A Case of Postpartum Preeclampsia
The patient is a multiparous female in her 20s, post-operative day 8 from an uncomplicated repeat low transverse cesarean section at 39 weeks gestation after an uncomplicated pregnancy, who presents with SOB. She was discharged home on post-operative day 2 with a healthy female infant. She returns today with complaints of shortness of breath for 3 days and swelling in her bilateral lower extremities for 6 days. Over the same time course she endorses orthopnea, paroxysmal nocturnal dyspnea, weight gain, and chest pain. She describes the chest pain as substernal and intermittent. She also feels as if her chest is making a crackling noise when she exhales. She denies fevers, cough, nausea, vomiting, headache, or abdominal pain. She reports that her incision is healing well. She denies pain or drainage from the incision. She is breast-feeding her daughter, who is doing well at home. She has not yet seen her Obstetrician in follow-up but did receive all appropriate prenatal care.
Past Medical/Surgical History: Nephrolithasis and Cesarean Section
Medications: Prenatal Vitamins
Social History: None
Vital Signs: T 98.8 HR 46 RR 18 BP 164/96 O2 Sat 95%
Exam significant for mild tachypnea, rales and diminished breath sounds in the bilateral lower lung fields, normal S1 and S2, no murmurs, rubs, or gallops, bradycardic with a regular rhythm, soft non-tender abdomean with a well healing incision, alert, oriented, normal speech, +2 reflexes bilaterally, and pedal edema +1 bilaterally
WBC 8.8 H/H 11.5/32.6 Plt 337
Troponin: 0.09 BNP: 915
Uric acid: 8.0 AST 69 ALT 94
The patient presented on postpartum day 8 in mild respiratory distress with edema, hyperreflexia, and hypertension. Her clinical picture was consistent with postpartum severe preeclampsia. She was admitted to labor and delivery and started on IV magnesium. Her edema was treated with Lasix and hypertension was adequately controlled with oral Nifedipine and PRN dosing of Hydralazine for SBP > 160. Given her elevated troponin, BNP, and nonspecific ECG findings, cardiology was consulted to evaluate for peripartum cardiomyopathy. Her ECHO was normal and cardiology attributed her elevated troponin to strain from preeclampsia. The patient was weaned off of magnesium after 36 hours. Over the course of her hospital stay, her troponins trended downward and her symptoms improved. She was discharged home without antihypertensives and instructions to follow-up as scheduled with both OB and her primary care physician.
Five percent of all pregnancies are complicated by preeclampsia. It is one of four disease processes in pregnancy that are diagnosed based on blood pressure elevation greater than 140/90 after 20 weeks gestation(Figure 2).  The presence of severe symptoms in preeclampsia, as described below, drives both thetreatment options and timing of delivery.  There are 2 subsets of preeclamptic patients: early onset, which occurs at <34 weeks gestation, and late onset which is seen after 34 weeks gestation and up until 6 weeks postpartum.  Early onset preeclampsia, which accounts for 5-20% of cases, is caused by impaired spiral artery remodeling in the placenta which leads to a release of inflammatory factors.  This inflammatory state and associated sympathetic response leads to a systemic vasoconstriction resulting in the defining feature of preeclampsia: elevated blood pressure.  This systemic vasoconstriction also leads to endothelial dysfunction which results in the proteinuria, soft tissue edema, pulmonary edema, and liver capsule stretch. The onset preeclampsia, which accounts for 80% of preeclamptic patients, is thought to be a manifestation of the patient’s predisposition to cardiovascular dysfunction secondary to the physiologic demands of pregnancy. 
Shortness of breath secondary to pulmonary edema can be present in both preeclampsia and peripartum cardiomyopathy. Therefore, B-naturtic peptide (BNP) can sometimes help practitioners differentiate between these two disease processes. However, as is evident with our patient, elevated BNP can also be seen in more severe cases of preeclampsia, thus limiting its specificity for postpartum cardiomyopathy. In one study, the median BNP levels in normal patients, mild preeclamptics, and severe preeclamptics were 17.8, 21.1, and 101 pg/mL, respectively.  Given the patient’s elevated BNP and troponin, there was a high suspicion for associated cardiomyopathy. Surprisingly, this patient did not have evidence of cardiomyopathy on ECHO.
One in 2,000 pregnant women will suffer from eclampsia, a well defined complication of preeclampsia that manifests as tonic clonic seizures.  Even though the term preeclampsia indicates that it’s severe features would precede eclamptic seizures, up to one third of patients will have only mild range blood pressures at the time they seize. [2,8] Even more concerning is that 10% of patients will have proteinuria as their only manifestation of preeclampsia at the time of onset of eclampsia.  This argues against the traditional teaching that eclamptic seizures are a form of hypertensive encephalopathy. Rather, this supports the current theory that eclamptic patients seize due to cerebral edema, yet another manifestation of endothelial dysfunction that is responsible for the other symptoms found in severe preeclampsia. [2,8]
Late Postpartum Preeclampsia
Traditionally, delivery of the placenta is taught to be the definitive treatment for preeclampsia. However, there is a small, but significant, portion of patients who will present with symptoms of preeclampsia postpartum. The most relevant of these to emergency physicians are the patients who present with late postpartum preeclampsia (LPP), which by definition presents greater than 48 hours and less than 6 weeks after delivery.  This population has been discharged from the hospital and are the most likely to present to the emergency department directly, without involvement of the obstetricians prior to arrival. The data on these presentations is limited. However, one study of approximately 50,000 deliveries revealed that 152 (0.3%) women were readmitted to the hospital for LPP.  On average, these women present with symptoms on postpartum day 8, as was the case with our patient.  Our patient’s pregnancy was uncomplicated. She did not suffer from pre-eclampsia prior to delivery. Her uncomplicated prenatal course may lead a less experienced practitioner to place LPP lower on their differential. However, in the above study 63.2% of patients readmitted for LPP and 77% readmitted with postpartum eclampsia did not have any antecedent diagnosis of hypertension in pregnancy. 
Shortness of breath was our patient’s presenting complaint and was the second most common complaint of patients in this study, behind headache.  Risk factors for developing LPP include a BMI greater than 30, maternal age ≥40, latino or black ethnicity, and a new diagnosis of gestational diabetes. 
Management of Preeclampsia
The goal of emergency department care of patients with LPP is two-fold: treatment of hypertension and prevention of eclampsia. The American College of Obstetrics and Gynecology recommends treating severe-range blood pressures of over 160/100 with IV Labetalol or Hydralazine.  As was the case with our patient, repeat doses are often required to achieve this goal.  Severe range blood pressures or mild range blood pressures plus any of the symptoms of severe preeclampsia should prompt treatment with magnesium to prevent eclamptic seizures. Emergency physicians should have a low threshold to initiate magnesium, as the number needed to treat for prevention of eclampsia is 90.  The most common cause of death in patients with LPP is cerebral hemorrhage secondary to loss of cerebral autoregulation and increased blood pressure.  As such, tight BP control and magnesium therapy are both vital to minimizing morbidity and optimizing survival.  Involvement of our Obstetric colleagues should happen early in the course of these patients treatment, regardless of the severity of disease.
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