Search

Abstract Background Hypertensive disorders of pregnancy (HDP) are the most common cause of postpartum readmission. Prior research led to clinical guidelines for postpartum management; however, the patient experience is often missing from this work. The objective of this study is to understand the perspective of patients readmitted for postpartum hypertension. Methods This was a qualitative study with data generated through semi-structured interviews. Patients readmitted with postpartum HDP at an urban academic medical center from February to December 2022 were approached and consented for an interview. The same researcher conducted all interviews and patient recruitment continued until thematic saturation was reached (n = 9). Two coders coded all interviews using Nvivo software with both deductive and inductive coding processes. Discrepancies were discussed and resolved with consensus among the two coders. Themes were identified through an initial a priori template of codes which were expanded upon using grounded theory, and researchers were reflexive in their thematic generation. Results Six themes were generated: every pregnancy is different, symptoms of preeclampsia are easily dismissed or minimized by both patient and providers, miscommunication regarding medical changes can increase the risk of readmissions, postpartum care coordination and readmission logistics at our hospital could be improved to facilitate caring for a newborn, postpartum care is often considered separately from the rest of pregnancy, and patient well-being improved when conversations acknowledged the struggles of readmission. Conclusions This qualitative research study revealed patient-identified gaps in care that may have led to readmission for hypertensive disorders of pregnancy. The specific recommendations that emerge from these themes include addressing barriers to blood pressure management prior to discharge, improving postpartum discharge follow-up, providing newborn care coordination, and improving counseling on the risk of postpartum preeclampsia during discharge. Incorporating these patient perspectives in hospital discharge policy can be helpful in creating patient-centered systems of care and may help reduce rates of readmission.

Introduction: Longitudinal effect of diet-induced obesity on bone is uncertain. Prior work showed both no effect and a decrement in bone density or quality when obesity begins prior to skeletal maturity. We aimed to quantify long-term effects of obesity on bone and bone marrow adipose tissue (BMAT) in adulthood. Methods: Skeletally mature, female C57BL/6 mice (n = 70) aged 12 weeks were randomly allocated to low-fat diet (LFD; 10% kcal fat; n = 30) or high-fat diet (HFD; 60% kcal fat; n = 30), with analyses at 12, 15, 18, and 24 weeks (n = 10/group). Tibial microarchitecture was analyzed by µCT, and volumetric BMAT was quantified via 9.4T MRI/advanced image analysis. Histomorphometry of adipocytes and osteoclasts, and qPCR were performed. Results: Body weight and visceral white adipose tissue accumulated in response to HFD started in adulthood. Trabecular bone parameters declined with advancing experimental age. BV/TV declined 22% in LFD (p = 0.0001) and 17% in HFD (p = 0.0022) by 24 weeks. HFD failed to appreciably alter BV/TV and had negligible impact on other microarchitecture parameters. Both dietary intervention and age accounted for variance in BMAT, with regional differences: distal femoral BMAT was more responsive to diet, while proximal femoral BMAT was more attenuated by age. BMAT increased 60% in the distal metaphysis in HFD at 18 and 24 weeks (p = 0.0011). BMAT in the proximal femoral diaphysis, unchanged by diet, decreased 45% due to age (p = 0.0002). Marrow adipocyte size via histomorphometry supported MRI quantification. Osteoclast number did not differ between groups. Tibial qPCR showed attenuation of some adipose, metabolism, and bone genes. A regulator of fatty acid β-oxidation, cytochrome C (CYCS), was 500% more abundant in HFD bone (p < 0.0001; diet effect). CYCS also increased due to age, but to a lesser extent. HFD mildly increased OCN, TRAP, and SOST. Conclusions: Long-term high fat feeding after skeletal maturity, despite upregulation of visceral adiposity, body weight, and BMAT, failed to attenuate bone microarchitecture. In adulthood, we found aging to be a more potent regulator of microarchitecture than diet-induced obesity.