headache and seizure-like activity. Neuroimaging revealed findings consistent with PRES as well as a rare complication of subarachnoid hemorrhage. This case highlights the importance of clinicians considering preeclampsia/eclampsia-induced PRES when encountering a postpartum patient with headache and hypertension to further reduce morbidity and mortality in this patient population.

Effectiveness of extended postpartum inpatient monitoring for hypertensive disorders of pregnancy to reduce the risk of readmission for preeclampsia with severe features.

BACKGROUND: Preeclampsia is an obstetrical disorder, which complicates 3% to 6% of pregnancies and contributes to 21.6% of readmissions in the postpartum period. The optimal strategy for inpatient monitoring of blood pressures to minimize readmissions for postpartum patients with hypertensive disorders is not known. We hypothesized that extended monitoring of postpartum patients with hypertensive disorders of pregnancy for at least 36 hours after the last blood pressure that was ≥150/100 mm Hg would result in decreased readmission rates for preeclampsia with severe features compared with those who were not observed by these blood pressure goals. OBJECTIVE: This study aimed to evaluate whether extended inpatient monitoring of postpartum patients with hypertensive disorders of pregnancy for at least 36 hours after their last blood pressure that was ≥150/100 mm Hg would improve readmission rates for preeclampsia with severe features within 6 weeks of delivery. STUDY DESIGN: This was a retrospective cohort study in patients with a singleton pregnancy and a diagnosis of a hypertensive disorder of pregnancy at their delivery admission or at any point during pregnancy who delivered 1 year before and 1 year after the implementation of extended inpatient monitoring of postpartum hypertension. The primary outcome was readmission for preeclampsia with severe features within 6 weeks of delivery. The secondary outcomes were length of stay during first admission, number of readmissions for any indication, intensive care unit admission, postpartum day at readmission, median systolic blood pressure in the 24-hour period before discharge, median diastolic blood pressure in the 24-hour period before discharge, intravenous antihypertensive medication required during first admission, and intravenous antihypertensive medication required during second admission. Univariable analysis was performed for the association between baseline maternal characteristics and the primary outcome. Multivariable analysis was performed, adjusting for baseline maternal characteristic differences between exposure groups. RESULTS: A total of 567 patients met the inclusion criteria of which 248 patients delivered before and 319 delivered after the implementation of extended monitoring. For baseline characteristics, the extended monitoring group had a significantly higher proportion of patients who were non-Hispanic Black and Hispanic, more diagnoses of hypertensive disorders and/or diabetes mellitus at the time of admission for delivery, a difference in the distribution of hypertensive diagnoses at the time of discharge from the first admission, and fewer discharged patients from their first admission on labetalol than the preintervention group. In a univariable analysis of the primary outcome, there was a significantly increased risk of readmission for preeclampsia with severe features in the extended monitoring group (62.5% vs 96.2% of total readmissions; P=.004). In multivariable analysis, patients in the extended monitoring group were more likely to be readmitted for preeclampsia with severe features than patients in the preintervention group (adjusted odds ratio, 3.45; 95% confidence interval, 1.03-11.5; P=.044). CONCLUSION: Extended monitoring with a strict blood pressure goal of <150/<100 mm Hg did not decrease readmissions for preeclampsia with severe features in patients with a previous diagnosis of a hypertensive disorder of pregnancy.

Changes in maternal heart rate in delayed post-partum preeclampsia.

AIM: Delayed-onset postpartum preeclampsia (PET) is defined as a new diagnosis of preeclampsia presenting 48 h to 6 weeks postpartum. This disorder is infrequent and associated with a higher incidence of complications as compared to antepartum PET. There seems to be a need to further characterize this disorder. The aim of the study was to investigate the difference of maternal heart rate in women with delayed onset postpartum preeclampsia as compared to healthy controls. METHODS: The medical files of all women who were readmitted with delayed onset postpartum preeclampsia during 2014-2020 were reviewed. Data on maternal physiological characteristics were compared to healthy control group of women at the same post-partum day, with uncomplicated pregnancies. RESULTS: Included 45 women with the diagnosis of delayed onset of preeclampsia at 6.3 ± 2.86 post-partum day. As compared to controls (n = 49), women with delayed post-partum were older, 34.6 ± 5.4 vs. 32.3 ± 4.7 years, p = 0.003. There were no differences between groups regarding maternal gravidity, parity, BMI (kg/m2) or Hb level at delivery day. Women with delayed post-partum preeclampsia had lower mean pulse rate as compared to controls, 58 ± 15 bpm vs. 83 ± 11.6 bpm, respectively, P < 0.0001. Only 17% of the women in the delayed onset group had pulse rate above 70 bpm as compared to 83% in the control group. CONCLUSIONS: Maternal low heart rate in cases with delayed onset of post-partum preeclampsia is an important clinical characteristic that may reflect baroreceptors response to maternal hypertension.

Risk factors for the development of new-onset and persistent postpartum preeclampsia: A case-control study in Ghana.

BACKGROUND: Postpartum preeclampsia has been implicated in increasing hospital re-admissions, maternal morbidity, and mortality worldwide. The knowledge of the risk factors of postpartum preeclampsia would be helpful in formulating strategies to aid in the prevention, early diagnosis, and timely treatment of this disorder. Thus, this study aimed to identify the risk factors associated with the development of new-onset postpartum preeclampsia and persistent postpartum preeclampsia in the Ghanaian setting. METHODS: This case-control study was conducted at the Obstetrics and Gynecology units of Komfo Anokye Teaching Hospital and the Kumasi Regional Hospital, both located in the Ashanti Region of Ghana. A total of 65 postpartum preeclamptic women (33 new-onset postpartum preeclampsia and 32 persistent postpartum preeclampsia) and 65 normotensive postpartum mothers were recruited from 48 h to 6 weeks post-delivery. Questionnaires were administered to assess the socio-demographic, lifestyle, obstetric characteristics, and past medical history of the study participants. RESULTS: Physical inactivity (p < 0.0001), infrequent antenatal visits (p < 0.0001), analgesic use (p < 0.0001), and cesarean delivery (p = 0.021) were significantly associated with both the new-onset postpartum preeclampsia and persistent postpartum preeclampsia. Contraceptive use was significantly associated with the development of new-onset postpartum preeclampsia (p < 0.0001) while women with low-birthweight babies are also at high risk of developing persistent postpartum preeclampsia (p < 0.0001). CONCLUSION: Physical inactivity, infrequent antenatal visits, analgesic use, contraceptive use, and cesarean delivery are major predisposing risk factors for the development of postpartum preeclampsia. Screening using these risk factors, close monitoring and follow-up observation of women after delivery would be beneficial in identifying and managing postpartum preeclampsia.

Postpartum preeclampsia or eclampsia: defining its place and management among the hypertensive disorders of pregnancy.

High blood pressure in the postpartum period is most commonly seen in women with antenatal hypertensive disorders, but it can develop de novo in the postpartum time frame. Whether postpartum preeclampsia or eclampsia represents a separate entity from preeclampsia or eclampsia with antepartum onset is unclear. Although definitions vary, the diagnosis of postpartum preeclampsia should be considered in women with new-onset hypertension 48 hours to 6 weeks after delivery. New-onset postpartum preeclampsia is an understudied disease entity with few evidence-based guidelines to guide diagnosis and management. We propose that new-onset hypertension with the presence of any severe features (including severely elevated blood pressure in women with no history of hypertension) be referred to as postpartum preeclampsia after exclusion of other etiologies to facilitate recognition and timely management. Older maternal age, black race, maternal obesity, and cesarean delivery are all associated with a higher risk of postpartum preeclampsia. Most women with delayed-onset postpartum preeclampsia present within the first 7 to 10 days after delivery, most frequently with neurologic symptoms, typically headache. The cornerstones of treatment include the use of antihypertensive agents, magnesium, and diuresis. Postpartum preeclampsia may be associated with a higher risk of maternal morbidity than preeclampsia with antepartum onset, yet it remains an understudied disease process. Future research should focus on the pathophysiology and specific risk factors. A better understanding is imperative for patient care and counseling and anticipatory guidance before hospital discharge and is important for the reduction of maternal morbidity and mortality in the postpartum period.

Preeclampsia and eclampsia: the conceptual evolution of a syndrome.

Preeclampsia, one of the most enigmatic complications of pregnancy, is considered a pregnancy-specific disorder caused by the placenta and cured only by delivery. This article traces the condition from its origins-once thought to be a disease of the central nervous system, recognized by the occurrence of seizures (ie, eclampsia)-to the present time when preeclampsia is conceptualized primarily as a vascular disorder. We review the epidemiologic data that led to the recommendation to use diastolic hypertension and proteinuria as diagnostic criteria, as their combined presence was associated with an increased risk of fetal death and the birth of small-for-gestational-age neonates. However, preeclampsia is a multisystemic disorder with protean manifestations, and the condition can be present even in the absence of hypertension and proteinuria. Toxins gaining access to the maternal circulation have been proposed to mediate the clinical manifestations-hence, the term "toxemia of pregnancy," which was used for several decades. The search for putative toxins has challenged investigators for more than a century, and a growing body of evidence suggests that products of an ischemic or a stressed placenta are responsible for the vascular changes that characterize this syndrome. The discovery that the placenta can produce antiangiogenic factors, which regulate endothelial cell function and induce intravascular inflammation, has been a major step forward in the understanding of preeclampsia. We view the release of antiangiogenic factors by the placenta as an adaptive response to improve uterine perfusion by modulating endothelial function and maternal cardiovascular performance. However, this homeostatic response can become maladaptive and lead to damage of target organs during pregnancy or the postpartum period. Early-onset preeclampsia has many features in common with atherosclerosis, whereas late-onset preeclampsia seems to result from a mismatch of fetal demands and maternal supply, that is, a metabolic crisis. Preeclampsia, as it is understood today, is essentially vascular dysfunction unmasked or caused by pregnancy. A subset of patients diagnosed with preeclampsia are at greater risk of the subsequent development of hypertension, ischemic heart disease, heart failure, vascular dementia, and end-stage renal disease. However, these adverse events may be the result of a preexisting vascular pathologic process; it is not known if the occurrence of preeclampsia increases the baseline risk. Therefore, the understanding, prediction, prevention, and treatment of preeclampsia are healthcare priorities.

Does race or ethnicity play a role in the origin, pathophysiology, and outcomes of preeclampsia? An expert review of the literature.

The burden of preeclampsia, a substantial contributor to perinatal morbidity and mortality, is not born equally across the population. Although the prevalence of preeclampsia has been reported to be 3% to 5%, racial and ethnic minority groups such as non-Hispanic Black women and American Indian or Alaskan Native women are widely reported to be disproportionately affected by preeclampsia. However, studies that add clarity to the causes of the racial and ethnic differences in preeclampsia are limited. Race is a social construct, is often self-assigned, is variable across settings, and fails to account for subgroups. Studies of the genetic structure of human populations continue to find more variations within racial groups than among them. Efforts to examine the role of race and ethnicity in biomedical research should consider these limitations and not use it as a biological construct. Furthermore, the use of race in decision making in clinical settings may worsen the disparity in health outcomes. Most of the existing data on disparities examine the differences between White and non-Hispanic Black women. Fewer studies have enough sample size to evaluate the outcomes in the Asian, American Indian or Alaskan Native, or mixed-race women. Racial differences are noted in the occurrence, presentation, and short-term and long-term outcomes of preeclampsia. Well-established clinical risk factors for preeclampsia such as obesity, diabetes, and chronic hypertension disproportionately affect non-Hispanic Black, American Indian or Alaskan Native, and Hispanic populations. However, with comparable clinical risk factors for preeclampsia among women of different race or ethnic groups, addressing modifiable risk factors has not been found to have the same protective effect for all women. Abnormalities of placental formation and development, immunologic factors, vascular changes, and inflammation have all been identified as contributing to the pathophysiology of preeclampsia. Few studies have examined race and the pathophysiology of preeclampsia. Despite attempts, a genetic basis for the disease has not been identified. A number of genetic variants, including apolipoprotein L1, have been identified as possible risk modifiers. Few studies have examined race and prevention of preeclampsia. Although low-dose aspirin for the prevention of preeclampsia is recommended by the US Preventive Service Task Force, a population-based study found racial and ethnic differences in preeclampsia recurrence after the implementation of low-dose aspirin supplementation. After implementation, recurrent preeclampsia reduced among Hispanic women (76.4% vs 49.6%; P<.001), but there was no difference in the recurrent preeclampsia in non-Hispanic Black women (13.7 vs 18.1; P=.252). Future research incorporating the National Institute on Minority Health and Health Disparities multilevel framework, specifically examining the role of racism on the burden of the disease, may help in the quest for effective strategies to reduce the disproportionate burden of preeclampsia on a minority population. In this model, a multilevel framework provides a more comprehensive approach and takes into account the influence of behavioral factors, environmental factors, and healthcare systems, not just on the individual.

New-onset postpartum preeclampsia: epigenetic mechanism and prediction.

OBJECTIVE: Placental cytosine (CpG) methylation was measured to predict new-onset postpartum preeclampsia (NOPP) and interrogate its molecular pathogenesis. METHODS: NOPP was defined as patients with a new diagnosis of postpartum preeclampsia developing ≥48 h to ≤6 weeks after delivery with no prior hypertensive disorders. Placental tissue was obtained from 12 NOPP cases and 12 normotensive controls. Genome-wide individual cytosine (CpG) methylation level was measured with the Infinium MethylationEPIC BeadChip array. Significant differential methylation (NOPP vs. controls) for individual CpG loci was defined as false discovery rate (FDR) p value <.05. Gene functional enrichment using Qiagen's ingenuity pathway analysis (IPA) was performed to help elucidate the molecular pathogenesis of NOPP. A logistic regression model for NOPP prediction based on the methylation level in a combination of CpG loci was generated. The area under the receiver operating characteristic curves (AUC [95% CI]) sensitivity, and specificity for NOPP prediction based on the CpG methylation level was calculated for each locus. RESULTS: There were 537 (in 540 separate genes) significantly (FDR p<.05 with a ≥ 2.0-fold methylation difference) differentially methylated CpG loci between the groups. A total of 143 individual CpG markers had excellent individual predictive accuracy for NOPP prediction (AUC ≥0.80), of which 14 markers had outstanding accuracy (AUC ≥0.90). A logistic regression model based on five CpG markers yielded an AUC (95% CI)=0.99 (0.95-0.99) with sensitivity 95% and specificity 93% for NOPP prediction. IPA revealed dysregulation of critical pathways (e.g., angiogenesis, chronic inflammation, and epithelial-mesenchymal transition) known to be linked to classic preeclampsia, in addition to other previously undescribed genes/pathways. CONCLUSIONS: There was significant placental epigenetic dysregulation in NOPP. NOPP shared both common and unique molecular pathways with classic preeclampsia. Finally, we have identified novel potential biomarkers for the early post-partum prediction of NOPP.

Predictors of readmission for postpartum preeclampsia.

Objective: To develop a predictive model for re-admission for postpartum preeclampsia (PPEC).Methods: A case-control study; cases were patients re-admitted for PPEC; controls were not re-admitted. Mixed linear modelling was used to develop a predictive model on the training set, then validated on the validation set.Results: Two-hundred-sixty-nine patients were readmitted, and matched to 538 controls. A risk calculator was developed and yielded a sensitivity and specificity for readmission of 80.9% and 53.5%, respectively.Conclusion: A predictive model using age, race, discharge blood pressures, and preeclampsia was able to predict re-admission for PPEC with a high level of sensitivity.

Factors associated with postpartum readmission for hypertensive disorders of pregnancy.

BACKGROUND: Postpartum readmission has negative implications for patients and health systems. Previous studies suggest that up to 5% of women with hypertensive disorders of pregnancy experience postpartum readmission. Studies examining factors associated with postpartum readmission for hypertension have had small sample sizes and conflicting results. OBJECTIVE: This study aimed to characterize the incidence of and risk factors for postpartum readmission for hypertensive disorders of pregnancy among a cohort of women with preexisting hypertensive disorders of pregnancy. STUDY DESIGN: This was a retrospective cohort study of pregnant women with known hypertensive disorders of pregnancy who delivered live births in a large managed care organization in 2018. The primary outcome was hospital readmission for a hypertensive diagnosis or stroke within 42 days after delivery. The primary exposure of interest was persistent postpartum hypertension, defined as a maximum systolic blood pressure of ≥140 mm Hg or maximum diastolic blood pressure of ≥90 mm Hg within 24 hours before discharge from delivery hospitalization. Continuous and categorical variables were compared using bivariate analysis. Risk factors independently associated with postpartum readmission were identified using multivariable logistic regression. RESULTS: Of 42,022 women who delivered in 2018, 7151 had hypertensive disorders of pregnancy-an incidence of 17%. The rate of postpartum readmission among women with hypertensive disorders of pregnancy was 4.43% (317 of 7151). The following risk factors were associated with increased odds of postpartum readmission in women with hypertensive disorders of pregnancy: systolic blood pressure of ≥140 mm Hg within 24 hours before discharge (adjusted odds ratio, 2.29; 95% confidence interval, 1.71-3.07), diastolic blood pressure of ≥90 mm Hg within 24 hours before discharge (adjusted odds ratio, 1.33; 95% confidence interval, 1.02-1.73), maternal age of ≥30 years (30-34: adjusted odds ratio, 1.57; 95% confidence interval, 1.12-2.19; 35-39: adjusted odds ratio, 2.36; 95% confidence interval, 1.70-3.28; ≥40: adjusted odds ratio, 2.95; 95% confidence interval, 1.95-4.46), receipt of magnesium sulfate (adjusted odds ratio, 1.47; 95% confidence interval, 1.11-1.94), and receipt of inpatient rapid-acting antihypertensive medication (adjusted odds ratio, 1.46; 95% confidence interval, 1.10-1.93). In addition, 1 blood pressure of ≥140/90 mm Hg within 24 hours before discharge increased the odds of readmission (adjusted odds ratio, 1.98; 95% confidence interval, 1.37-2.87). Furthermore, 2 or more elevated blood pressure values further increased the odds (adjusted odds ratio, 3.14; 95% confidence interval, 2.33-4.24). Median postpartum day of readmission was day 5 (interquartile range=3). CONCLUSION: Hospital readmission for postpartum hypertension was associated with persistent postpartum hypertension (blood pressure of ≥140/90 mm Hg), increasing maternal age, and more severe antepartum hypertension. Women with these characteristics may be targeted in future quality initiatives to mitigate readmission.

Epstein-Barr virus-associated hemophagocytic lymphohistiocytosis in a postpartum patient with preeclampsia: a case report.

Hemophagocytic lymphohystiocytosis is an extremely life-threatening immune deregulatory syndrome. It is characterized by pathologic activation of immune cells, leading to excessive cytokine production, multiorgan failure, and potentially, death. A 28-year-old primigravida at 32 weeks and 3 days of gestation presented with newly-diagnosed preeclampsia with severe features, fever, and fetal tachycardia. She was delivered by cesarean delivery. After delivery, she had a fever of unknown origin, with evidence of a hyperinflammatory state. Extensive infectious work-up was significant for positive Epstein-Barr Virus. A bone marrow biopsy demonstrated hemophagocytosis. She was diagnosed with Epstein-Barr-Virus-associated hemophagocytic lymphohystiocytosis and was treated with immunosuppression and chemotherapy. Hemophagocytic lymphohistiocytosis is a rare, life-threatening immune dysregulatory syndrome with both genetic and extragenic triggers that can occur in the postpartum period. Rituximab is an effective add-on therapy to conventional treatment.

Magnesium sulfate prophylaxis attenuates the postpartum effects of preeclampsia by promoting M2 macrophage polarization.

Preeclampsia is a complex disorder that is characterized by new onset hypertension and proteinuria at or after 20 weeks of gestation. Preeclampsia is a leading cause of maternal and fetal morbidity and mortality. MgSO4 is commonly used to treat severe preeclampsia, but its mechanism of action is poorly understood, and investigations into the effects of MgSO4 during the postpartum period are lacking. In this study, timed-pregnant Sprague-Dawley rats received low-dose lipopolysaccharide (LPS) on gestational day 14 to induce preeclampsia. Maternal and fetal outcomes and the macrophage profile 1 week after delivery were explored. On postpartum day (PD) 7, the maternal systolic blood pressure and urinary protein level were significantly increased, the number of M1 macrophages was increased and the number of M2 macrophages was decreased in the maternal kidney and brain; the median duration of gestation, the number of live fetuses, and the fetal weight/placenta weight ratio were significantly decreased; and the percentage of growth-restricted pups and fetal mortality were significantly increased in preeclampsia rats compared to normal pregnant control rats. Prophylactic MgSO4 decreased blood pressure at PD7, improved pregnancy outcomes, and promoted the polarization of M2 macrophages in the kidney and of M2 microglia in the brain of preeclampsia rats. These findings confirm that the pathophysiology of preeclampsia involves the dysregulation of the inflammatory response and the activation of M1 macrophages in several target organs during pregnancy. MgSO4 prophylaxis attenuates the postpartum effects of preeclampsia by promoting M2 macrophage polarization in the maternal kidney and brain.

Pilot study: placental biomarker predictive capability (sFlt-1, PlGF and their ratio) of postpartum maternal outcome.

BACKGROUND: Prenatal measurement of placental biomarkers was able to improve screening and diagnosis of preeclampsia. Little is known about the clinical role of placental biomarkers in the postpartum period. METHODS: This study is a prospective monocentric trial that included a total of 30 women with preeclamptic pregnancies. Serum placental biomarkers including soluble fms-like tyrosine kinase 1 (sFlt-1) and placental growth factor (PlGF) were measured before and 2 h after delivery by Enzyme-Linked Immunosorbent Assay (ELISA) using commercially available kits according to manufacturer's instructions and correlated with the postpartum outcome. RESULTS: Postpartum higher serum PlGF level was associated with postpartum elevation of the systolic blood pressure. Yet, the placental biomarkers were not able to predict general worsening of postpartum preeclampsia or other individual clinical or laboratory parameters. CONCLUSION: Serum concentrations of sFlt-1 and PlGF or their ratio in our study cohort did not completely predict the occurrence of postpartum preeclampsia. Yet, postpartum higher serum PlGF level was associated with postpartum elevation of the systolic blood pressure.

Modified ISTH pregnancy-specific DIC score in parturients with liver rupture: population-based case series.

OBJECTIVES: Liver rupture and hematoma are rare life-threatening complications of pregnancy. The aims of the current study are to: (1) characterize in a population-based study all cases of liver hematoma and/or rupture; and (2) validate the utility of the International Society on Thrombosis and Haemostasis (ISTH) modified pregnancy specific disseminated intravascular coagulation (DIC) score in those cases. STUDY DESIGN: A retrospective cohort study including all patients with liver subcapsular hematoma or rupture between the years 1996 and 2012 was conducted. Information on maternal characteristics, clinical presentation, diagnostic studies, therapeutic modalities, as well as maternal and fetal outcomes was collected. The pregnancy-specific modified ISTH DIC scores were calculated from admission to discharge, a score >26 is suggestive of DIC. RESULTS: Out of 175,000 births in our database, seven patients were identified with liver rupture or subcapsular hematoma, representing a prevalence of 4:100,000 deliveries. Of those, six had liver rupture and one had subcapsular liver hematoma. One patient died of hemorrhagic shock. Four patients underwent surgical liver packing and one also underwent hepatic artery ligation. Four out of seven patients were diagnosed during the immediate postpartum period with severe features of preeclampsia or with hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome. Modified ISTH pregnancy-specific DIC scores were calculated for five out of seven patients, and three (60%) had a score higher than 26. Patients with higher scores received more blood product transfusions, had longer hospitalizations, and their neonates had lower 1 and 5 minutes Apgar scores. CONCLUSIONS: Elevated pregnancy-specific modified ISTH DIC score (>26) in patients with liver hematoma or rupture was associated with adverse maternal and neonatal outcomes and appeared to perform well in distinguishing high and low-risk cases. Postpartum preeclampsia may be associated with severe features and a more complicated disease course.

Labor therapeutics and BMI as risk factors for postpartum preeclampsia: A case-control study.

OBJECTIVES: This study aims at identifying associations between therapeutics used during labor and the occurrence of postpartum preeclampsia (PPPE), a poorly understood entity. STUDY DESIGN AND MAIN OUTCOME MEASURES: This is a case-control study of women who received an ICD-9 code for PPPE (cases) during the years 2009-2011, compared to women with a normotensive term pregnancy, delivery and postpartum period until discharge (controls), matched on age (±1year) and delivery date (±3months). Cases were defined as women having a normotensive term pregnancy, delivery and initial postpartum period (48h post-delivery) but developing hypertension between 48h and 6weeks postpartum. Single variable and multiple variable models were used to determine significant risk factors. RESULTS: Forty-three women with PPPE were compared to 86 controls. Use of vasopressors and oxytocin did not differ between cases and controls, but rate of fluids administered during labor (OR=1.68 per 100cc/h; 95% CI: 1.09-2.59, p=0.02) and an elevated pre-pregnancy/first trimester BMI (OR=1.18 per kg/m2, 95% CI: 1.07-1.3, p=0.001) were identified as significant risk factors in multivariate analysis. CONCLUSIONS: We identified two potentially modifiable risk factors for PPPE; further studies are needed to better define the role of these two variables in the development of PPPE.