O ne of the major causes of maternal morbidity and mortality during pregnancy are hypertensive disorders. Hypertension requiring treatment may occur before, during, or after pregnancy. Postpartum hypertension may be related to gestational hypertension (GH), preeclampsia, preexist- ing chronic hypertension, or it can develop secondary to other causes. Of the studies looking at GH-preeclampsia, those patients readmitted with postpartum hypertension- preeclampsia are often not considered when evaluat- ing outcomes; therefore there are little data to support the evaluation, management, and complications of post- partum hypertension-preeclampsia. As a result of this lack of evidence, the author focused on the prevalence, etiology, evaluation, and management of women with new-onset or persistent postpartum hypertension. The exact incidence of postpartum hypertension is difficult to calculate. Most women with mild hypertension are usually not reported, whereas those who have hyper- tension associated with headaches or blurred vision are often seen by an emergency physician and not reported as hypertensive unless hospitalized. Even with these limi- tations, the prevalence of new-onset postpartum hyper- tension or preeclampsia is reported to be 0.3% to 27.5%. Postpartum hypertension has extensive etiologies and differential diagnoses with GH-preeclampsia the most com- mon cause. New-onset postpartum hypertension or pre- eclampsia can be caused by an introduction of a large volume of fluid into the intravascular space which causes a state of volume overload resulting in hypertension. Medi- cations often used for pain relief (ibuprofen) are also vaso- constrictors and cause water retention, potentially leading to hypertension. No solid data are available detailing the period over which maternal hypertension and proteinuria resolve in women with GH-preeclampsia. Those with preeclampsia generally show a decrease in blood pressure within 48 hours, but blood pressure can increase again between 3 and 6 days postpartum. Cerebral manifestations or deterioration may only become manifest postpartum and can lead to the development of eclampsia or preeclampsia with hemolysis, elevated liver enzymes, low platelets syndrome. The risk of hypertension exacerbation increases in women with undiag- nosed chronic hypertension or superimposed preeclampsia. Maternal outcome is dependent upon existing problems; those with isolated hypertension or preeclampsia generally face a positive outcome, whereas those diagnosed with an issue such as pheochromocytoma or stroke, or those who have a delayed diagnosis face a poor outcome. A multidisciplinary approach is recommended for managing women with postpartum hypertension. Pre- delivery risk factors, time of onset in relation to delivery, presence of signs or symptoms, results of laboratory or imaging findings, and response to initial therapy should all be taken into account during patient evaluation. Pre- viously prescribed medications should be considered and discontinued if they are likely to cause adverse reactions. Patients who present with only hypertension should be given antihypertensive medications to control blood pres- sure. If problems persist, the presence of renal artery stenosis or primary hyperaldosteronism should be consid- ered. Pulmonary edema and/or postpartum cardiomyop- athy, hyperthyroidism, or pheochromocytoma may be considered in women presenting with hypertension and shortness of breath, orthopnea, tachycardia, or palpita- tions. Severe preeclampsia is the presumed diagnosis when women present with postpartum and new-onset persistent headaches, visual changes, or proteinuria. If a hypertensive woman has a seizure, she should be treated for eclampsia with magnesium sulfate and intravenous antihyperten- sive medications. Those who experience refractory or thunderclap headaches, visual disturbances, or neurological deficits should undergo diagnostic neuroimaging to identify a possible cerebrovascular complication. Women with hypertension accompanied by persistent nausea, vomiting, or epigastric pain should be screened for preeclampsia with hemolysis, elevated liver enzymes, low platelets syndrome and treated with magnesium sulfate, antihypertensives, and monitoring of laboratory values. When evaluating women for postpartum hyper- tension, a wide index of secondary causes should be con- sidered. A detailed history, careful physical exam, selective laboratory and imaging studies, and response to initial treatments are vital in diagnosing and treating postpartum hypertension. Management of Obstructive Sleep Apnea in Pregnant Women J. Louis, D. Auckley, and N. Bolden (Obstet Gynecol. 2012;119(4):864–8) Department of Medicine, Case Western Reserve University, Cleveland, OH Copyright r 2013 by Lippincott Williams & Wilkins DOI: 10.1097/01.aoa.0000429109.36501.b5 Topics: Nonobstetric Maternal Disease, Maternal Obesity A 32-year-old woman at 37-week gestation presented for repeat cesarean delivery. She was morbidly obese (body mass index, 53.1) and had chronic hypertension and obstructive sleep apnea (OSA). Her antenatal course was uneventful. On repeat polysomnography (PSG) at 20 weeks mild OSA was confirmed, with an apnea-hypopnea index of 9 events per hour. Her lowest oxygen saturation on over- night PSG was 76%, with 3.9% of total sleep time with a level <90%. She began continuous positive airway pres- sure (CPAP) at 12 cm H 2 O at 26 weeks. She had an uncomplicated cesarean delivery and tubal ligation under combined spinal-epidural anesthesia. Neonatal Apgar scores were 9 at both 1 and 5 minutes. Postoperatively, she declined CPAP and within 4 hours, she had intermittent hypoxemia with a pulse oximetry nadir of 83%. Her lungs were clear, she had no tachycardia, and she denied chest pain. Later, pulse oximetry ranged between 93% and 94% but because of the OSA, she was maintained on continuous pulse oximetry monitoring. After the first 24 hours post- operatively, physician assessment of vital signs was neces- sary before narcotics and ketorolac could be given for analgesia. Hypoxemia was most profound during the first 24 hours. On postoperative day 2, oxygen saturation was consistently B96% and by day 3, it was at her preoperative baseline level of 98% with no desaturations on room air. Echocardiography to evaluate for the presence of pulmo- nary hypertension was normal. She was discharged home on postoperative day 4. Editorials and Reviews Obstetric Anesthesia Digest  Volume 33, Number 2, June 2013 78 | www.obstetricanesthesia.com r 2013 Lippincott Williams & Wilkins