Postpartum subarachnoid hemorrhage - questions on gestational hypertension diagnosis and treatment threshold: A case report.

Hypertensive disorders of pregnancy (HDP) are a leading cause of morbidity and mortality for pregnant patients, but how aggressively to address non-severe hypertension in pregnancy remains controversial. The American College of Obstetrics and Gynecology (ACOG) currently recommends a blood pressure treatment threshold of 140/90 mmHg during pregnancy. However, 2017 American College of Cardiology/American Heart Association (ACC-AHA) guidelines define stage 1 hypertension by blood pressures of >130/80 mmHg within the general population. There is now an understudied population of pregnant patients considered to have stage 1 hypertension by ACC-AHA guidelines but who do not meet the treatment threshold by ACOG's standards. This article presents a patient who met ACC-AHA-defined stage 1 hypertension throughout her pregnancy and went on to develop severe hypertension and a postpartum subarachnoid hemorrhage (SAH) secondary to venous hemorrhage. She presented to the emergency department 17 days postpartum complaining of an extreme headache and with a blood pressure of 230/125 mmHg. Magnetic resonance imaging showed SAH in the parietal region adjacent to the superior sagittal sinus. Magnesium and labetalol were administered followed by a clevidipine drip. The patient was continued on antihypertensives and made a full recovery. This article's objective is to draw attention to the urgent need for increased clarity of practice guidelines, consensus between societies, and further study of peripartum health outcomes for pregnant patients defined as having stage 1 hypertension by 2017 ACC-AHA criteria.

Caspase activation independent of cell death is required for proper cell dispersal and correct morphology in PC12 cells.

Caspase activation is indispensable for the proper execution of apoptosis. However, to date, little is known about other possible physiologic functions for this class of enzymes in addition to their well-defined role in apoptosis. In this report, we described an action of caspase-3 involving cell dispersion that is independent of cell death. Using an in vitro neuronal model system consisting of PC12 cells, we observed a transient activation of caspase-3 both in situ and by Western blot analysis that was evident at 1 h following plating, was maximal by 3 h, and was attenuated by 24 h. Preincubation of PC12 cells with either the caspase-3 inhibitor, DEVD, or antisense caspase-3 oligonucleotides caused cells to be more rounded in appearance and led to a failure of cells to disperse properly. Additional experiments demonstrated a possible target for caspase cleavage to be the cytoskeletal protein, tau. These data suggest a requirement for caspase activation and subsequent disassembly of the cytoskeleton during cell dispersion and represent a novel role for caspases that may allow for proper migration of neurons to target locations during development.