Preeclampsia with Severe Features Case File

Preeclampsia with Severe Features Case File

Eugene C. Toy, MD, Patti Jayne Ross, MD, Benton Baker III, MD, John C. Jennings, MD

CASE 16

A 19-year-old G1P0 woman at 29 weeks’ gestation arrives to the hospital because of severe dyspnea of 6 hours’ duration. Her prenatal course has been unremarkable, and she denies any medical problems. Her blood pressure (BP) is 160/114 mm Hg, heart rate (HR) is 105 beats per minute (bpm), respiratory rate (RR) is 40 breaths per minute and labored, and oxygen saturation is 90%. The fetal heart tones are in the range of 140 bpm. A urine protein to creatinine ratio is 0.6. The serum alanine transaminase (ALT) is 84 IU/L (normal < 35) and aspartate transaminase (AST) is 90 IU/L (normal < 35). The prenatal records show the following:

Gestational Age	BP (mm Hg)	Urine Protein	FHT (bpm)	Fundal Height (cm)
8 weeks	100/60	0	140
12 weeks	110/70	0	148
16 weeks	100/76	0	150
20 weeks	105/58	0	138	20
26 weeks	130/89	1+	142	25

» What is the most likely diagnosis?

» What is your immediate next step?

» What are your priority laboratory tests?

» What is your management plan?

ANSWER TO CASE 16:

Preeclampsia with Severe Features                                        

Summary: A 19-year-old G1P0 woman at 29 weeks’ gestation has acute onset of severe dyspnea, RR of 40 breaths per minute and labored, new onset severely elevated BP of 160/114 and elevated protein/ creatinine ratio, and elevated liver function tests. The prenatal records show normal BPs in the pregnancy with a borderline elevated BP and 1+ proteinuria at the last visit (26 weeks).

• Most likely diagnosis: Preeclampsia with severe features
• Immediate next step: The highest priority must be to improve oxygenation. Sufficient oxygen must be provided to raise the O2 saturation >94%, and if the patient is tiring, ventilator support may be required. The second priority is to lower the BP with intravenous (IV) antihypertensive agents. If pulmonary edema is confirmed, IV diuresis such as furosemide should be given.
• Priority Lab tests: Complete blood count (CBC) with platelet count and renal function test (creatinine).
• Management: Stabilize maternal status (optimize oxygenation, lower BP to safe level below 160/110 mm Hg), stabilize fetal status, administer corticosteroids for fetal lung maturity, start magnesium sulfate for seizure prophylaxis, and move toward delivery.

ANALYSIS

Objectives

1. Know the clinical presentation and diagnostic criteria for four categories of hypertensive disorders of pregnancy.
2. Know the serious sequelae of severe features of preeclampsia, including pulmonary edema.
3. Understand the management of preeclampsia with severe features at the preterm and term gestations.

Considerations

The patient is nulliparous, which is a risk factor for preeclampsia. She has preeclampsia based on new onset BP exceeding 140/ 90 mm Hg with proteinuria (urine protein/ creatinine ratio exceeding 0.3). The patient has a record of normal BPs in her first 24 weeks of pregnancy (with borderline BP and 1+ proteinuria at 26 weeks), which is evidence that she does not have chronic hypertension. She has preeclampsia with severe features based on any one of three criteria: blood pressure, elevated liver function tests, and likely pulmonary edema. An O2 saturation of 60% correlates to a pO2 level of 60 mm Hg. Thus, the most immediate next step would be to improve oxygenation. The patient should be given 100% oxygen by face mask and if lung auscultation confirms pulmonary edema, then IV furosemide should be given. Concurrently, the BP needs to be lowered from the severe level (≥ 160/ 110 mm Hg) to prevent stroke. The physical exam and an urgent portable chest x-ray can help to assess for cardiomyopathy, pulmonary embolism, or asthma. Stabilization of maternal status has priority over fetal status; however, there should not be undue delay to evaluate the fetal status: fetal heart rate pattern and ultrasound for fetal weight, and amniotic fluid measurement. Deciding whether to deliver a preeclamptic patient with severe features depends on the risk to maternal/ fetal well being, the stability of the patient, and the gestational age. In the face of pulmonary edema, delivery must be enacted, since the pregnant woman’s life is in immediate jeopardy. In the face of marked prematurity, some severe features such as mildly elevated but stable liver function tests may be observed carefully without delivery. The key laboratories to draw are the CBC with platelet count, LFTs, and the serum creatinine. The management of this patient includes magnesium sulfate for seizure prophylaxis and delivery. Because of the preterm gestation, antenatal corticosteroid administration is important to promote lung maturity, and GBS prophylaxis such as with IV penicillin.

APPROACH TO:

Hypertensive Disease in Pregnancy                                   

DEFINITIONS

CHRONIC HYPERTENSION: Blood pressure of 140/ 90 mm Hg before pregnancy or at less than 20 weeks’ gestation, or persisting more than 12 weeks’ postpartum.

GESTATIONAL HYPERTENSION: Hypertension without proteinuria (or other features of preeclampsia) at > 20 weeks’ gestation persistent for at least 4 hours.

PREECLAMPSIA: Hypertension (140 systolic or 90 diastolic) measured twice 6 hours apart with the new onset of proteinuria (>300 mg over 24 hours, or a urine protein to creatinine ratio >0.3) usually at a gestational age greater than 20 weeks. In the absence of proteinuria, hypertension and one of the following findings may suffice: thrombocytopenia, impaired liver function tests, renal insufficiency, pulmonary edema, cerebral disturbances, or visual impairment.

ECLAMPSIA: Seizure disorder associated with preeclampsia.

HELLP SYNDROME: Hemolysis, elevated liver function tests, low platelets, possibly a subset of severe preeclampsia, associated with significant fetal/maternal morbidity and mortality.

POSTERIOR REVERSIBLE ENCEPHALOPATHY SYNDROME (PRES): A cliniconeuroradiological syndrome with headache, encephalopathy, seizures, cortical visual disturbances, usually diagnosed with clinical features and magnetic resonance imaging (MRI) (showing enhancement in the posterior parietal areas). Prompt recognition and treatment of PRES with antihypertensives, antiepileptics, and intensive care unit (ICU) monitoring is important to prevent long-term neurological sequelae.

SEVERE FEATURE OF PREECLAMPSIA: Vasospasm associated with preeclampsia of such extent that maternal end organs are threatened, usually necessitating delivery of the baby regardless of gestational age.

SUPERIMPOSED PREECLAMPSIA: Development of preeclampsia in a patient with chronic hypertension, often diagnosed by an increased blood pressure and/ or new onset proteinuria, which can be with or without severe features.

SUPERIMPOSED PREECLAMPSIA WITH SEVERE FEATURES: Development of preeclampsia in a patient with chronic hypertension with severe hypertension despite maximum therapy, cerebral/ visual symptoms, pulmonary edema, low platelets, elevated LFT, or new onset renal insufficiency (Cr ≥ 1.1 mg/ dL).

CLINICAL APPROACH

Hypertensive disorders complicate 3% to 4% of pregnancies and can be organized into several categories:

• Gestational hypertension
• Preeclampsia with or without severe features
• Chronic hypertension
• Superimposed preeclampsia with or without severe features
• Eclampsia

Gestational Hypertensive patients have only increased blood pressures without proteinuria or other features of preeclampsia. Up to 1/ 3 of those who are thought to have gestational hypertension are later found to have preeclampsia.

Preeclampsia is characterized by hypertension and proteinuria; less commonly, there is absence of proteinuria but evidence of vasospastic disease via other endorgan manifestations (see Table 16– 1). Although not a criterion, nondependent edema is also usually present. An elevated blood pressure is diagnosed with a systolic blood pressure at or >140 mm Hg or diastolic blood pressure at or >90 mm Hg. Two elevated BPs, measured 6 hours apart (BP taken in the seated position), are needed for the formal diagnosis of preeclampsia, although at term, presumptive diagnoses with persistent hypertension over a shorter interval often guides management. Proteinuria is usually based on timed urine collection, defined as equal to or greater than 300 mg of protein in 24 hours, although a P/ Cr ratio ≥ 0.3 is accurate.

Table 16–1 • DIAGNOSIS OF PREECLAMPSIA

New onset hypertension (140 systolic or 90 diastolic) twice over 6 hours with any one of: • Proteinuria (≥300 mg/24 hours, or protein/Cr ≥ 0.3 mg/dL, or dipstick ≥ 1 + or greater) • Thrombocytopenia (platelets < 100 000/mm3) • Impaired LFT (2× normal) • Renal insufficiency (Cr ≥ 1.1 mg/dL) • Pulmonary edema • New onset cerebral disturbance or visual impairment

Table 16–2 • SEVERE FEATURES OF PREECLAMPSIA (ANY ONE OF THE FOLLOWING)

• Systolic BP ≥ 160 mm Hg or diastolic BP ≥ 110 mm Hg on two occasions 4 hours apart • Platelets < 100 000/mm3 • Impaired LFT (2× normal) or severe persistent epigastric or RUQ pain • Progressive renal insufficiency (Cr ≥ 1.1 mg/dL) • Pulmonary edema • New onset cerebral or visual disturbance

Preeclampsia is further categorized as with or without severe features. See Table 16– 2. With severe vasospasm to the brain, headache or visual disturbances can occur. Capillary leakage can lead to pulmonary edema. Right upper quadrant or epigastric pain or elevated LFTs result from hepatic injury.

Chronic hypertension includes preexisting hypertension or hypertension that develops prior to 20 weeks’ gestation. These patients are at risk for intrauterine growth restriction (IUGR), fetal demise, or placental abruption. A patient with chronic hypertension is at risk for developing preeclampsia and, if this develops, her diagnosis is labeled as superimposed preeclampsia; this diagnosis is made on the basis of new onset of severe and uncontrollable hypertension, or new onset proteinuria, or a severe feature (Table 16–2). Eclampsia occurs when the patient with preeclampsia develops convulsions or seizures, but can occur without elevated blood pressure or proteinuria.

Pathophysiology

The underlying pathophysiology of preeclampsia is vasospasm and “leaky vessels,” but its origin is unclear. It is cured only by termination of the pregnancy, and the disease process almost always resolves after delivery. Vasospasm and endothelial damage result in leakage of serum between the endothelial cells and cause local hypoxemia of tissue. Hypoxemia leads to hemolysis, necrosis, and other end-organ damage. The vasospasm leads to increased systemic vascular resistance (hypertension), decreased intravascular volume, and decreased oncotic pressure; these changes place a patient more susceptible to pulmonary edema and sensitive to fluid shifts (fluid overload with IV fluids, and hypotension with blood loss).

Clinical Evaluation

Patients are usually unaware of the hypertension and proteinuria, and typically the presence of symptoms indicates severe disease. Hence, one of the important roles of prenatal care is to identify patients with hypertension and proteinuria prior to severe disease. Complications of preeclampsia include placental abruption, eclampsia (with possible intracerebral hemorrhage), coagulopathies, renal failure, hepatic subcapsular hematoma, hepatic rupture, and uteroplacental insufficiency. Fetal growth restriction, poor Apgar scores, and fetal acidosis are also more often seen.

Risk factors for preeclampsia include nulliparity, extremes of age, African-American race, personal history of severe preeclampsia, family history of preeclampsia, chronic hypertension, chronic renal disease, obesity, antiphospholipid syndrome, diabetes, and multifetal gestation. The history and physical examination is focused on end-organ disease.

It is important to review and evaluate the blood pressures prior to 20 weeks’ gestation (to assess for chronic hypertension). Patients with chronic hypertension may sometimes already have mild proteinuria, so it is important to establish a baseline to later document superimposed preeclampsia (substantial increase in proteinuria). Also one should document any sudden increase in weight (indicating possible edema). On physical examination, serial blood pressures should be checked along with a urinalysis.

Laboratory tests should include a complete blood count (CBC; check platelet count and hemoconcentration), urinalysis and 24-hour urine protein collection or protein/creatinine ratio (check for proteinuria), liver function tests, LDH (elevated with hemolysis), and creatinine. Fetal testing (such as biophysical profile) is also usually performed to evaluate uteroplacental insufficiency.

Management

After the diagnosis of preeclampsia is made, the management will depend on the gestational age of the fetus and the severity of the disease (see Table 16– 3 and Figure 16– 1 for one management scheme). Gestational hypertensive or preeclamptic patients without severe features can be observed and delivered at term (37 weeks), and magnesium sulfate use is individualized. Chronic hypertensive patients who are well controlled and uncomplicated can be observed and delivered at 38 to 39 weeks. When severe features complicate preeclampsia or superimposed preeclampsia, the risks of the preeclampsia must be weighed against the risk of prematurity. When the fetus is premature, the following issues are considered:

1. What are the immediate threats to maternal status, how stable is the patient, and can these threats be ameliorated?
2. What are the immediate threats to fetal status, how stable is the fetus, and can these threats be ameliorated?
3. What is the gestational age? If <34 weeks’ gestation, can delivery be safely delayed for 48 hours to allow corticosteroids to have maximum efficacy?
4. What is the natural history of the severe feature and does it seem to be worsening rapidly?

Observation of a patient with severe features should be performed in a tertiary center, since the risks to both the woman and the fetus are substantial. With an unstable patient, delivery is always warranted regardless of gestational age. NSAIDs may elevate the BP in postpartum preeclamptic patients and should be avoided.

Acute Management of Severe Hypertension

The acute-onset of severe hypertension (160 systolic or 110 diastolic, NOTE “or”) that persists >15 minutes is considered a hypertensive emergency. Therapy should be initiated quickly to avoid stroke. Systolic hypertension is as important or even more important as a predictor of cerebral injury. First line agents include IV labetolol, IV hydralazine, or oral nifedipine; typically after an initial dose, the BP is retaken 20 minutes later and further higher dose therapy is given if the BP is still in the severe range.

Table 16–3 • MANAGEMENT OF HYPERTENSION IN PREGNANCY
Category	Assessment	Management
Gestational hypertension or preeclampsia without severe features	1. Check for symptoms 2. Check BP 2×/week 3. Check platelet count, LFT, Cr 1×/week 4. Check serial US for fetal growth* 5. BPP once a week for fetal well being	No bed rest needed No anti-BP meds needed Delivery at 37 0/7 weeks (magnesium sulfate use individualized)
Chronic hypertension without severely elevated BP (uncomplicated)	1. Oral antihypertensive agent if BP ≥ 150/100, or on agent prepregnancy 2. Check BP and urine protein at prenatal visits 3. Serial US to assess for fetal growth 4. BPP starting at 30–32 weeks	Delivery at 38-39 weeks
Preeclampsia or superimposed preeclampsia with severe features	1. Stabilize maternal status, such as control BP if ≥ 160 systolic or 110 diastolic 2. Assess for maternal and/ or fetal threats (CBC, LFT, Cr) 3. Assess fetal weight, FHR pattern, and/or BPP	• If ≥34 weeks, administer magnesium sulfate and deliver • If <34 weeks, corticosteroids, magnesium sulfate, and assess maternal/fetal stability a. <34 weeks and maternal/fetal status stable= wait at least 48 hours, then delivery (with magnesium sulfate) b. With greater prematurity, if delivery delayed, monitor carefully and reassess daily in tertiary center c. If fetal or maternal status unstable, deliver immediately (with magnesium sulfate) • Regardless of gestation age, deliver for uncontrollable severe hypertension (max meds), eclampsia, pulmonary edema, abruption, DIC, nonreassuring fetal status • NOTE: If IUGR, use BPP and umbilical art Dopplers to guide
Acutely elevated BP (160 systolic or 110 diastolic)		Use IV labetolol or IV hydralazine or oral nifedipine immediately (reassess 20 minutes later) and escalate dose or alternate agent to bring BP to safe level

*If IUGR found, then BPP and umbilical artery Doppler testing.

Figure 16–1 Algorithm for management of hypertension in pregnancy.

Eclampsia

Eclampsia is one of the most feared complications of preeclampsia, and the greatest risk for occurrence is just prior to delivery, during labor (intrapartum), and within the first 24 hours’ postpartum. During labor, the preeclamptic patient should be started on the anticonvulsant magnesium sulfate. Since magnesium is excreted by the kidneys, it is important to monitor urine output, respiratory depression, dyspnea (side effect of magnesium sulfate is pulmonary edema), and abolition of the deep tendon reflexes (first sign of toxic effects is hyporeflexia). Hypertension is not affected by the magnesium. Severe hypertension needs to be controlled with antihypertensive medications such as hydralazine or labetalol. After delivery, magnesium sulfate is discontinued approximately 24 hours’ postpartum. The hypertension and proteinuria frequently will resolve. Occasionally, the patient’s blood pressure remains high and an antihypertensive medication is needed after delivery. After discharge, the patient usually follows up in 1 to 2 weeks to check blood pressures and proteinuria.

Emerging Concepts

There may be different mechanisms of preeclampsia. There is evidence that early disease (prior to 34 weeks) may be due to placental factors, such as inadequate or abnormal trophoblastic invasion into the spiral arteries. Investigators have noted abnormal “notching” uterine artery Doppler waveforms in patients prior to the clinical development of preeclampsia; these individuals seem to have worse and earlier-onset disease. In contrast, women with late-onset preeclampsia may be predisposed due to “constitutional” factors such as obesity. These patients tend to have a more favorable course. Also, there is some evidence that in significantly obese patients, bariatric surgery prior to pregnancy may reduce the risk of preeclampsia (and the risks of obesity). Low dose aspirin (started in late first trimester) may slightly reduce the recurrence of preeclampsia. Women who have had one or more pregnancies complicated by severe features <34 weeks’ gestation are candidates. Women with preeclampsia may have an increased risk of cardiovascular disease in later life, and may benefit from screening for hypertension and cardiovascular risk factors throughout their life.

CASE CORRELATION See also Case 14 on intrahepatic cholestasis of pregnancy (ICP) and the discussion of acute fatty liver of pregnancy. A common differential diagnosis of abnormal liver function tests in pregnancy includes preeclampsia, AFLP, HELLP syndrome, and ICP. The following features can help differentiate: AFLP—nausea and vomiting, icteric, hypoglycemia, coagulopathy Preeclampsia—LFTs 100 to 300 IU/ L range, hypertension, proteinuria HELLP—hemolysis, LFTs can be up to 1000 IU/ L, platelet < 100 000/ μL ICP—generalized itching, mildly elevated LFTs, elevated bile salts

COMPREHENSION QUESTIONS

16.1 A 29-year-old G1P0 woman at 28 weeks’ gestation is admitted to the hospital for preeclampsia. Her blood pressure (BP) is 150/ 100 mm Hg and protein excretion is 500 mg in 24 hours. On day 7 in the hospital, she is diagnosed with severe features of preeclampsia and the decision is made to administer magnesium sulfate and deliver the baby. Which of the following findings is most likely present in this patient to necessitate delivery?

A. Elevated uric acid levels

B. 5 g of proteinuria excreted in a 24-hour period

C. 4+ pedal edema

D. Platelet count of 115 000/ μL

E. PT INR of 1.9 and PTT of 50 s

16.2 Which of the following is the best management of an 18-year-old G1P0 woman at 28 weeks’ gestation with a blood pressure of 160/ 110 mm Hg, elevated liver function tests, and a platelet count of 60 000/ μL?

A. Oral antihypertensive therapy

B. Platelet transfusion

C. Magnesium sulfate therapy and induction of labor

D. Intravenous immunoglobulin therapy

16.3 A 19-year-old G1P0 woman at 39 weeks’ gestation is diagnosed with preeclampsia based on a blood pressure in the range of 150/ 90 mm Hg and 2+ proteinuria on urine dipstick. She complains of a severe headache. The patient is placed on magnesium sulfate and develops flushing and fatigue. She asks about the need for the magnesium sulfate. You explain that it is to prevent the seizures that may complicate preeclampsia and may even cause death. The patient asks how seizures associated with preeclampsia can cause mortality. Which of the following is the most common mechanism?

A. Intracerebral hemorrhage

B. Myocardial infarction

C. Electrolyte abnormalities

D. Aspiration

16.4 A 33-year-old woman at 29 weeks’ gestation is noted to have a blood pressure of 150/ 90 mm Hg and a protein/ creatinine ratio of 0.6. The platelet count, liver function tests, and creatinine are normal. Which of the following is the best management for this patient?

A. Induction of labor

B. Cesarean section

C. Antihypertensive therapy

D. Expectant management

16.5 A 25-year-old G1P0 woman at 28 weeks is diagnosed with severe preeclampsia based on a BP of 160/100 mm Hg and a platelet count of 98 000/mm3. The patient is treated with hydralazine for the hypertension. Which of the following is the most appropriate reason for delivery?

A. Blood pressures persist in the range of 150/ 95 mm Hg

B. Urine protein increases to 5 g over 24 hours

C. The patient reaches 32 weeks’ gestation

D. Patient develops pulmonary edema

E. Repeat platelet count is 95 000/mm3

16.6 On postpartum day 1, a 28-year-old G1P1 woman reports some headache and problems with her vision bilaterally. Her BP is 150/ 95 mm Hg and P/C ratio is 0.5. Her neurological examination is normal but her vision is impaired in both eyes. Which of the following is the best next step?

A. Antihypertensive agent

B. IV Mannitol

C. MRI of the brain

D. CT imaging of the brain

E. Ophthalmic eye drops to both eyes

Choose the best management plan (A-E) for each of the clinical scenarios (16.7-16.10):

A. Corticosteroids

B. Antihypertensive agent

C. Biophysical profile

D. Magnesium sulfate and delivery

E. Continued observation

16.7 A 32-year-old G2P1 woman is at 35 weeks with chronic hypertension. The BP is in the 140/ 95 range.

16.8 A 28-year-old G1P0 woman is at 30 weeks’ gestation with superimposed preeclampsia. The BP is 150/ 100. The platelet count is 95 000 and LFT is 2× normal. BPP is 10/10.

16.9 A 30-year-old G2P1 woman is at 31 weeks with chronic hypertension, using oral labetolol. Her BP in the office is 160/95 and 162/90. The urine protein is negative.

16.10 A 24-year-old G3P2 woman at 34 weeks’ gestation is noted to have preeclampsia. The BP is 150/90 and P/C ratio is 0.5. A fetal ultrasound shows the estimated fetal weight is at the 8th percentile.

ANSWERS

16.1 E. A severe feature of preeclampsia (Table 16– 2) may or may not necessitate immediate delivery. In this case, DIC is the most concerning condition and requires delivery at any gestational age. Pedal edema is not pathologic; nondependent edema, such as of the face and hands, may be consistent with preeclampsia but does not indicate severity of disease. Low platelets are associated with HELLP syndrome, a form of hemolytic anemia in pregnancy, and are very worrisome. Uric acid levels are known to be elevated with preeclampsia; however, it is not a criterion for severe preeclampsia. In general, the criteria for severe preeclampsia indicate end-organ threat, and generally require delivery for gestational age at or >34 weeks, and depending on the nature of the threat and the stability of the patient, perhaps delivery at an earlier gestational age.

16.2 C. Although the pregnancy is only 28 weeks, in light of the severe feature of preeclampsia with marked thrombocytopenia, the best treatment is magnesium sulfate and delivery. When preeclampsia with severe features is diagnosed, delivery depends on the nature of the threat, the stability of the patient/ fetus, and the gestational age. If the platelet count was higher (90 000), expectant management may be entertained at a tertiary center. Oral antihypertensive therapy, such as labetalol, may be given to the patient to control blood pressure; however, it should not be used as the “treatment” for severe preeclampsia. The platelet levels are not low enough to require transfusion; intravenous immunoglobulin (IVIG) is used for various autoimmune diseases, but not indicated in this patient.

16.3 A. The most common cause of maternal death due to eclampsia is intracerebral hemorrhage. Eclampsia is one of the most feared complications of preeclampsia, and the greatest risk for occurrence is just prior to delivery, during labor (intrapartum), and within the first 24 hours’ postpartum. Patients with gestational hypertension or preeclampsia without severe features do not necessarily require magnesium sulfate for seizure prophylaxis. This patient has a severe headache which is a severe feature. Magnesium sulfate has been proven to be superior to other anticonvulsants such as valium, Dilantin, or phenobarbital. One dictum that is useful in the emergency room or obstetrical unit is that “a pregnant patient greater than 20 weeks’ gestation without a history of epilepsy who presents with seizures has eclampsia until otherwise proven.”

16.4 D. In the preterm patient with mild preeclampsia, expectant management is generally employed until severe features are noted or the pregnancy reaches 37 weeks. In other words, the risks of prematurity usually outweigh the risks of the preeclampsia until end-organ threat is manifest. Had this

patient been at term, the best step in management would be to induce labor; this is because at term, the risks of prematurity are minimal. Severe, but not mild hypertension associated with preeclampsia, should be controlled with hypertensive medication. Antihypertensive agents are useful in chronic hypertension but not in preeclampsia unless the BP is in the severe range; lowering these BPs can help avoid stroke. For the patient in this scenario, neither induction nor cesarean section is indicated since she is not yet at term. It is not a requirement for a preeclamptic patient to deliver by cesarean. This patient can be followed as an outpatient with twice weekly BP checks and once a week platelet count, Cr, and LFTs.

16.5 D. Pulmonary edema is an indication for delivery at a preterm gestation. Proteinuria of 5 g over 24 hours is no longer criteria of a severe feature of preeclampsia and does not correspond to maternal or fetal outcome. Mild thrombocytopenia (80 000-100 000) that is stable may be judiciously observed in this patient (in a tertiary care center). A DIC panel should be performed to ensure there is not a coagulopathy, since that would be an indication for immediate delivery.

16.6 C. This patient is postpartum and likely has preeclampsia based on the elevated BP and the proteinuria. The symptoms may be due to PRES syndrome, which needs to be quickly diagnosed by MR imaging, since aggressive therapy must be enacted to prevent long-term brain dysfunction. An

antihypertensive agent does not generally need to be used unless the BP is severe (160 systolic or 110 diastolic). CT imaging can discern an intracranial bleed, and is useful if the patient had an eclamptic episode. Eye drops would be indicated with a conjunctivitis.

16.7 C. A biophysical profile should be performed. A patient with chronic hypertension that is well controlled should be monitored carefully for superimposed preeclampsia, complications such as abruption, serial ultrasound examinations to assess for IUGR, fetal testing such as BPP weekly, and delivered at 38 to 39 weeks.

16.8 A. Corticosteroid therapy is the single most important intervention to impact on the neonatal outcome in a pregnancy < 34 weeks when delivery is expected imminently (within 7 days). Magnesium sulfate is often given during this time of carefully monitoring the platelet count and liver function tests, but not necessarily delivery. This change in carefully observing patients with stable mild thrombocytopenia and stable elevated LFTs is based on the knowledge of antenatal corticosteroid impact on neonatal outcome.

16.9 B. This patient has severely elevated BP and must receive an antihypertensive agent ASAP to reduce the risk of stroke. This may be IV labetolol, IV hydralazine, or oral nifedipine. Although corticosteroids and BPP are viable answer choices, the highest priority is to lower the BP.

16.10 C. This patient likely has IUGR. The next step would be to evaluate possible fetal compromise with BPP and umbilical artery Doppler studies. At 34 weeks, corticosteroid therapy is not effective. Magnesium sulfate and delivery is an option, but more information such as assessment of fetal status would give a more complete picture. The BPs are in the mild range, and so an antihypertensive agent is not needed.

    CLINICAL PEARLS    

» In general, the treatment of gestational hypertension or preeclampsia without severe features at or beyond 37 weeks’ gestation is delivery. Use of magnesium sulfate is individualized. » The management of preeclampsia without severe features in a preterm pregnancy is observation until severe features are noted, or term gestation is reached. » Severe features complicating preeclampsia or superimposed preeclampsia at a gestational age of 34 weeks or higher should be given magnesium sulfate and delivered. Those <34 weeks may be judiciously observed in specialized facilities. » The most common cause of significant proteinuria in pregnancy is preeclampsia. » Magnesium sulfate is the best anticonvulsant to prevent eclampsia. » The first sign of magnesium toxicity is loss of deep tendon reflexes. » Chronic hypertension is diagnosed when a pregnant woman has hypertension prior to 20 weeks’ gestation, or if the hypertension persists beyond 12 weeks’ postpartum. » Gestational hypertension is when a pregnant woman has hypertension after 20 weeks of gestation without proteinuria or other evidence of preeclampsia. » Acute onset severe hypertension (160 systolic or 110 diastolic) persisting > 15 minutes is considered a hypertensive emergency. IV labetolol, IV hydralazine, or oral nifedipine are first line agents.

REFERENCES

American College of Obstetricians and Gynecologists. Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin 33. Washington, DC; 2012. 

Castro LC. Hypertensive disorders of pregnancy. In: H acker NF, Gambone JC, H obel CJ, eds. Essentials of Obstetrics and Gynecology. 5th ed. Philadelphia, PA: Saunders; 2009:173-182. 

Cunningham FG, Leveno KJ, Bloom SL, et al. Pregnancy hypertension. In: Williams Obstetrics. 24th ed. New York, NY: McGraw-Hill; 2014:706-756. 

Task Force on Hypertension in Pregnancy. American College of Obstetricians and Gynecologists. Hypertension in Pregnancy; 2013.

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