A 37-year-old woman, gravida 1 para 0, at 37 weeks gestation comes to the emergency department due to severe epigastric pain. The pain started yesterday and has progressively worsened. She developed nausea today but has had no fever, vomiting, or diarrhea. The patient has no contractions, leakage of fluid, or vaginal bleeding. Fetal movement is normal. She has no chronic medical conditions and has had no surgeries. Temperature is 37.3 C (99.1 F), blood pressure is 168/94 mm Hg, and pulse is 98/min. BMI is 29 kg/m². Fetal heart tones are 140/min. The patient appears anxious and in moderate distress. The abdomen is tender in the epigastrium with no rebound, rigidity, or guarding. The uterus is gravid and nontender. Urinalysis shows 3+ protein. Ultrasound of the right upper quadrant is normal. This patient is at increased risk for developing which of the following complications?

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Explanation: 11ec25c8_da71_551f_bc81_017c090806a7_MD0003_00 This patient with new-onset epigastric pain, hypertension, and proteinuria at 37 weeks gestation has preeclampsia with severe features, a potentially life-threatening condition. Preeclampsia is most likely caused by abnormal placentation and narrowed spiral artery formation. The resulting placental hypoperfusion, hypoxia, and ischemia trigger the release of antiangiogenic factors causing maternal endothelial cell damage. This damage may manifest in multiple organ systems, including the liver (eg, referred epigastric pain from stretching of the hepatic capsule) and kidneys (eg, proteinuria from acute kidney injury). In the brain, endothelial cell damage can precipitate an acute stroke via the following mechanisms: Activation of the coagulation system, platelet aggregation, and vascular microthrombi formation, leading to cerebral vessel occlusion (ischemic stroke). Dysregulated cerebral blood flow that causes inappropriate cerebral vasospasm, severely elevated perfusion pressure, and ruptured intracerebral vessels (hemorrhagic stroke). To decrease these risks, patients with severe-range hypertension (ie, systolic ≥160 or diastolic ≥110 mm Hg) require prompt antihypertensive therapy (eg, IV labetalol, IV hydralazine). Treatment of preeclampsia with severe features is with delivery because removal of the placenta is typically curative. (Choice B) The primary risk factor for ascending cholangitis is biliary calculi, which can present with epigastric pain and nausea. However, this patient's ultrasound of the right upper quadrant is normal. (Choice C) Patients with increased intraesophageal pressure (eg, vomiting) are at risk for Boerhaave syndrome (ie, effort rupture of the esophagus). This patient has had no vomiting. (Choice D) The risk of intraamniotic infection is increased in patients with prolonged rupture of membranes. This patient has had no leakage of fluid. (Choice E) Subarachnoid hemorrhage typically occurs due to a ruptured intracranial saccular (berry) aneurysm; risk factors include cigarette smoking and chronic hypertension, which are not seen in this patient. Preeclampsia is not a risk factor. Educational objective: Preeclampsia with severe features increases the risk of acute stroke due to endothelial cell damage, dysregulation of cerebral blood flow, cerebral vasospasm, and vascular microthrombi formation, particularly in patients with severe hypertension (ie, systolic ≥160 or diastolic ≥110 mm Hg). References: Ischemic stroke during pregnancy and puerperium. (http://www.ncbi.nlm.nih.gov/pubmed/21331336) Preeclampsia: association with posterior reversible encephalopathy syndrome and stroke. (http://www.ncbi.nlm.nih.gov/pubmed/29438078) Cerebrovascular complications in pregnancy and puerperium. (http://www.ncbi.nlm.nih.gov/pubmed/24431615)

A 37-Year-Old Woman, Gravida 1 Para 0, at 37 Weeks