TYPE	DESCRIPTION
GESTATIONAL HYPERTENSIVE DISORDERS
Gestational hypertension	Development of mild hypertension after week 20 of pregnancy in previously normotensive woman without proteinuria
Preeclampsia	Development of hypertension and proteinuria in previously normotensive woman after 20 weeks of gestation or in early postpartum period; in presence of trophoblastic disease, preeclampsia can develop before 20 weeks of gestation
Eclampsia	Development of convulsions or coma not attributable to other causes in preeclamptic woman
CHRONIC HYPERTENSIVE DISORDERS
Chronic hypertension	Hypertension or proteinuria (or both) in pregnant woman present before pregnancy or diagnosed before 20 weeks of gestation and persistent after 6 weeks postpartum
Superimposed preeclampsia or eclampsia	• In women with hypertension before 20 weeks of gestation: new-onset proteinuria (≥0.5 g protein in a 24-hr collection) • In women with both hypertension and proteinuria before 20 weeks of gestation: significant increase in hypertension, plus one of the following: new onset of symptoms, thrombocytopenia, or elevated liver enzymes

Sources: American College of Obstetricians and Gynecologists (ACOG). (2002). Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. Washington DC: ACOG; Sibai, B. M. (2007). Hypertension. In S. Gabbe, J. Niebyl, & J. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (5th ed.) Philadelphia: Churchill Livingstone.

Gestational hypertension

Gestational hypertension is the onset of hypertension without proteinuria after week 20 of pregnancy (ACOG, 2002; Working Group, 2000). Hypertension is defined as a systolic blood pressure (BP) greater than 140 mm Hg or a diastolic BP greater than 90 mm Hg. The hypertension should be recorded on at least two separate occasions at least 4 to 6 hours apart but within a maximum of a 1-week period (ACOG, 2002; Sibai, 2007; Working Group, 2000). Both the Working Group and the American Heart Association (AHA) have published extensive recommendations for accurately measuring BP (Pickering et al., 2005; Working Group, 2000). Box 21-1 provides detailed instructions for measuring BP.

BOX 21-1 Blood Pressure Measurement

• Measure blood pressure with the woman seated (ambulatory) or in the left lateral recumbent position with the arm at heart level.

• After positioning, allow the woman at least 10 minutes of quiet rest before blood pressure measurement to encourage relaxation.

• Instruct the woman to refrain from tobacco or caffeine use 30 minutes before blood pressure measurement.

• Use the right arm each time for blood pressure measurement.

• Hold the arm in a horizontal position at heart level.

• Use the proper-sized cuff (cuff should cover approximately 80% of the upper arm or be times the length of the upper arm).

• Maintain a slow, steady deflation rate.

• Take the average of two readings at least 6 hours apart to minimize recorded blood pressure variations across time.

• Use Korotkoff phase V (disappearance of sound) for recording the diastolic value.

• Use accurate equipment. The mercury sphygmomanometer is the most accurate device.

• If interchanging manual and electronic devices, use caution in interpreting different blood pressure values.

Gestational hypertension is the most frequent cause of hypertension during pregnancy, with an incidence of 6% to 17% in primigravidas and 2% to 4% in multiparous women. It occurs much more frequently in women with multifetal pregnancies than in other women (Sibai, 2007). Gestational hypertension usually develops at or after 37 weeks of gestation. Women with gestational hypertension have no evidence of preexisting hypertension, and their BPs return to normal levels within 6 weeks after giving birth. Women with mild gestational hypertension usually have good pregnancy outcomes. Some women who are initially thought to have gestational hypertension will eventually be diagnosed with chronic hypertension instead. Others will go on to develop proteinuria, thereby changing their diagnosis to preeclampsia. Women who are diagnosed with gestational hypertension before 35 weeks of gestation are more likely to progress to preeclampsia than women whose onset of hypertension occurs closer to term (Sibai).

Critical Thinking Exercise: Preeclampsia

Case Study: Preeclampsia

Preeclampsia

Preeclampsia is a pregnancy-specific condition in which hypertension and proteinuria develop after 20 weeks of gestation in a previously normotensive woman. A significant contributor to maternal and perinatal morbidity and mortality, preeclampsia complicates approximately 3% to 7% of all pregnancies (American Academy of Pediatrics [AAP] & ACOG, 2007). Preeclampsia is a vasospastic, systemic disorder and is usually categorized as mild or severe for purposes of management (ACOG, 2002; Working Group, 2000). Table 21-2 lists criteria for mild and severe preeclampsia, and Table 21-3 gives common laboratory changes that occur in mild and severe preeclampsia.

TABLE 21-2

Differentiation between Mild and Severe Preeclampsia

	MILD PREECLAMPSIA	SEVERE PREECLAMPSIA
MATERNAL EFFECTS
Blood pressure (BP)	BP reading ≥140/90 mm Hg × two, at least 4-6 hr apart but within a maximum of a 1-week period	Rise to ≥160/110 mm Hg on two separate occasions 6 hr apart with pregnant woman on bed rest
Proteinuria
Qualitative dipstick	≥1+ on dipstick	≥3+ on dipstick
Quantitative 24-hr analysis	Proteinuria of ≥300 mg in a 24-hr specimen	Proteinuria of ≥5 g in 24-hr specimen
Urine output	Output matching intake, ≥25-30 ml/hr	<400-500 ml/24 hr
Headache	Absent or transient	Persistent or severe
Visual problems	Absent	Blurred, photophobia
Irritability or changes in affect	Transient	May be severe
Epigastric or right upper quadrant pain, nausea, and vomiting	Absent	May be present
Thrombocytopenia	Absent	May be present
Impaired liver function	Normal	May be present
Pulmonary edema	Absent	May be present
FETAL EFFECTS
Placental perfusion	Reduced	Decreased perfusion expressing as IUGR in fetus; nonreassuring fetal status on antepartum testing

FHR, Fetal heart rate; IUGR, intrauterine growth restriction.

Sources: American College of Obstetricians and Gynecologists (ACOG). (2002). Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. Washington, DC: ACOG; Sibai, B. M. (2007). Hypertension. In S. Gabbe, J. Niebyl, & J. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (5th ed.) Philadelphia: Churchill Livingstone.

TABLE 21-3

Common Laboratory Changes in Preeclampsia

	NORMAL NONPREGNANT	PREECLAMPSIA	HELLP
Hemoglobin, hematocrit	12-16 g/dl, 37%-47%	May ↑	↓
Platelets (cells/mm³)	150,000-400,000/mm³	Unchanged or <100,000/mm³	<100,000/mm³
Prothrombin time (PT), partial thromboplastin time (PTT)	12-14 sec, 60-70 sec	Unchanged	Unchanged
Fibrinogen	200-400 mg/dl	300-600 mg/dl	↓
Fibrin split products (FSP)	Absent	Absent or present	Present
Blood urea nitrogen (BUN)	10-20 mg/dl	↑	↑
Creatinine	0.5-1.1 mg/dl	>1.2 mg/dl	↑
Lactate dehydrogenase (LDH)*	45-90 units/L	↑	↑ (>600 units/L)
Aspartate aminotransferase (AST), serum glutamic oxaloacetic transaminase (SGOT)	4-20 units/L	Unchanged to minimal ↑	↑ (>70 units/L)
Alanine aminotransferase (ALT)	3-21 units/L	Unchanged to minimal ↑	↑
Creatinine clearance	80-125 ml/min	130-180 ml/min	↓
Burr cells or schistocytes	Absent	Absent	Present
Uric acid	2-6.6 mg/dl	>5.9 mg/dl	>10 mg/dl
Bilirubin (total)	0.1-1 mg/dl	unchanged or ↑	↑ (>.1.2 mg/dl)

^*LDH values differ according to the test or assays being performed.

Sources: American College of Obstetricians and Gynecologists (ACOG). (2002). Diagnosis and management of preeclampsia and eclampsia. ACOG Practice Bulletin No. 33. Washington, DC: ACOG; Cunningham, F., Leveno, K., Bloom, S., Hauth, J., Gilstrap, L., & Wenstrom, K. (Eds.). (2005). Williams obstetrics (22nd ed.). New York: McGraw-Hill; Dildy, G. (2004). Complications of preeclampsia. In G. Dildy, M. Belfort, G. Saade, J. Phelan, G. Hankins, & S. Clark (Eds.), Critical care obstetrics (4th ed.). Malden, MA: Blackwell Science; Sibai, B. M. (2007). Hypertension. In S. Gabbe, J. Niebyl, & J. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (5th ed.). Philadelphia: Churchill Livingstone.

Proteinuria is defined as a concentration at or above 30 mg/dl (≥1+ on dipstick measurement) or more in at least two random urine specimens collected at least 6 hours apart with no evidence of urinary tract infection. In a 24-hour specimen, proteinuria is defined as a concentration at or above 300 mg/24 hours. Because of the discrepancy between random protein determinations the diagnosis of proteinuria should be based on a 24-hour urine collection if possible or a timed collection corrected for creatinine excretion if a 24-hour specimen is not feasible (ACOG, 2002; Longo, Dola, & Pridjian, 2003). To ensure accurate results, proteinuria should be determined using only a urine specimen that has been collected either by catheterization or by a thorough clean-catch technique.

Preeclampsia

Etiology

Preeclampsia is a condition unique to human pregnancy; signs and symptoms develop only during pregnancy and disappear quickly after birth of the fetus and placenta. The cause of preeclampsia is not known. Although preeclampsia is generally a disease of primigravidas, its cause may not be the same for all women. For example, the pathogenesis for a healthy nulliparous woman who develops mild preeclampsia near term or in labor may be very different than that of the woman who has preexisting vascular disease or diabetes, a multifetal pregnancy, or who develops severe preeclampsia earlier in the pregnancy (Sibai, 2007). Box 21-2 lists risk factors for the development of preeclampsia.

BOX 21-2

Risk Factors Associated with the Development of Preeclampsia

• Nulliparity

• Family history of preeclampsia

• Obesity

• Multifetal gestation

• Preeclampsia in previous pregnancy

• Poor outcome in previous pregnancy:

Intrauterine growth restriction

Placental abruption

Fetal death

• Preexisting medical—genetic conditions:

Chronic hypertension

Renal disease

Type 1 (insulin-dependent) diabetes mellitus

Thrombophilias:

Antiphospholipid antibody syndrome

Protein C, protein S, antithrombin deficiency

Source: Sibai, B. (2007). Hypertension. In S. Gabbe, J. Niebyl, & J. Simpson (Eds.), Obstetrics: Normal and problem pregnancies (5th ed.). Philadelphia: Churchill Livingstone.

Many theories have been suggested to explain the cause of preeclampsia. Current theories that are still being considered include abnormal trophoblast invasion, coagulation abnormalities, vascular endothelial damage, cardiovascular maladaptation, and dietary deficiencies or excesses. Immunologic factors and genetic predisposition may also play an important role (Sibai, 2007).

Pathophysiology

Preeclampsia can progress along a continuum from mild to severe preeclampsia to eclampsia. Current thought is that the pathologic changes that occur in the woman with preeclampsia are caused by disruptions in placental perfusion and endothelial cell dysfunction (Gilbert, 2007; Peters, 2008). These pathologic changes are present long before the clinical diagnosis of preeclampsia is made (Roberts & Funai, 2009). Normally in pregnancy the spiral arteries in the uterus widen from thick-walled muscular vessels to thinner, saclike vessels with much larger diameters. This change increases the capacity of the vessels, allowing them to handle the increased blood volume of pregnancy. Because this vascular remodeling does not occur or only partially develops in women with preeclampsia, decreased placental perfusion and hypoxia result (Peters). Placental ischemia is thought to cause endothelial cell dysfunction by stimulating the release of a substance that is toxic to endothelial cells. This anomaly causes generalized vasospasm, which results in poor tissue perfusion in all organ systems, increased peripheral resistance and BP, and increased endothelial cell permeability, leading to intravascular protein and fluid loss and ultimately to less plasma volume. The main pathogenic factor is not an increase in BP but poor perfusion as a result of vasospasm and reduced plasma volume (Fig. 21-1) (Gilbert; Peters; Roberts & Funai). Fig. 21-2 demonstrates how endothelial cell dysfunction causes many of the common signs and symptoms of preeclampsia.

Fig. 21-1 Etiology of preeclampsia: disruptions in placental perfusion and endothelial cell dysfunction.

Reduced kidney perfusion decreases the glomerular filtration rate and leads to degenerative glomerular changes and possibly oliguria. Pathologic changes in the endothelial cells of the glomeruli (glomerular endotheliosis) are uniquely characteristic of preeclampsia. Protein, primarily albumin, is lost in the urine. Uric acid clearance is decreased. Serum uric acid levels, however, increase. Sodium and water are retained. Acute tubular necrosis and renal failure may occur (Gilbert, 2007; Peters, 2008; Roberts & Funai, 2009).

Plasma colloid osmotic pressure decreases as serum albumin levels decrease. Intravascular volume is reduced as fluid moves out of the intravascular compartment, resulting in hemoconcentration, increased blood viscosity, and tissue edema. The hematocrit value increases as fluid leaves the intravascular space. In severe preeclampsia, blood volume may decrease to or below nonpregnancy levels; severe edema develops, and rapid weight gain is seen. Arteriolar vasospasm can cause endothelial damage and contribute to an increased capillary permeability, which increases edema and further decreases intravascular volume, predisposing the woman with preeclampsia to pulmonary edema (see Fig. 21-2) (Gilbert, 2007; Roberts & Funai, 2009).

Decreased liver perfusion results in impaired liver function. Liver enzyme levels increase in the wake of liver damage. If hepatic edema and subcapsular hemorrhage develop, the woman may complain of epigastric or right upper quadrant pain. Rupture of a subcapsular hematoma is a life-threatening complication and a surgical emergency (Gilbert, 2007) (see Fig. 21-2).

Arteriolar vasospasms and decreased blood flow to the retina lead to visual symptoms such as scotomata (blind spots) and blurring. Neurologic complications associated with preeclampsia include cerebral edema and hemorrhages and increased central nervous system (CNS) irritability, the last of which causes headache, hyperreflexia, positive ankle clonus, and seizures (Gilbert, 2007; Longo et al., 2003; Roberts & Funai, 2009) (see Fig. 21-2).

Preeclampsia contributes significantly to restriction of fetal growth and the incidence of placental abruption (Hull & Resnik, 2009; Peters, 2008). Impaired placental perfusion leads to early degenerative aging of the placenta. The rate of fetal complications is directly related to the severity of the disease (Longo et al., 2003).

HELLP Syndrome

HELLP syndrome is a laboratory diagnosis for a variant of severe preeclampsia that involves hepatic dysfunction, characterized by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP), not a separate illness. No consensus has been reached, however, regarding which laboratory tests should be used to diagnose HELLP syndrome or what values should be considered abnormal (Sibai, 2007). Table 21-3 lists laboratory changes that occur in HELLP syndrome. A unique form of coagulopathy occurs with HELLP syndrome. The platelet count is low, but coagulation factor assays, prothrombin time (PT), partial thromboplastin time (PTT), and bleeding time remain normal. In some instances, hemolysis does not occur, and the condition is termed ELLP or partial HELLP syndrome (Sibai, Dekker, & Kupferminc, 2005).

Because no agreement has been reached on diagnostic criteria for HELLP syndrome, its reported incidence varies. It has been reported to occur in anywhere from 5% to 20% of women with preeclampsia (Emery, 2005; Gilbert, 2007). HELLP syndrome appears to occur more frequently in Caucasian women than in women of other races. A diagnosis of HELLP syndrome is associated with an increased risk for adverse perinatal outcomes, including pulmonary edema, acute renal failure, disseminated intravascular coagulation (DIC), placental abruption, liver hemorrhage or failure, adult respiratory distress syndrome (ARDS), sepsis, and stroke (Sibai, 2007). The syndrome is associated with an increased risk of maternal death. Perinatal mortality rates range from 7.4% to 20.4%, with a maternal mortality of approximately 1% (Sibai). The rate of preterm birth in women with HELLP syndrome is approximately 70%, with 15% of these occurring before 28 weeks of gestation. Most of the perinatal deaths occur before 28 weeks of gestation, in association with placental abruption or severe intrauterine growth restriction (IUGR) (Sibai).

HELLP syndrome is often nonspecific in clinical presentation. A majority of patients report a history of malaise for several days and some have a nonspecific viral-like syndrome. Many women (30%-90%) experience epigastric or right upper quadrant abdominal pain, nausea, and vomiting. Headaches are reported by 33% to 61% of all women with the syndrome. A small number of women may exhibit symptoms related to thrombocytopenia, such as bruising or hematuria (Sibai, 2007).

Nursing Alert

An extremely important point to understand is that many women with HELLP syndrome may not have the signs or symptoms usually associated with severe preeclampsia. For example, although most women have hypertension, the BP may be only mildly elevated in up to one half of all cases. Proteinuria may be absent. As a result, women with HELLP syndrome are often misdiagnosed with a variety of other medical or surgical disorders (Sibai, 2007).

Care Management

Identifying and preventing preeclampsia

Numerous clinical trials have been conducted studying various methods for preventing preeclampsia. These interventions included the use of low-dose aspirin, antioxidants, calcium, magnesium, and zinc; restricted protein or sodium intake; and fish oil supplementation. None of the interventions demonstrated a significant benefit in preventing or reducing the severity of preeclampsia (Sibai, 2007).

No reliable test has been developed that can be used as a routine screening tool for predicting preeclampsia. Research findings reported by Cockey (2005) suggested that women were increasingly likely to develop preeclampsia if they had low levels of placental growth factor (PIGF) in their urine. The low levels of PIGF were apparent beginning at weeks 25 through 28 of pregnancy. This finding sets the stage for the development of a screening tool for women who are at high risk for preeclampsia (Cockey).

Evidence-Based Practice

Preeclampsia Risk Factors and Prevention