Hypertensive Disorders of Pregnancy, Pre-eclampsia and HELLP Nursing CE Course for APRNs

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Hypertensive Disorders of Pregnancy for APRNs

Disclosure Statement

This learning activity aims to increase learners’ knowledge of hypertensive disorders of pregnancy (HDP) and the effects on pregnant individuals and their fetuses. Advanced practice registered nurses (APRNs) will understand the pathophysiology of the distinct types of HDP, including chronic hypertension, gestational hypertension, and preeclampsia. APRNs will also understand the risk factors, maternal complications, diagnosis, and treatment of each HDP.

This learning activity is designed to allow learners to:

• describe the causes of HDP
• explain the complications of HDP in pregnant individuals and their fetuses
• identify risk factors for developing HDP
• outline diagnostic criteria for the different types of HDP
• distinguish the treatments of the different types of HDP
• summarize the long-term complications of a pregnancy complicated by HDP

Background

Hypertension in pregnancy is caused by four different disorders collectively known as hypertensive disorders of pregnancy (HDP). HDP consists of chronic hypertension, gestational hypertension, preeclampsia, and preeclampsia superimposed over chronic hypertension. Globally, chronic hypertension affects 1% to 2% of pregnancies, gestational hypertension affects 5% to 6% of pregnancies, and preeclampsia affects 2% to 4% of pregnancies. Individuals who have already been diagnosed with chronic hypertension and begin to have preeclampsia symptoms after 20 weeks are considered to have preeclampsia superimposed over chronic hypertension. In the US, the prevalence of gestational hypertension increased from 10.8% in 2017 to 13% in 2019. During that same period, the rate of chronic hypertension increased from 2% to 3% (Ford et al., 2022; Garovic et al., 2022; Magee & von Dadelszen, 2021).

HDP affects 10% of pregnancies and causes 14% of maternal and perinatal deaths worldwide, second only to maternal hemorrhage. Preeclampsia and eclampsia are responsible for approximately 10% of maternal deaths worldwide. This equates to over 50,000 deaths, with one occurring every 7 minutes. HDP is a common pregnancy complication in the US and the leading maternal mortality cause. The prevalence of HDP increased from 13.3% in 2017 to 15.9% in 2019. HDP affects 31% of pregnant individuals aged 45-55, 18% of pregnant individuals aged 35-44, 14.3% of pregnant individuals aged 30-34, 13.5% of pregnant individuals aged 25-29, and 13.9% of pregnant individuals aged 12-24. Non-Hispanic Black individuals had the highest rate of HDP at 20.9%, followed by American Indian or Alaska Native individuals at 16.4%, Non-Hispanic Whites at 14.7%, Hispanics at 12.5%, and Asian or Pacific Islanders at 9.3%. Of all the reported deaths during hospitalization for delivery, 31.6% had a documented diagnosis of HDP. Among those, 24.3% had hypertension induced by pregnancy (i.e., gestational hypertension or preeclampsia), and the other 7.4% had a diagnosis of chronic hypertension (American College of Obstetricians and Gynecologists [ACOG] 2020; Ford et al., 2022; Lowdermilk et al., 2016; UNICEF, 2021).

Hypertension induced by pregnancy is classified as systolic blood pressure (SBP) above 140 mmHg, diastolic blood pressure (DBP) above 90 mmHg, or a combination of elevated SBP and DBP that occurs after 20 weeks of gestation. Typically, blood pressure readings must be elevated on two separate readings at least 4 hours apart. In cases where the readings are extremely elevated (SBP ≥ 160 or DBP ≥ 110), a shorter interval between readings is indicated to expedite treatment (ACOG, 2019).

Pathophysiology

Hemodynamic changes occur during pregnancy, exacerbating chronic hypertension or increasing a pregnant individual's risk of developing hypertension. During a normal pregnancy, intravascular fluid volume increases, leading to increased cardiac output. Due to hormonal changes, vasodilation and decreased vascular resistance also occur. This vasodilation and decreased vascular resistance can decrease blood pressure by 10% by the second trimester. For patients with chronic hypertension, this decrease can lead to the normalization of blood pressure without using antihypertensive medications. This improvement is short-lived, and blood pressure measurements usually return to baseline by the third trimester. This can lead to a misdiagnosis of gestational hypertension instead of chronic hypertension if a patient’s elevated blood pressure is not recognized until after 20 weeks (ACOG, 2019; Garovic et al., 2022).

 When pregnancy occurs, the spinal arteries are also supposed to thin and widen to compensate for the increased intravascular volume that accompanies pregnancy. This process does not occur in individuals with preeclampsia, or there is only a partial widening. This restricts the amount of blood that can flow through the spinal arteries to the placenta, leading to poor placental perfusion and ischemia (Norwitz, 2021).

Measuring Blood Pressure

The criteria for diagnosing hypertension require accurate blood pressure measurements. Blood pressure measurements that are elevated enough to classify as any form of HDP should be repeated. However, there should be at least a 10-minute refractory period between measurements. Instructing the patient on proper positioning when obtaining blood pressure is essential for accuracy. The patient should be seated with their legs uncrossed, feet planted on the floor, and their back supported. Ideally, the patient should be seated for a least 5 minutes prior to assessing blood pressure. Neither the patient nor the healthcare professional (HCP) obtaining the blood pressure should speak during the assessment. Improper positioning can lead to an elevated result. To eliminate falsely elevated readings, the patient should not have ingested caffeine, nicotine, or other stimulants in the 30 minutes before the blood pressure assessment. It is essential to use a cuff that is the appropriate size for the patient. A cuff that is not the proper size can affect the blood pressure reading. A cuff that is too small can elevate blood pressure, while a cuff that is too large can show falsely reduced blood pressure. Ensure the cuff has a length that is 1.5 times the circumference of the upper arm or the bladder of the cuff fits around 80% of the arm width and 40% of the circumference. The right arm is preferred when measuring blood pressure unless contraindicated due to another medical condition (ACOG, 2019; Lowdermilk et al., 2016). More specific guidelines can be followed based on the measurement of the arm circumference:

• 22-26 cm: small adult cuff
• 27-34 cm: adult cuff
• 35-44 cm: large adult cuff
• 45-52 cm: adult thigh cuff (ACOG, 2019)

When placed on the patient's arm, the cuff should be positioned at the level of the heart. Patients who cannot sit and must have their blood pressure assessed in a recumbent position should be turned onto their left side. Not using proper techniques when measuring blood pressure can lead to inaccurate results (ACOG, 2019).

Classifications

As discussed above, different disorders make up the various classifications of HDP. Table 1 outlines the ACOG definition of the different types of hypertension diagnosed in pregnancy.

Table 1

ACOG Definitions of HDP 

(ACOG, 2019, 2020; Norwitz, 2021)

Chronic Hypertension 

The ACOG defines chronic hypertension as hypertension diagnosed prior to pregnancy or during the first 20 weeks of pregnancy. The term chronic hypertension can also be used to describe hypertension diagnosed during pregnancy that does not resolve in the first 12 weeks of the postpartum period as expected. As stated above, chronic hypertension affects 2% to 3% of all pregnancies. The rate of chronic hypertension increased by 67% from 2000 to 2009. This increase in prevalence is attributed to rising obesity rates in the US and the older average maternal age at the time of pregnancy (ACOG, 2019).

There are two types of chronic hypertension, primary and secondary. Approximately 90% of individuals with chronic hypertension have primary hypertension. This type of hypertension has an unknown cause. Secondary hypertension affects fewer individuals but leads to poorer maternal and fetal outcomes. Secondary hypertension is attributed to another medical condition, such as sleep apnea, renal disease, or aldosteronism. Secondary hypertension should be considered for pregnant individuals older than 35, those without a family history of hypertension, those with abnormal serum laboratory results (i.e., hypokalemia, elevated creatinine, or albuminuria), or those with hypertension that is resistant to treatment (Garovic et al., 2022).

Although the ACOG defines hypertension in pregnancy as an SBP above 140 mmHg or DBP above 90 mmHg, the American College of Cardiology (ACC) and the American Heart Association (AHA) have adjusted their guidelines for the diagnosis of hypertension in non-pregnant individuals. According to the AHA guidelines, stage 1 hypertension is defined as an SBP of 130-139 mmHg or DBP of 80-89 mmHg, and stage 2 hypertension as an SBP above 140 mmHg or DBP above 90 mmHg. The AHA recommends initiating treatment for non-pregnant individuals with stage 1 hypertension and current cardiovascular disease or when risk factors are present that increase the risk of developing cardiovascular disease. Due to these new recommendations, an individual with stage 1 hypertension may already be on medications to treat high blood pressure even though they do not meet the ACOG guidelines for hypertension. For these individuals, treatment should be continued during pregnancy. Unfortunately, due to the difference in guidelines, there is some disagreement about whether treatment should be initiated if a pregnant individual presents in the first trimester with blood pressure measurements that fall within the range of stage 1 hypertension, as defined by the AHA and ACC (ACOG, 2019; Garovic et al., 2022).

Treatment Adjustments

Pregnant individuals who are not taking antihypertensive medications prior to pregnancy, or are not taking an effective regimen, are often started on labetalol (Trandate) or nifedipine (Procardia) as indicated. These medications have been used extensively during pregnancy and have well-documented safety profiles for this patient population. For patients who become pregnant while already following an effective medication regimen, the risks versus benefits of continuing that regimen must be weighed based on the individual patient and clinical presentation. Patients taking angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) to manage their chronic hypertension should be counseled on the risks of becoming pregnant while taking these medications. Before pregnancy, these medications should be discontinued, and the treatment regimen should be adjusted since ACE inhibitors and ARBs have been associated with fetal malformations and neonatal complications, including intrauterine growth restriction (IUGR) and kidney failure. Aldosterone antagonists, including spironolactone (Aldactone) and eplerenone (Inspra), should also be discontinued or avoided, as they can cause a male fetus to develop feminine features (Chandrasekaran et al., 2022; Friel, 2022).

Tests for Baseline Evaluation

All pregnant individuals with chronic hypertension should undergo baseline monitoring of organ function with repeat monitoring periodically throughout their pregnancy (ACOG, 2019). Laboratory testing recommendations include:

• serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT)
• serum creatinine
• serum electrolytes (especially potassium)
• complete blood count (CBC)
• random urine protein/creatinine ratio
• electrocardiogram (ECG; ACOG, 2019; Friel, 2022)

An echocardiogram should be completed for any pregnant individual with chronic hypertension diagnosed over 4 years prior to their pregnancy. After the initial fetal anatomy scan conducted at around 20 weeks of gestation, it is recommended that ultrasounds be completed every month beginning at 28 weeks to monitor fetal growth and catch IUGR early. If other complications are present such as renal impairment, this monitoring should begin before 28 weeks (Friel, 2022).

Complications

Most individuals diagnosed with chronic hypertension will have an uncomplicated pregnancy if their hypertension is controlled (Chandrasekaran et al., 2022). Those with uncontrolled hypertension or comorbidities are at an increased risk of developing the following maternal and fetal complications:

• maternal
• death
• stroke
• pulmonary edema
• renal insufficiency leading to renal failure
• myocardial infarction
• superimposed preeclampsia
• hypertensive urgency
• cesarean delivery
• postpartum hemorrhage
• gestational diabetes
• placental abruption (ACOG, 2019; Chandrasekaran et al., 2022)
• fetal and neonatal
• stillbirth or intrauterine fetal demise (IUFD)
• IUGR
• preterm birth
• congenital anomalies (e.g., heart defects, hypospadias, and esophageal atresia; ACOG, 2019)

Gestational Hypertension 

As defined above, gestational hypertension occurs in an individual with no history of hypertension after 20 weeks of gestation and subsides within the first 6 weeks of the postpartum period. Patients are usually asymptomatic, with elevated blood pressure as the only indication of the disorder. Gestational hypertension is considered severe when the SBP is greater than 160 mmHg, or the DBP is greater than 110 mmHg. Although blood pressure readings are typically taken 4 hours apart, the time between readings is shorted to expedite treatment initiation when the first reading is severely elevated. Severe hypertension requires treatment in an inpatient setting where close monitoring of the pregnant patient and the fetus can occur (ACOG, 2020).

Risk Factors

Certain factors can increase the risk of an individual developing gestational hypertension (ACOG, 2020). Some of these risk factors are:

• obesity
• nulliparity (i.e., never giving birth to a live infant)
• primigravida when younger than 19 or older than 40 years old
• multifetal gestation
• history of gestational hypertension or preeclampsia in a previous pregnancy
• family history of preeclampsia (either a parent or a sibling)
• Black or Hispanic ethnicity
• low socioeconomic status
• prepregnancy body mass index (BMI) greater than 30
• underlying kidney disease
• underlying chronic hypertension (ACOG, 2020; Ying et al., 2018)

The outcomes of individuals diagnosed with gestational hypertension are predominantly positive; however, gestational hypertension does increase a person’s risk of experiencing adverse effects. In 50% of patients, gestational hypertension will eventually lead to preeclampsia with the development of proteinuria or organ dysfunction (ACOG, 2020).

Preeclampsia 

Preeclampsia is a hypertensive disorder that presents during pregnancy. Like gestational hypertension, preeclampsia is new-onset hypertension that appears after 20 weeks of gestation; however, it is typically distinguished from gestational hypertension by the presence of proteinuria. Preeclampsia occurs in 3% to 4% of pregnancies in the US and is responsible for 9% of maternal deaths. Although preeclampsia can develop any time after 20 weeks of gestation, 90% of cases occur after 34 weeks. Although the onset of preeclampsia typically occurs during pregnancy, it can manifest after delivery. Typically, this form of preeclampsia develops within 48 hours of delivery but can present up to 6 weeks later. For most patients, any organ injury sustained as a result of preeclampsia resolves within the first few days or weeks of the postpartum period (ACOG, 2020).

Pathophysiology 

The exact cause of preeclampsia is not fully understood at this time. There is evidence that placental abnormalities are the leading cause of the disease since clinical manifestations of preeclampsia begin to improve once the placenta is delivered (ACOG, 2020; Flint et al., 2019). The ACOG lists the following mechanisms thought to be the possible causes of preeclampsia:

• poor placental perfusion, leading to ischemia
• immune maladaptation
• toxicity from an excess of very low-density lipoproteins (VLDLs)
• genetic abnormalities
• rapid apoptosis or necrosis of trophoblasts (cells that form the outer layer of the blastocyte that eventually develop into the placenta)
• increased inflammatory response
• the release of excess antiangiogenic factor Feline McDonough sarcoma (FMS)-like tyrosine kinase-1 (sFlt-1), which binds circulating proangiogenic vascular endothelial growth factor (VEGF) and placental growth factor (PIGF), leading to vascular dysfunction and insufficiency; VEGF and PIGF promote the vascular changes that occur during pregnancy (ACOG, 2020; Flint et al., 2019)

Risk Factors 

Risk factors for developing preeclampsia are similar to those for gestational hypertension (ACOG, 2020). Additional risk factors that are specific to preeclampsia include:

• infection during pregnancy (i.e., urinary tract infection [UTI])
• pregestational or gestational diabetes
• thrombophilia (a blood disorder that increases the risk of blood clots)
• systemic lupus erythematosus (SLE) or rheumatoid arthritis 
• antiphospholipid antibody syndrome or Hughes syndrome (an autoimmune disease that increases the risk of blood clots)
• advanced maternal age (older than 35)
• the use of assisted reproductive technology (i.e., in vitro fertilization)
• history of obstructive sleep apnea (ACOG, 2020; Lowdermilk et al., 2016)

Diagnosis

The classic diagnostic features of preeclampsia are hypertension with the presence of proteinuria. The criteria for diagnosing preeclampsia based on blood pressure follow the same guidelines as diagnosing gestational hypertension. A patient is considered to have proteinuria when there is 300 mg or more protein present in a 24-hour urine collection, a protein/creatinine ratio of 0.3 or more, or a dipstick reading of 2+. A dipstick reading should only be used when other testing methods for proteinuria are unavailable, or a rapid diagnosis is required (ACOG, 2020). If proteinuria is not present, the patient may still be diagnosed with preeclampsia if any of the following develop:

• thrombocytopenia: platelet count less than 100 x 10⁹/L
• renal insufficiency: a creatinine level greater than 1.1 mg/dL or a 2-fold increase of baseline creatinine levels without any other contributing renal disease
• impaired liver function: an increase of liver enzyme levels to twice the upper limit of the normal range
• a rapid, new-onset headache that is unresponsive to treatment with acetaminophen (Tylenol), cannot be attributed to another cause and does not include visual changes (ACOG, 2020)

To diagnose preeclampsia with severe features, a patient must present with an SBP greater than 160 mmHg or DBP greater than 110 mmHg on at least two readings 4 hours apart unless the patient is already taking antihypertensive medications (ACOG, 2020). Other potential symptoms include all those associated with preeclampsia with and without proteinuria described above, in addition to the following:

• severe and persistent right upper quadrant pain or epigastric pain that is resistant to treatment and cannot be attributed to any other cause
• massive proteinuria with over 500 mg of protein present in a 24-hour urine collection
• progressive renal insufficiency
• pulmonary edema
• visual disturbances with or without associated headaches that are resistant to treatment (ACOG, 2020; Lowdermilk et al., 2016)

Most individuals with preeclampsia are asymptomatic. When patients do experience symptoms, they may attribute them to the changes the body undergoes during pregnancy and not report them to the provider. It is essential to educate pregnant patients to report headaches that are persistent and do not resolve, any vision changes (e.g., blurry vision, double vision, seeing flashing lights or lines across the visual field, or blind spots), shortness of breath, and pain in the epigastric area that be compared to severe heartburn (Norwitz, 2021).

Complications 

Both maternal and fetal complications can occur as a result of preeclampsia. Preeclampsia can increase the risk of IUGR, oligohydramnios (reduced amniotic fluid volume), placental abruption, IUFD, delivery via cesarian section, preterm birth, and maternal and fetal morbidity and mortality. Preeclampsia can also progress and become HELLP syndrome or eclampsia. Due to complications, the infant may require admission to a neonatal intensive care unit (NICU) for monitoring following delivery (Wheeler et al., 2022; USPSTF, 2017).

HELLP Syndrome. A variant of severe preeclampsia known as HELLP syndrome is named for its defining characteristics: hemolysis, elevated liver enzymes, and low platelet levels. HELLP syndrome complicates 0.5% to 0.9% of all pregnancies in the US. Over 70% of cases occur during the third trimester between 26 and 40 weeks, with the remaining 30% occurring within 48 hours of delivery. Although HELLP syndrome is considered a progression of preeclampsia, 12% to 18% of patients diagnosed are not hypertensive, and 13% present without proteinuria. Up to 24% of cases result in maternal mortality, and up to 37% lead to perinatal mortality (Khalid et al., 2022; Leeman et al., 2016).

Although the pathophysiology is not entirely understood, HELLP syndrome is thought to begin with abnormal placental development resulting in poor perfusion, which leads to systemic inflammation mediated by the activation of the complement system. This amplified activation leads to even greater inflammation of the hepatic system compared to what occurs with preeclampsia. In HELLP syndrome, the coagulation cascade is activated when platelets adhere to the damaged endothelium of the placenta. These platelets release serotonin and thromboxane A, which cause vasoconstriction and platelet aggregation, leading to further endothelial damage. This excessive use of platelets leads to a decrease in the circulating number, resulting in thrombocytopenia. As circulating blood flows through the affected blood vessels, they begin to break down, causing microangiopathic hemolytic anemia. A subset of HELLP patients present with hemolytic uremic syndrome (HUS) as a result of thrombotic microangiopathy (Khalid et al., 2022).

Individuals with HELLP syndrome may experience a variety of non-specific symptoms. For most patients, the symptoms improve during the day and worsen overnight. Symptoms seen in individuals with HELLP syndrome include excessive fatigue, malaise, flu-like symptoms, edema, excessive weight gain, headaches, gastrointestinal (GI) upset with nausea and vomiting, pain in the epigastric area, vision changes including blurred vision, hypofibrinogenemia (reduced fibrinogen levels), nosebleeds, and seizures. HELLP syndrome occurs more frequently in White pregnant individuals than in any other population(Genetic and Rare Diseases Information Center [GARD], n.d.; Lowdermilk et al., 2016).

Laboratory testing required to diagnose HELLP syndrome consists of liver function tests, CBC, peripheral blood smear, and serum creatinine levels. A diagnosis of HELLP syndrome requires confirmed hemolysis, liver enzymes (ALT or AST) elevated to twice the normal upper limit, and platelet levels below 100 x 10⁹/L. For hemolysis to be confirmed, at least 2 of the following must be present: schistocytes of helmet cells on a peripheral blood smear, serum bilirubin above 1.2 mg/dL, lactate dehydrogenase (LDH) twice the normal upper limit, or anemia with hemoglobin (Hgb) below 8 g/dL that cannot be attributed to hemorrhage (Khalid et al., 2022). The laboratory changes that occur in preeclampsia or HELLP syndrome are outlined in Table 2.

Table 2

Laboratory Changes in Preeclampsia and HELLP Syndrome

(Lowdermilk et al., 2016)

HELLP syndrome can lead to complications that affect the pregnant individual and their fetus (Khalid et al., 2022). Maternal complications associated with the development of HELLP syndrome include:

• eclampsia
• placental abruption (in 11% to 25% of cases)
• cesarean section
• disseminated intravascular congestion (DIC, in 15% to 62.5% of cases)
• acute renal failure (in 36% to 50% of cases)
• liver rupture
• fulminant liver failure
• cerebral hemorrhage
• cerebral edema
• pulmonary edema
• acute respiratory distress syndrome (ARDS)
• retinal detachment
• infection leading to possible sepsis
• postpartum hemorrhage (in 12.5% to 40% of cases)
• maternal mortality (Khalid et al., 2022; Lowdermilk et al., 2016)

Fetal complications that can occur as a result of HELLP syndrome include:

• IUGR
• preterm birth
• thrombocytopenia, leukopenia, or neutropenia
• respiratory distress syndrome
• perinatal death (Khalid et al., 2022)

Eclampsia. A progression of preeclampsia, known as eclampsia, presents with tonic-clonic seizures and coma. Eclampsia can be prevented with the timely delivery of the fetus once preeclampsia is diagnosed or through the prophylactic use of anticonvulsants, including magnesium sulfate. Benzodiazepines can be used when magnesium sulfate is contraindicated or ineffective. In 78% to 83% of cases, symptoms occur before the development of eclampsia, including persistent occipital or frontal headaches, vision changes such as blurred vision and photophobia, severe epigastric or right upper quadrant pain, abdominal pain, and mental status changes. For some patients, seizures may occur without warning or in the presence of symptoms associated with preeclampsia. Some patients progress to eclampsia with minimal blood pressure changes (ACOG, 2020; Lowdermilk et al., 2016).

There are three stages of tonic-clonic seizures: invasion, contraction, and convulsion. The stage of invasion can last 2-3 seconds. During this stage, the patient exhibits fixed eyes and twitching facial muscles. The stage of contraction lasts 15-20 seconds. During this stage, the eyes may appear bloodshot and bulging. There is also tonic contraction of the muscles, resulting in flexed arms, clenched fists, and inverted legs. During the stage of convulsion, the muscles intermittently contract and relax. Respirations often cease and then resume as long, deep inhalations. During the seizure, the patient may also have an episode of urine or stool incontinence. Following seizure cessation, the patient may experience hypotension, disorientation, muscle twitching, or amnesia that may persist for a time. After the seizure, the patient may not regain consciousness and become comatose (ACOG, 2020; Lowdermilk et al., 2016).

Maintaining patient safety during an active seizure in the clinical setting is essential. The priority is to keep the airway patent. This is achieved by turning the patient's head to the side or placing them in a lateral decubitus position. It is important to stay with the patient and call for assistance using the call light or other means. If the patient is in a hospital bed, raise the side rails to keep them from falling and lower the bed if not already in the lowest position to decrease the distance to the floor. If not already done, attempt to pad the side rails with pillows or blankets to prevent injury. Ideally, patients at risk of developing seizures should have the side rails of their bed padded upon admission for safety and suction placed at the bedside for airway management if needed. Observe the patient during convulsions and monitor their length. Once the patient enters the postictal stage, they should not be left unsupervised until they are alert and oriented and their vital signs are stable. The patient's airway should be suctioned to remove excess secretions if needed. Oxygen should be initiated at 10 L/min continuously via a nonrebreather mask to improve oxygenation. Continuous pulse oximetry should also be initiated to monitor the patient’s oxygenation and response to oxygen administration. Complete vital signs—including blood pressure, respirations, and heart rate—should be monitored frequently (based on organization policy). If not already present, a peripheral intravenous (IV) catheter should be placed, and IV fluids, magnesium sulfate, or another anticonvulsant should be initiated (Lowdermilk et al., 2016).

Fetal monitoring should be initiated after any seizure activity. During a seizure, the fetus can experience prolonged decelerations and bradycardia. There may also be an increase in uterine contractility and tone. Maternal respiratory changes and hypoxia can lead to fetal hypoxia and hypercarbia. Post-seizure fetal monitoring may also show recurrent deceleration, reduced variability, and tachycardia. Fetal monitoring changes often resolve following maternal stabilization (ACOG, 2020).

Prevention 

Low-Dose Acetylsalicylic Acid (Aspirin) 

Low-dose (81 mg) acetylsalicylic acid (ASA; Aspirin) has been used successfully to delay the onset or prevent the development of preeclampsia. The ACOG, the Society for Maternal-Fetal Medicine (SMFM), and the US Preventive Services Task Force (USPSTF) recommend initiating treatment for individuals with any high-risk factor or more than one moderate risk factor for developing preeclampsia. Treatment should begin after 12 weeks of gestation but optimally before 16 weeks. The dose of ASA (Aspirin) used for pregnant individuals is one low-dose (81 mg) tablet orally every day until delivery (ACOG Practice Advisory, 2021; USPSTF, 2021). Based on the guidelines set by the ACOG, SMFM, and USPSTF, individuals with the following risk factors are considered at high risk for developing preeclampsia:

• a history of preeclampsia
• multifetal gestation
• chronic hypertension
• pregestational diabetes
• underlying kidney disease
• SLE
• antiphospholipid antibody syndrome (ACOG Practice Advisory, 2021)

The following are considered moderate risk factors for the development of preeclampsia, and low-dose ASA (Aspirin) should be initiated when more than one is present:

• nulliparity
• BMI above 30
• a period between subsequent pregnancies of greater than 10 years
• pregnancy via invitro fertilization
• immediate family history of preeclampsia (ACOG Practice Advisory, 2021)

In October 2020, the US Food and Drug Administration (FDA) released a warning addressing the safety of using ASA (Aspirin) during pregnancy after 20 weeks. The warning advised that using nonsteroidal anti-inflammatory (NSAID) drugs after 20 weeks, including ASA (Aspirin), can cause serious kidney problems in the fetus. Although rare, this complication can lead to oligohydramnios. Using NSAIDs after 30 weeks can increase the risk that the ductus arteriosus closes prematurely. The FDA did release an exception to this warning stating that the use of 81 mg ASA (Aspirin) is permissible under the direct supervision of an HCP when the risk of the disease being treated outweighs the risk of fetal complications from the treatment (USPSTF, 2021).

Although the dose of ASA (Aspirin) used for prevention is low, there are still adverse effects and contraindications that HCPs should consider before initiating treatment. Adverse effects of ASA (Aspirin) include headaches, lethargy, hypotension, tachycardia, tinnitus, nausea, GI distress, vomiting, prolonged pregnancy and labor, proteinuria, prolonged bleeding time, rash, increased bruising, low birth weight in the infant(s), and IUFD. ASA (Aspirin) is contraindicated in patients with a known hypersensitivity to the drug, those who have a history of G6PD deficiency (can lead to hemolytic anemia), or those with other bleeding disorders such as hemophilia, von Willebrand disease, and bleeding ulcers. ASA (Aspirin) should be used cautiously in patients with vitamin K deficiency, thrombocytopenia, and impaired renal function. ASA (Aspirin) should be taken with food, milk, or a large glass of water to reduce GI side effects. The medication should not be stopped unless instructed by an HCP (Woods, 2023).

Dietary Modifications

Making lifestyle changes can decrease the risk of hypertension during pregnancy or decrease the effects of chronic hypertension on a pregnant individual and their developing fetus. Prepregnancy BMI is a significant risk factor for the development of HDP. Although pregnant individuals are not advised to lose weight during pregnancy, there are recommendations on how much weight they should gain based on their prepregnancy BMI (Perry et al., 2022). Weight gain recommendations are outlined in Table 3.

Table 3

Recommendations for Weight Gain During Pregnancy

(Perry et al., 2022)

Dietary modifications can limit weight gain during pregnancy and decrease the risk of HDP. The majority of caloric intake should come from plant-based foods and vegetable-based oils. It is recommended that a pregnant individual should aim to consume at least 400 g/day of fruits and vegetables. Foods high in fat, sugar, or salt should be limited or avoided. Pregnant individuals are encouraged to consume 25 to 30 g/day of dietary fiber. Increased dietary fiber can contribute to the maintenance of a healthy weight and decrease an individual's risk of cardiovascular disease. A high-fiber diet is also associated with a reduction in blood pressure and inflammation. Incorporating food-based probiotics has also been shown to reduce the incidence of preeclampsia. Probiotics help decrease inflammation in the placenta's trophoblast cells, leading to reduced systemic inflammation and blood pressure. One randomized control study that included 33,399 pregnant individuals found that when a probiotic yogurt was consumed for 9 weeks in late pregnancy, there was a significant reduction in c-reactive protein levels and a lower risk of developing preeclampsia (Perry et al., 2022).

Specific diets that can reduce the risk of HDP include the dietary approaches to stop hypertension (DASH) diet and the Mediterranean diet. The DASH diet focuses on consuming high amounts of fruits, vegetables, whole grains, low-fat dairy products, and plant-based protein while limiting the consumption of red meat, sweets, and sugary drinks. The Mediterranean diet prioritizes the consumption of fruits, vegetables, and whole grains. The Mediterranean diet limits the consumption of red meat, poultry, and dairy products (Perry et al., 2022).

Treatment 

Treatment options vary based on the class of hypertension being treated. The types of treatment options include delivery of the fetus or medical management based on fetal gestational age and maternal and fetal presentation. The only true cure for gestational hypertension or the various forms of preeclampsia is delivery. The goal of medication management for non-severe hypertension is to obtain an SBP between 110-135 mmHg and a DBP between 70-85 mmHg. For severe hypertension or hypertension with severe features, the goal is to decrease blood pressure below 160/110 mmHg and manage symptoms until delivery can occur (Wiles et al., 2021).

Chronic Hypertension, Gestational Hypertension, and Preeclampsia Without Severe Symptoms

Treatment of chronic hypertension, gestational hypertension, and preeclampsia without severe features focuses on reducing the patient's blood pressure and preventing the progression to a more severe type of hypertension with systemic effects. These are the only hypertensive conditions that can be appropriately managed in an outpatient setting. Pharmaceutical management and continued observation is an appropriate treatment plan for individuals with controlled chronic hypertension, gestational hypertension, or preeclampsia without severe symptoms until 37 0/7 weeks of gestation. Observation of these individuals includes regular ultrasounds to monitor fetal development and growth and amniotic fluid levels, weekly laboratory testing to evaluate changes related to preeclampsia, and weekly antepartum testing (i.e., biophysical profile, non-stress test [NST], and doppler monitoring), and frequent blood pressure monitoring. The frequency of monitoring may be adjusted based on patient presentation and clinical findings (ACOG, 2020).

When treating chronic hypertension, gestational hypertension, or preeclampsia without severe symptoms, methyldopa (Aldomet) is the first-line treatment. Second-line treatments include labetalol (Normodyne), nifedipine (Procardia), hydralazine (Apresoline), and hydrochlorothiazide (HydroDiuril; ACOG, 2019).

Methyldopa (Aldomet) 

Methyldopa is the first-line and most widely used medication to treat non-severe hypertension in pregnant patients. Methyldopa decreases blood pressure by acting as a central alpha-receptor agonist, thereby reducing sympathetic tone and peripheral vascular resistance. The use of methyldopa (Aldomet) can prevent the progression of hypertension in pregnancy to severe hypertension. Initial dosing is 250 mg administered orally 2 to 3 times daily, increasing to 500 to 3,000 mg/day in 2 to 4 divided doses. This medication has been used in pregnant individuals for over 40 years, and there is no indication of any effect on uteroplacental or fetal hemodynamics. When used in pregnancy, the most common adverse effects are related to central nervous system depression, including drowsiness, decreased mental alertness, impaired sleep leading to daytime fatigue, and depression. Other adverse effects consist of edema, nasal congestion, salivary gland inflammation leading to xerostomia (dry mouth), nausea, vomiting, diarrhea, constipation, flatulence, and abdominal distention. Less common but more severe adverse effects include hepatitis, hepatic necrosis, and jaundice. Methyldopa (Aldomet) is contraindicated in patients with a previous hypersensitivity reaction to the drug and those with active hepatic disease, including hepatitis or cirrhosis (ACOG, 2019; Magee & van Dadelszen, 2021; Woods, 2023).

Labetalol (Normodyne)

Labetalol (Normodyne) is a beta-adrenergic blocker that decreases blood pressure through vasodilation due to the blockage of alpha and non-selective beta receptors. Labetalol decreases blood pressure without causing reflex tachycardia or decreasing cardiac output. Initial dosing is 100 to 200 mg orally twice daily, increasing to 200 to 2,400 mg/day in divided doses 2 or 3 times per day as needed to maintain an SBP below 140 mmHg and DBP below 90 mmHg. Labetalol (Normodyne) is often added to methyldopa (Aldomet) treatment when monotherapy is ineffective. Adverse effects include dizziness, fatigue, headaches, syncope, vertigo, somnolence, edema, orthostatic hypotension, vision changes, nausea, vomiting, dyspnea, wheezing, and pruritus. If adverse effects are not tolerated, dosing may be moved to bedtime or changed to 3 times daily. Since labetalol (Normodyne) is a non-selective beta receptor antagonist, it should be used cautiously in patients with preexisting respiratory conditions, including asthma, and is contraindicated if the respiratory condition is not well controlled. Treatment is also contraindicated in patients with a history of myocardial disease, decompensated cardiac function, heart block greater than first-degree, or bradycardia (ACOG, 2019; Magee & von Dadelszen, 2021; Woods, 2023).

Nifedipine (Procardia)

Nifedipine (Procardia) is a calcium channel blocker used to control hypertension in pregnant individuals. For routine maintenance of hypertension, the extended-release formulation should be used; the immediate-release form is reserved for the treatment of severe hypertension. Initial dosing is 30 to 60 mg orally once daily, increasing to a maximum dose of 120 mg/day as needed to control blood pressure. The sublingual formulation should not be used in pregnant patients. Patients must be educated to store the medication out of direct sunlight, take whole tablets, and not break or crush them. Adverse effects include dizziness, fatigue, lightheadedness, weakness, mood changes, sleep disturbances, flushing, peripheral edema, palpitations, nasal congestion, a sore throat, blurred vision, nausea, heartburn, diarrhea, constipation, muscle cramps, joint stiffness, coughing, wheezing, shortness of breath, and pruritus. Nifedipine (Procardia) can be taken with a low-fat meal to reduce flushing. Nifedipine (Procardia) is contraindicated in patients with tachycardia due to the reflex tachycardia that can occur. This medication should be used cautiously in patients with renal insufficiency or hepatic disorders (ACOG, 2019; Woods, 2023).

Hydrochlorothiazide (HydroDiuril) 

The thiazide diuretic, hydrochlorothiazide (HCTZ; HydroDiuril), is primarily used to treat chronic hypertension during pregnancy or as a third-line agent to treat hypertension resistant to treatment with antihypertensive drugs. Thiazide diuretics work by inhibiting the reabsorption of sodium and chloride in the distal portion of the nephron, resulting in decreased intravascular volume. There are concerns that decreasing intravascular volume can have adverse fetal outcomes, including IUGR and oligohydramnios; however, there are mixed results in clinical studies regarding this. Initial dosing in pregnancy is 12.5 to 50 mg orally once daily. Patients should take the medication in the morning to prevent nocturia. Adverse effects include dizziness, vertigo, headaches, hypotension, blurred vision, anorexia, nausea, vomiting, abdominal pain, diarrhea or constipation, hypokalemia, hyperglycemia and glucose intolerance, dehydration, muscle cramps, photosensitivity, and rash. HCTZ (HydroDiuril) is contraindicated in patients with a sensitivity to other thiazide diuretics or sulfonamide derivatives and those with SLE. This medication should be used cautiously in patients with gout due to its effects on uric acid excretion, diabetes due to glucose intolerance, renal disease, and impaired hepatic function. If the patient is already being treated with HCTZ (HydroDiuril) before pregnancy, the dose may need to be adjusted based on electrolyte levels, especially potassium, due to the risk of hypokalemia and resulting clinical manifestations (ACOG, 2019; Woods, 2023).

Severe Hypertension/Preeclampsia with Severe Features 

 Many of the same medications used to treat chronic hypertension, gestational hypertension, and preeclampsia without severe features are also used for urgent blood pressure control. When used for urgent blood pressure control, the initial dose of labetalol (Normodyne) is 10 to 20 mg given IV, then 20 to 80 mg every 10 to 30 minutes with a maximum cumulative dose of 300 mg. Labetalol (Normodyne) may also be administered via continuous IV infusion at 1 to 2 mg/min. Blood pressure effects occur quickly since the onset of action of labetalol (Normodyne) is only 1 to 2 minutes. The benefits of treatment with labetalol (Normodyne) include fewer adverse effects than other antihypertensive agents used for urgent blood pressure control and a lower risk of reflex tachycardia (ACOG, 2020).

Nifedipine (Procardia), in its immediate release form, is also used to treat severely elevated blood pressure urgently. Initial dosing is 10 to 20 mg administered orally. Repeat dosing with 10 to 20 mg orally is indicated if there is no response within 20 minutes after the initial dose. Nifedipine (Procardia) is then administered every 2 to 6 hours up to a maximum daily dose of 180 mg. When using nifedipine (Procardia) to treat severe hypertension, the patient may experience reflex tachycardia and headaches (ACOG, 2020).

Hydralazine (Apresoline) is a peripheral vasodilator used for urgent blood pressure control in severe hypertension. It works by relaxing arteriole smooth muscle, decreasing vascular resistance. The onset of action of hydralazine (Apresoline) is 10 to 20 minutes, which is slower than other antihypertensives. The initial dose is 5 mg administered IV or intramuscularly (IM). Repeat dosing is 5 to 10 mg administered IV every 20 to 40 minutes with a maximum cumulative dose of 20 mg. Hydralazine (Apresoline) can also be administered via continuous IV infusion at 0.5 to 10 mg/hr. Administering high doses or utilizing the medication frequently can lead to maternal hypotension, headaches, dizziness, angina, palpitations, tachycardia, edema, flushing, anemia, urinary retention, dyspnea, and rash. Fetal adverse effects include abnormal fetal heart rate tracing, a complication seen more frequently when using hydralazine (Apresoline) than other antihypertensive agents. Hydralazine (Apresoline) should be used cautiously with diuretics, as severe hypotension can result. Other contraindications include a patient history of hypersensitivity to aspirin, coronary artery disease (CAD), or mitral valve disease. Hydralazine (Apresoline) should be used cautiously in patients with severe renal impairment, stroke, or cardiac disease. The ACOG has published example treatment algorithms to follow when treating severe hypertension. These algorithms are outlined in Table 4 (ACOG, 2020; Woods, 2023).

Table 4

ACOG Treatment Algorithm Examples

(ACOG, 2022)

HELLP Syndrome

The only true treatment for HELLP syndrome is delivery. Patients with this syndrome can deteriorate quickly and are best managed in an acute care facility that can care for a critical pregnant individual and a critical fetus both in utero and after delivery. Medical management focuses on symptom management and addressing complications as they arise if delivery is not an immediate option. To expedite delivery in pregnancy at less than 34 0/7 weeks of gestation, it is recommended that betamethasone (Diprolene) or dexamethasone (Decadron) be administered to the pregnant individual to accelerate fetal lung development. Per the ACOG, there is not enough evidence to recommend one medication over the other. The recommended dose of betamethasone (Diprolene) is 12 mg administered IM twice, 24 hours apart. The recommended dose of dexamethasone (Decadron) is 6 mg administered IM every 12 hours for four doses. Treatment with either corticosteroid should be initiated even if it is unlikely that the treatment will be finished before delivery. Currently, there is no evidence that shortening the interval between doses—known as "accelerated dosing"—increases the benefit to the fetus when administration on a standard schedule is not expected to be completed prior to delivery (ACOGs' Committee on Obstetric Practice, 2020).

Individuals who have developed HELLP may require pain control, vasopressors, volume expanders, blood transfusions, nutritional supplementation, and respiratory support up to ventilation if necessary. When platelet levels drop below 20 x 10⁹/L before vaginal delivery or below 50 x 10⁹/L before cesarean delivery, the administration of platelets is indicated. Regional anesthesia used during cesarean delivery is contraindicated when platelet levels drop below 50 x 10⁹/L. Magnesium sulfate should also be administered from the time of admission to an inpatient facility until 24 to 48 hours post-delivery. Magnesium sulfate is used to prevent seizure activity and the progression to eclampsia (Khalid et al., 2022; Leeman et al., 2016).

Eclampsia 

Magnesium sulfate is used to prevent eclampsia from developing in patients with preeclampsia with severe features, HELLP syndrome, or who have already experienced a seizure. Magnesium sulfate is a high-alert medication and should never be abbreviated as MgSO₄. Treatment begins with a loading dose of 4 to 6 grams of 10% magnesium sulfate in 100 mL of 0.9% sodium chloride, lactated ringers, or D5W infused over 20 minutes. Following the loading dose, the maintenance dose is 1 to 2 g/hr until 24 hours after delivery. If a seizure occurs despite the initial treatment with magnesium sulfate, an additional 2-gram bolus may be given over 3 to 5 minutes. If prompt treatment is needed and there is no IV access, magnesium sulfate can be administered IM. The IM dose is 10 grams of 50% solution divided into two doses of 5 grams administered into each dorsogluteal muscle (ACOG, 2022; Bernstein et al., 2017).

The administration of magnesium sulfate for the prevention and treatment of seizures can lead to magnesium toxicity in patients with poor renal function. Magnesium toxicity can cause central nervous system depression, respiratory arrest, and cardiac arrest. Urine output should be strictly monitored at least hourly. Often, an indwelling catheter is placed for a more accurate measurement of urinary output. Respiratory rate is often measured continuously along with oxygen saturation, and deep tendon reflexes are assessed frequently. The magnesium sulfate infusion should be discontinued immediately if signs of magnesium toxicity appear, such as the loss of deep tendon reflexes, respiratory rate decreasing to fewer than 12 breaths/min, or urine output decreasing to less than 30 mL/hr. The patient’s serum magnesium level should then be monitored every 2 hours. The infusion can be restarted once the serum magnesium level drops below 7 mEq/L or 8.4 mg/dL. If the patient shows signs of impending respiratory arrest, magnesium toxicity can be reversed rapidly with the administration of 10 mL of 10% calcium gluconate (1000 mg); the administration should be done slowly over 2 to 5 minutes to prevent bradycardia or hypotension (ACOG, 2020; Bernstein et al., 2017; Leeman et al., 2016). Table 5 outlines the laboratory ranges of magnesium.

Table 5 

Serum Magnesium Concentration

(ACOG, 2020)

Magnesium sulfate is contraindicated in patients with myasthenia gravis, hypocalcemia, heart block, myocarditis, pulmonary edema, or moderate to severe renal failure. If magnesium is contraindicated or recurrent seizures occur despite treatment, the initiation or addition of other anticonvulsants, such as lorazepam (Ativan) or diazepam (Valium), can be used to prevent recurrent seizures. The dosing of lorazepam (Ativan) is 2 to 4 mg IV and can be repeated once after 10 to 15 minutes. The dosing of diazepam (Valium) is 5 to 10 mg IV every 5 to 10 minutes until a maximum dose of 30 mg is reached (ACOG, 2022; Bernstein et al., 2017).

Delivery 

For patients with hypertension that is controlled without any underlying complications, delivery should occur between 37 0/7 and 39 0/7 weeks of gestation. If the patient's blood pressure is poorly controlled, presents with severe features, or has underlying complications such as IUGR or superimposed preeclampsia, delivery before 37 0/7 weeks is recommended based on disease severity and clinical presentation. If severe features develop after 34 0/7 weeks of gestation, delivery is recommended once the pregnant individual is stabilized. Postponing delivery to administer steroids is not indicated if the pregnancy is beyond 34 0/7 weeks (ACOG, 2020). Delivery is indicated if the patient develops any of the following:

• severe hypertension (SBP ≥ 160 mmHg or DBP ≥ 110 mmHg)
• persistent headaches that are resistant to treatment
• severe epigastric or right upper quadrant pain that is not relieved with analgesics
• visual disturbances
• mental status changes
• stroke
• myocardial infarction
• HELLP syndrome
• eclampsia
• pulmonary edema
• placental abruption
• vaginal bleeding without a history of placental previa (ACOG, 2020)

Similarly, delivery is indicated for the following fetal complications:

• abnormal fetal test results
• fetal demise
• a poor prognosis before reaching 34 0/7 weeks of gestation (ACOG, 2020)

In these cases, the administration of corticosteroids to promote lung development is indicated; however, based on assessment data, delaying delivery until the completion of the treatment regimen may be contraindicated due to the risk to the fetus and the patient. If severe features appear before a viable gestational age is reached, options must be discussed with the patient regarding termination versus management of symptoms. Management of symptoms is only indicated until any of the listed symptoms appear; however, based on recent legislation, options for pre-viable management may be limited based on specific state laws (ACOG, 2020; Chandrasekaran et al., 2022).

Long-Term Complications

Cardiovascular Effects 

Individuals with gestational hypertension or preeclampsia during pregnancy have an increased risk of cardiovascular disease, stroke, peripheral artery disease, and cardiovascular mortality later in life. Their risk is nearly doubled compared to individuals who did not have hypertension during pregnancy. For individuals with recurrent preeclampsia in subsequent pregnancies or early onset preeclampsia, this risk increases to 4 to 8 times higher than an individual who remained normotensive during pregnancy. Due to this increased risk, follow-up monitoring of blood pressure and weight should occur 6 to 8 weeks after pregnancy and then again 6 to 12 months after pregnancy. Assessments of blood pressure, cholesterol levels, fasting glucose, and hemoglobin A1C should be completed annually until the age of 50 to monitor for the development of cardiovascular complications (ACOG, 2020; Benschop et al., 2019).

Mental Health Effects 

For many pregnant individuals, this life-changing experience can have significant mental health effects. Worldwide, 10% of pregnant individuals and 13% of postpartum individuals suffer from a mental health disorder, with the majority experiencing depression. A pregnancy complicated by hypertension, especially for pregnancies with poor outcomes or severe complications, can elicit or aggravate feelings of anxiety, depression, or even post-traumatic stress disorder (PTSD). Often, mental health symptoms go unreported, leaving the condition untreated, which can result in poor outcomes for both the postpartum individual and their infant (if in the care of the postpartum individual). If an individual with HDP is at higher risk of developing a mental health disorder, routine intrapartum and postpartum monitoring should be completed, and treatment must be initiated promptly (Roberts et al., 2019). For more information, see the NursingCE course Peripartum Mental Health. 

References

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