SOAP. – Preeclampsia (PIH)

Merita O’Sullivan

Definition

A.Preeclampsia, also called PIH (antiquated term toxemia), is the new onset of hypertension with proteinuria that develops after 20 weeks’ gestation in pregnancy or develops up to 6 weeks postpartum in a previously normotensive woman. In the absence of proteinuria, any of the following can establish the diagnosis: new-onset thrombocytopenia, impaired liver function, renal insufficiency, pulmonary edema, or visual or cerebral disturbances.

B.Preeclampsia with severe features: In 2013, the American Congress of Obstetricians and Gynecologists (ACOG) replaced the term severe preeclampsia with the term preeclampsia with severe features. In a patient with preeclampsia, the presence of one or more of the following indicates a diagnosis of preeclampsia with severe features:

1.Symptoms of central nervous system (CNS) dysfunction:

a.New-onset cerebral or visual disturbances, such as:

i.Photopsia, scotomata, cortical blindness, retinal vasospasm.

ii.Severe incapacitating headache (the worst headache in my life) or a headache that persists and progresses despite analgesic therapy.

iii.Altered mental status.

2.Hepatic abnormality:

a.Severe persistent right upper quadrant (RUQ) or epigastric pain unresponsive to medication and not accounted for by an alternative diagnosis or a serum transaminase concentration greater than 2 times the upper limit of the upper range, or both.

3.Severe blood pressure (BP) elevation:

a.Systolic BP greater than 160 mmHg or diastolic BP greater than 110 mmHg on two or more occasions at least 4 hours apart. Antihypertensive therapy may be initiated upon confirmation of severe hypertension in which case criteria for severe BP elevation can be satisfied without waiting until 4 hours have lapsed.

4.Thrombocytopenia:

a.Platelets less than 100,000 per microliter.

5.Renal abnormality:

a.Progressive renal insufficiency (serum creatinine >1.1 mg/dL [97.2 micromol/L] or a doubling of the serum creatinine concentration in the absence of other renal disease).

6.Pulmonary edema.

C.Hypertension: The 2017 changes in the definition for elevated BP and hypertension in nonpregnant adults do not affect diagnostic criteria for pregnancy-related hypertensive disorders:

1.Either a systolic BP more than 140 mmHg or a diastolic BP more than 90 mmHg, or both. The values must be elevated on at least two separate occasions at least 4 hours apart. Severity of hypertension is not necessarily associated with the severity of preeclampsia.

2.Eclampsia is the development of grand mal seizures in a patient with preeclampsia in the absence of other neurologic conditions that could account for the seizures.

3.HELLP syndrome: HELLP = hemolysis, elevated liver enzymes, and low platelets. It probably represents a severe form of preeclampsia, but this relationship is controversial; HELLP may be an independent disorder.

4.Chronic hypertension in pregnancy is often complicated by superimposed preeclampsia.

5.Gestational hypertension (GHTN) is hypertension without proteinuria or other signs and symptoms of preeclampsia or related end-organ dysfunction that develops after 20 weeks’ gestation and resolves by 12 weeks postpartum. Between 10% and 25% of women with GHTN may develop signs and symptoms of preeclampsia.

Incidence

A.Hypertensive disorders are the most common medical complication of pregnancy, with a reported incidence of up to 10% worldwide. Incidence varies among different regions and countries. The incidence of preeclampsia has increased by 25% in the United States during the past two decades and 4.6% of all pregnancies worldwide are complicated by preeclampsia. The risk of recurrent preeclampsia is between 5% and 70%. Women who develop severe features of preeclampsia prior to 30 weeks’ gestation have the highest risk of preeclampsia in future pregnancies.

B.Prognosis:

1.Women with preeclampsia are at an increased risk for life-threatening obstetric or medical complications. Worldwide, 10% to 15% of direct maternal deaths (resulting from obstetric complications of pregnancy) are associated with preeclampsia/eclampsia. In the United States, preeclampsia/eclampsia is one of the four leading causes of maternal death, along with hemorrhage, cardiovascular conditions, and thromboembolism. There is approximately one maternal death caused by preeclampsia/eclampsia per 100,000 live births, with a case-fatality rate of 6.4 deaths per 10,000 cases.

2.Fetal implications: Preeclampsia can lead to intrauterine growth retardation (IUGR) and oligohydramnios, as well as medically or obstetrically indicated preterm birth (PTB). As a result, perinatal morbidity and mortality are increased.

C.Prevention:

1.Low-dose aspirin: This reduces the frequency of preeclampsia, as well as related adverse pregnancy outcomes (PTB, growth restriction), by about 10% to 20% when given to women at moderate to high risk of the disease; it has an excellent maternal/fetal safety profile in pregnancy.

2.Candidates: There is no consensus on the criteria that confer high risk for developing preeclampsia.

3.U.S. Preventive Services Task Force (USPSTF) criteria for high risk include one or more of the following (the incidence of preeclampsia is estimated to be at least 8% in a pregnant woman with one of these risk factors):

a.Previous pregnancy with preeclampsia, especially early onset and with an adverse outcome.

b.Multifetal gestation.

c.Chronic hypertension.

d.Type 1 or 2 diabetes mellitus (DM).

e.Chronic kidney disease.

f.Autoimmune disease (antiphospholipid syndrome, systemic lupus erythematosus).

4.USPSTF criteria for moderate risk include the following (the incidence of preeclampsia is estimated to be less than 8% in a pregnant woman with only one of these risk factors):

a.Nulliparity.

b.Obesity (body mass index [BMI] >30 kg/m²).

c.Family history of preeclampsia in mother or sister.

d.Age ≥35 years.

e.Sociodemographic characteristics (African American race, low socioeconomic level).

f.Personal risk factors (previous pregnancy with low birth weight or small for gestational age infant, previous adverse pregnancy outcome [fetal demise], interval >10 years between pregnancies).

D.The following summaries represent the recommendations of some national organizations:

1.The American Heart Association and American Stroke Association recommend low-dose aspirin for women with chronic primary or secondary hypertension or previous pregnancy-related hypertension for prevention of preeclampsia-related stroke.

2.The USPSTF recommends the use of low-dose aspirin 81 mg/d in women at high risk of developing preeclampsia to reduce the risk for preeclampsia, PTB, and fetal growth restriction.

Women with ≥1 high-risk factors should receive low-dose aspirin. For women with multiple moderate risk factors, the benefit of aspirin therapy is less clear, so clinicians should use clinical judgment and talk with their patients about the benefits and harms of low-dose aspirin use. Aspirin should be initiated between 12 and 28 weeks of gestation.

3.In July 2016, ACOG endorsed the USPSTF recommendation for use of low-dose aspirin 81 mg/d in women at high risk of developing preeclampsia and based high-risk status on the same high-risk factors designated by the USPSTF. Prior to July 2016, ACOG defined high risk more narrowly: history of early-onset preeclampsia and preterm delivery less than 34⁰/⁷ weeks of gestation or more than one prior pregnancy complicated by preeclampsia.

4.The World Health Organization recommends the use of low-dose aspirin 75 mg/d for high-risk women (history of preeclampsia, diabetes, chronic hypertension, renal or autoimmune disease, or multifetal pregnancies).

Pathogenesis

A.The etiology of preeclampsia is unknown, although several theories exist. Generalized vascular endothelial damage is a hallmark of the pathophysiologic responses.

Predisposing Factors

A.Nulliparity.

B.Chronic hypertension.

C.Age extreme (<18 years and >35 years old).

D.Race (African American women are at higher risk).

E.Pregestational and gestational diabetes.

F.Renal disease.

G.Family history of preeclampsia in a sister or mother.

H.Previous pregnancy with PIH.

I.Multiple gestation.

J.Hydatidiform mole.

K.Obesity (BMI >30).

L.Autoimmune disease (systemic lupus erythematosus or antiphospholipid syndrome).

M.Hydrops fetalis.

N.Vascular disease.

O.IUGR, abruptio placenta, or fetal demise in a previous pregnancy.

P.Prolonged inter-pregnancy interval if previous pregnancy was normotensive.

Q.Short inter-pregnancy interval if previous pregnancy was preeclamptic.

Common Complaints

A.Persistent and/or severe headache unrelieved by analgesics.

B.RUQ epigastric pain.

C.Severe heartburn unrelieved by antacids.

D.Nausea and vomiting.

E.Edema: Peripheral and/or facial.

F.Visual disturbances (photophobia, scotomata, ametropia).

Other Signs and Symptoms

A.Hypertension (BP of 140 mmHg systolic or greater or 90 mmHg diastolic or greater that occurs after 20 weeks’ gestation in a woman without a previous history of hypertension).

First-trimester signs of PIH require ultrasonographic evaluation for the presence of a gestational trophoblastic disease (molar pregnancy) as well as the other differential diagnoses.

B.Proteinuria:

1.Random urine protein: Creatinine ratio of greater than 0.3 mg protein/mg creatinine.

2.Timed excretion of greater than 0.3 g protein in a 24-hour urine collection specimen. The completeness of the 24-hour collection can be estimated from the creatinine excretion, which should be 15 to 20 mg/kg of lean body weight in women.

C.Brisk deep tendon reflexes (DTRs; hyperreflexia) or ankle clonus.

Potential Complications

A.Multiple organ involvement.

B.HELLP syndrome.

C.Eclampsia, which may lead to maternal demise.

D.Fetal complications: IUGR, oligohydramnios, abruptio placenta.

Subjective Data

A.Elicit information about headaches, their onset and duration, the progression of headache, and/or other symptoms.

B.What part of the head hurts? Differentiate headache from sinus headache. Note severity and any relief measure tried (acetaminophen, massage, sleep).

C.Is the headache new? Does the patient have a previous history of migraines? Is this like a previous migraine?

D.What are other concurrent symptoms? Nausea, vomiting, RUQ pain, and visual changes?

E.Question the patient about edema. If edema is present, has it significantly worsened over the past few days? Has she been able to wear rings up to this point? Has she had to wear different shoes because of pedal edema?

F.What are her usual weight and today’s weight (on the same scales)? Has she gained more than 2 pounds in 1 week?

G.Ask specifics about RUQ pain, sometimes identified as severe heartburn. Note the duration, severity, and relief measures tried. Have the patient point to the area of discomfort (midsternum or under right breast).

H.Are there any visual disturbances, such as black dots she can’t see through?

I.Review other gastrointestinal symptoms such as diarrhea, abdominal pain, and gallbladder attack.

J.Review for signs of fever and thyroid storm.

K.Review the patient’s history for seizures.

L.Review for signs of pulmonary edema: dyspnea, chest pain, and/or decreased (≤93%) oxygen saturation by pulse oximetry.

Physical Examination

A.Check BP, pulse, respirations, oxygen saturation via pulse oximetry, weight, and fetal heart tones.

B.Inspect:

1.Check pedal, hand, and facial edema.

2.Check fundal height.

C.Palpate:

1.Palpate the abdomen, noting any hepatosplenomegaly and RUQ tenderness to the palpation.

2.Palpate the lower extremities for pitting edema. Peripheral edema may be related to capillary leaking or overfill edema.

D.Percuss:

1.Gently check for liver enlargement or pain. Hepatic tenderness is caused by stretching of Glisson capsule from hepatic swelling or bleeding.

2.Perform neurologic exam for hyperreflexia: Check lower extremities for DTR and ankle clonus.

E.Auscultate:

1.Auscultate the heart and lungs.

2.Auscultate the fetal heart tone.

Diagnostic Tests

A.Complete blood count (CBC) and platelets.

B.Liver profile (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]).

C.Renal workup: