Caring for the Laboring Woman with Hypertensive Disorders Complicating Pregnancy
Patricia M. Witcher
Objectives
As you complete this module, you will learn:
The epidemiology of hypertensive disorders in pregnancy
Current terminology and a current classification system recommended for hypertensive disorders of pregnancy
The definition and characteristics of each hypertensive disorder encountered during pregnancy
Risk factors associated with chronic hypertension and pregnancy outcomes in women with chronic hypertension
Factors that predispose a woman to preeclampsia/eclampsia and pregnancy outcomes in women with the preeclampsia/eclampsia
Current theoretical and known pathophysiologic alterations that occur in women with preeclampsia
The significance of signs and symptoms that correlate with pathophysiologic alterations of body systems in hypertensive disorders during pregnancy
Diagnostic criteria (including laboratory tests) considered valid and reliable for screening and monitoring women at risk for preeclampsia
Triggers in the prenatal record during the admission process that guide nursing assessment
Physical examination of patients with hypertensive disorders
Priorities for treatment and nursing care
Issues of intrapartum pain management
Recommended anticonvulsant treatment regimens for administering magnesium sulfate to the woman with preeclampsia and eclampsia
Recommendations for monitoring and the therapeutic blood level range appropriate for the woman receiving magnesium sulfate
Signs of toxicity in magnesium sulfate overdose and treatment
Guidelines for antihypertensive therapy in hypertensive emergencies in pregnancy
Mechanism of action for antihypertensive agents commonly administered to women with hypertension during pregnancy
Indications for maternal transport of a preeclamptic woman to a high-risk regional center
Special preparations for delivery of a potentially high-risk pregnancy
Postpartum care and education
Key Terms
When you have completed this module, you should be able to recall the meaning of the following terms. You should also be able to use the terms when consulting with other health professionals. Terms are defined in this module or in the glossary at the end of this book.
angiogenesis
antiangiogenic proteins
disseminated intravascular coagulation (DIC)
endothelium (endothelial lining)
epigastric pain
gestational hypertension
hydralazine (Apresoline)
iatrogenic
ischemia
labetalol
microangiopathy
nifedipine (Procardia)
oliguria
prostacyclin (PGI2)
proteinuria
scotomata
thrombocytopenia
thromboxane
vasopressor
Introduction
Hypertension is the most common medical condition in pregnant women and nonpregnant individuals,1 affecting 10% of pregnancies world-wide.2 Although hypertension was the second leading cause of pregnancy-related deaths in the United States from 1987 to 1997,3,4,5 cardiovascular and other medical conditions have emerged as greater contributors to the causes of pregnancy-related death than the traditional pregnancy complications during the most recent surveillance period (2006–2009).6 There remains an increasing trend for hospitalizations for hypertensive disorders of pregnancy in the United States7 which suggests an opportunity for intervention to prevent the progression from morbidity to mortality for hypertensive women during pregnancy and postpartum.
Hypertension, along with other chronic conditions such as diabetes mellitus or chronic renal disease, increases the risk for preeclampsia, a pregnancy-specific hypertensive disorder that poses more significant risks to the woman and fetus2 when it is superimposed upon pre-existing hypertension or presents alone. An understanding of the dynamic and progressive nature of the disease process, current diagnostic criteria, and management recommendations provide the foundation for reducing adverse outcomes. Astute and early assessments as well as patient education on premonitory signs and symptoms of preeclampsia are critical to appropriate diagnosis and early intervention. The etiology and pathophysiology of hypertension in pregnancy have been intensively researched over the years, and although a great deal is still unknown, there has been substantial improvement in the understanding of preeclampsia. This module presents what is currently reflected in the literature as well as guidelines from the American College of Obstetricians and Gynecologists (ACOG) Task Force on Hypertensive in Pregnancy.2 The Task Force on Hypertensive in Pregnancy bases the guidelines for management of hypertensive disorders of pregnancy on evidence and consensus among obstetrical experts. This module reinforces prior understanding of pathophysiology and management guidelines and provides the changes in diagnostic criteria along with more precise recommendations that have evolved for management of hypertension.
Terminology and Classification
Different classification schemes and terminology in the literature have confused healthcare professionals and perpetuate imprecise diagnostic categories, which contributes to a lack of conformity in determining outcomes of hypertensive disorders complicating pregnancy in different research studies. The ACOG Task Force on Hypertension in Pregnancy currently uses the classification schema first introduced by ACOG in 19722 and modified reports of The National High Blood Pressure Education Program, Working Group Report on High Blood Pressure in Pregnancy (Working Group) published through the National Institutes of Health; and the National Heart, Lung, and Blood Institute; and outlines current accepted terminology for the hypertensive disorders of pregnancy8,9,10 to classify hypertensive disorders in pregnancy.
A major goal of the classification system is to differentiate hypertensive disorders that precede pregnancy from those that develop during pregnancy or that are exacerbated by the pregnancy. Preeclampsia is peculiar to pregnancy and manifests with a wide range of clinical manifestations that arise from decreased end-organ perfusion secondary to arteriolar vasospasm, increased capillary permeability from endothelial injury, and hemostatic alterations.11,12
These pathophysiologic alterations typically progress in severity as pregnancy advances and do not resolve until after the infant’s birth. Delivery at the optimal time requires a balanced consideration of the risks to the woman and fetus of continuing the pregnancy to a timeframe sufficient for fetal development and maturity. This timing is challenged by the dynamic and progressive nature of the disease and difficulty in differentiating worsening chronic hypertension versus superimposition of preeclampsia.2
Clarification of Terms
Preeclampsia versus Pregnancy-Induced Hypertension
The term, pregnancy-induced hypertension (PIH) has been used inconsistently to either broadly describe all new onset hypertension in pregnancy with or without accompanying proteinuria or it has been used interchangeably with the term, preeclampsia. Therefore, the term pregnancy-induced hypertension has been abandoned by classification systems used in the United States. This module incorporates this new classification system.2
Gestational Hypertension versus Transient Hypertension
The term, transient hypertension previously described a group of women with gestational hypertension that resolves during the postpartum period.5 Gestational hypertension is defined as blood pressure elevation with onset after 20 weeks’ gestation without proteinuria that often presents near term. Gestational hypertension may manifest for the first time postpartum, but resolves postpartum. Failure of blood pressure to normalize in the postpartum period (which is no longer specified to the specific postpartum day) constitutes chronic hypertension. The term, transient hypertension has been abandoned as well.2
Preeclampsia with or without Severe Features versus Mild and Severe Preeclampsia
Mild preeclampsia is no longer used to describe preeclampsia with the absence of severe manifestations because the Task Force on Hypertension in Pregnancy2 believed it to misrepresent the dynamic and progressive nature of the disease. Even without severe manifestations, there remains a significant risk for morbidity and mortality. ACOG has further recommended that the term severe preeclampsia be replaced with preeclampsia with severe features for similar reasons.
Classification of Hypertensive Disorders Complicating Pregnancy
Each hypertensive disorder complicating pregnancy has distinguishing characteristics, diagnostic criteria, and risks of perinatal morbidity and mortality. The discussion in this module follows the Task Force on Hypertension in Pregnancy.2
Preeclampsia/eclampsia
NOTE: HELLP syndrome—preeclampsia subtype—is discussed within this category
Chronic hypertension
Chronic hypertension with superimposed preeclampsia
Gestational hypertension
Preeclampsia/Eclampsia
Usually occurring after 20 weeks’ gestation, preeclampsia is a pregnancy-specific syndrome with multiple organ system involvement from ischemia
New onset hypertension plus new onset proteinuria
Some women present with new onset hypertension without proteinuria. In the absence of proteinuria, preeclampsia may be diagnosed when new onset hypertension is accompanied by one of the following features that reflect the multisystem involvement:
Thrombocytopenia
Impaired liver function
New development of renal insufficiency
Pulmonary edema
New onset cerebral or visual disturbances
Eclampsia—the onset of convulsions in the woman diagnosed with preeclampsia, which is a severe manifestation
Chronic Hypertension
Hypertension known to be observed prior to pregnancy
OR
Onset of elevated blood pressure before 20 weeks’ gestation when prepregnancy blood pressure is unknown
Chronic Hypertension with Superimposed Preeclampsia
Occurrence of preeclampsia in a woman with pre-existing hypertension
Gestational Hypertension
New onset of hypertension after the 20th week of pregnancy in the absence of proteinuria
NOTE: Hypertension with an onset after 20 weeks’ gestation that fails to normalize postpartum changes the diagnosis to chronic hypertension.
Observations that reflect current understanding of the hypertensive disorders in pregnancy include the following:
Hypertension during pregnancy represents a continuum of disease processes. Hypertension may be the first sign, but the underlying pathophysiology can involve major organ systems.
Hypertensive states are classified according to certain signs or symptoms based upon the timing in pregnancy in which they present. Women diagnosed with gestational hypertension established by onset of hypertension after 20 weeks without accompanying proteinuria, may actually have preeclampsia before either proteinuria or multisystem disturbances are manifested. These patients require surveillance for proteinuria and multisystem signs and symptoms, and should these develop, are no longer considered to have gestational hypertension, but preeclampsia.
Chronic hypertension is associated with fetal morbidity, such as intrauterine fetal growth restriction and an increased risk for superimposed preeclampsia. Maternal and fetal morbidity increase substantially when preeclampsia is superimposed upon chronic hypertension.
Chronic hypertension may not be accurately diagnosed until after childbirth in the setting of hypertension that initially manifests later in pregnancy because these women may have been presumed to have been normotensive prior to the pregnancy. These women may have had pre-existing hypertension, but experienced the normal physiologic decline in blood pressure during pregnancy; the return to a hypertensive state may reflect the physiologic return of blood pressure to prepregnancy levels. Postpartum follow-up is warranted in order to ascertain persistent elevations in blood pressure that may necessitate referral to a physician specializing in hypertension management.
Preeclampsia may progress to severe disease rapidly, necessitating timely recognition of relevant signs and symptoms. Diagnosis of preeclampsia is not constrained to rigid criteria for diagnosis in order to optimize maternal and fetal management.
HELLP syndrome is not included in the classification system because it is considered a preeclampsia subtype. HELLP syndrome is addressed later in this module.
NOTE: Although hypertensive disorders are discussed as separate diagnoses, recognition that preeclampsia may be superimposed upon gestational hypertension or chronic hypertension and progress to severe disease rapidly provides the foundation for ongoing assessment of these patients. Because the classification system is not precise and a missed diagnosis may lead to increased risk of adverse maternal and perinatal outcomes, a more prudent approach for clinical management is to overdiagnose preeclampsia.
Diagnosis of Preeclampsia and Eclampsia
How are hypertensive disorders specific to pregnancy diagnosed?2
The Task Force on Hypertension in Pregnancy and others9,10,13 identify reliable diagnostic criteria and guidelines for the evaluation of hypertensive disorders in pregnancy. Table 11.1 illustrates the diagnostic criteria for each.
TABLE 11.1 DIAGNOSTIC CRITERIA FOR HYPERTENSIVE DISORDERS OF PREGNANCY | ||||||||||||||||||||||||||||||
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Preeclampsia
Preeclampsia is a syndrome with multiple organ system involvement that manifests in the second half of pregnancy with new onset hypertension and new onset proteinuria.
Hypertension is defined by a persistent elevation in either the systolic blood pressure of 140 mm Hg or higher or the diastolic blood pressure of 90 mm Hg or higher on two occasions at least 4 hours apart.
Proteinuria is defined as protein of greater than 300 mg in a 24-hour urine specimen. Alternatively, proteinuria may be defined as a protein/creatinine ratio of at least 0.3 (both measured in mg/dL) because this ratio has been demonstrated to be equivalent to or exceed a 24-hour urine protein collection of 300 mg. A urine dipstick reading of +1 may also be used to fulfill criteria for proteinuria in the absence of quantifiable tests.
Proteinuria is not required for the diagnosis of preeclampsia. In the absence of proteinuria, new onset hypertension (as defined above) with any of the following constitutes preeclampsia:
Thrombocytopenia (less than 100,000/μL)
Impaired liver function (increase in blood levels of liver transaminases twice their normal value)
New development of renal insufficiency (serum creatinine greater than 1.1 mg/dL or doubling of serum creatinine
Pulmonary edema
New onset cerebral or visual disturbance
Hypertension is defined as either a systolic BP of 140 mm Hg or higher or diastolic BP of 90 mm Hg or higher on two occasions at least 4 hours apart.
NOTE: Preeclampsia is a syndrome that occurs only during pregnancy (the placenta plays a key role). Functional and structural changes in the developing placenta are believed to cause preeclampsia based upon the observation that the disease resolves after removal of the products of conception. Preeclampsia evolves from a complex interaction between placental-derived products and exaggerated adaptive mechanisms of normal pregnancy that lead to tissue ischemia.
Preeclampsia with Severe Features
Preeclampsia with severe features may be diagnosed with any of the following findings:
Systolic blood pressure of 160 mm Hg or higher on two occasions at least 4 hours apart
Diastolic blood pressure 110 mm Hg or higher on two occasions at least 4 hours apart
Thrombocytopenia (less than 100,000/μL)
Impaired liver function (increase in blood levels of liver transaminases twice their normal value or severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnosis or both)
New development of renal insufficiency (serum creatinine greater than 1.1 mg/dL or doubling of serum creatinine in the absence of other renal disease)
Pulmonary edema
New onset cerebral or visual disturbance
NOTE: Some clinical findings have been removed from the criteria for preeclampsia with severe features because they do not correlate with outcome or are not managed any differently than if the patient were not diagnosed with preeclampsia. The clinical findings that have been removed from consideration of severe disease include urine proteinuria greater than 5 g in 24 hours, intrauterine fetal growth restriction, and oliguria.
Preeclampsia is no longer categorized as mild or severe because of the progressive and dynamic nature of the disease. A woman who fulfills the basic criteria for hypertension (systolic blood pressure 140 to 159 mm Hg or diastolic blood pressure 90 to 109 mm Hg), but manifests with organ system derangements as outlined above are considered to have a severe form of the disease.
Early identification of worsening preeclampsia in a patient at a level I or II hospital is critical for timely transport to a high-risk regional center while the patient is stable and before a critical state is reached.
Eclampsia
Eclampsia is defined as new onset grand mal seizure activity in the woman diagnosed with preeclampsia.
Seizures can occur before, during, or after labor.
HELLP Syndrome
HELLP syndrome is a preeclampsia subtype; the acronym represents Hemolysis, Elevated Liver enzymes, and Low Platelets and is typically characterized by the following laboratory findings11:
Hemolysis, defined as the presence of microangiopathic hemolytic anemia, which includes:
Abnormal peripheral blood smear (schistocytes, burr cells, echinocytes)
Elevated serum bilirubin (Serum bilirubin of 1.2 mg/dL or higher)
Low serum haptoglobin levels
Elevated lactate dehydrogenase (LDH) (usually greater than 600 U/L)
Significant decline in hemoglobin, unrelated to blood loss
Elevated Liver Enzymes:
Aspartate transaminase (AST), twice the upper level of normal or greater
Alanine transaminase (ALT), twice the upper level of normal or greater
Elevated LDH
Low platelets, less than 100,000/mm3
Gestational Hypertension
Gestational hypertension is new onset hypertension after 20 weeks’ gestation without proteinuria.
Multisystem features consistent with preeclampsia are also absent.
Failure of hypertension to resolve postpartum fulfills the criteria for diagnosis of chronic hypertension.
NOTE: Some women will experience severe blood pressure elevations, yet not fulfill the criteria for diagnosis of preeclampsia but still experience similar outcomes to women with preeclampsia.
Women who present with hypertension initially during pregnancy, especially after 20 weeks’ gestation, are presumed to have been normotensive prior to pregnancy and will usually be diagnosed with either gestational hypertension or preeclampsia based upon clinical presentation and fulfillment of diagnostic criteria, when in actuality, these patients may have pre-existing hypertension that was not diagnosed due the physiologic decline in blood pressure that normally occurs after the first trimester. This warrants further assessment of blood pressure postpartum in order to ensure that hypertension resolves. In the event that hypertension persists beyond the postpartum period, the patient more than likely has chronic hypertension that necessitates referral to a physician specializing in hypertension management. However, during the pregnancy, it is prudent to manage the patient in accordance with guidelines for preeclampsia in order to optimize the short-term outcomes for both mother and fetus.
Pathophysiology of Preeclampsia
Preeclampsia is believed to originate from abnormal implantation of the placenta. Normally, through a complex process early in placental development, placental trophoblast cells invade the uterine spiral arteries, converting them from small, high-resistance vessels to dilated, low-resistance vessels, to increase placental circulation. This process of vascular growth, termed angiogenesis, is essential to sustain the fetus throughout the pregnancy.14 In pregnancies with preeclampsia, the partial invasion of trophoblasts into the superficial decidua fails to achieve this transformation, resulting in constricted and narrowed uterine arteries, compromising uteroplacental perfusion. Placental ischemia leads to the production of placental factors that enter the maternal circulation giving rise to widespread maternal endothelial dysfunction ensuing in a variety of manifestations of the disease from reduced end-organ perfusion.2,11,14 Some of the placental factors released into the maternal circulation have received a great deal of attention; among them are inflammatory factors and antiangiogenic factors.2 Antiangiogenic
proteins (soluble fms-like tyrosine kinase-1 [sFlt-1] and soluble endoglin) antagonize proangiogenic proteins (vascular endothelial growth factor [VEGF] and placental like growth factor [PLGF]), thereby reducing free levels of these proangiogenic proteins that normally stimulate uteroplacental vascular growth and dilation and maintain endothelial integrity.11 Increased circulating levels of sFLT-1 precede the development of preeclampsia by weeks to months and are accompanied by decreased circulating-free PLGF and VEGF levels.2,14 Appearance of these biomarkers is being further studied to determine their value in predicting preeclampsia.2
proteins (soluble fms-like tyrosine kinase-1 [sFlt-1] and soluble endoglin) antagonize proangiogenic proteins (vascular endothelial growth factor [VEGF] and placental like growth factor [PLGF]), thereby reducing free levels of these proangiogenic proteins that normally stimulate uteroplacental vascular growth and dilation and maintain endothelial integrity.11 Increased circulating levels of sFLT-1 precede the development of preeclampsia by weeks to months and are accompanied by decreased circulating-free PLGF and VEGF levels.2,14 Appearance of these biomarkers is being further studied to determine their value in predicting preeclampsia.2
The cause of preeclampsia remains unknown. Yet many mechanisms have been proposed to establish the pathophysiologic progression from abnormal placentation to development of the maternal syndrome. Predominant pathophysiologic mechanisms that have been implicated in the disease process include2,11 oxidative stress, an exaggerated inflammatory response, and altered coagulation.
Oxidative Stress
Under normal conditions, maternal blood flow to the placenta increases oxygen tension along with an increase in antioxidant enzymes. In preeclampsia, there is a diminished antioxidant response to oxygen stimulation, leading to the generation of oxygen-free radicals that promote tissue damage with resultant neutrophil activation that extends the generation of cytotoxic superoxide ions and ultimately, activation of the vascular endothelium. Reduced antioxidant activity and increased oxidative stress in the placenta and in the maternal circulation15 have instigated clinical trials that study the role of antioxidants, such as Vitamin C and Vitamin E, in preventing preeclampsia. Further study may conclude a risk reduction for preeclampsia; until definitive data demonstrate a clear benefit, Vitamin C and Vitamin E supplements are not currently recommended.2 The lipid profile in preeclamptic women (increased concentrations of serum free fatty acids, triglycerides, and very-low density lipoprotein [VLDL]) may predispose to oxidative stress. The VLDL particles are smaller in preeclamptic women when compared to normotensive women, which may facilitate their oxidative degradation.15
Inflammatory Response
During normal pregnancy, the maternal immune system adaptations directed at establishing an immune tolerance to fetal antigens manifests as a systemic inflammatory response. Preeclampsia further enhances the immune response, as evidenced by elevated levels of proinflammatory mediators, interleukin-6, interleukin-8, tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein 1 (MCR-1).16 Neutrophil activation may contribute to vascular injury as a result of leukocyte adhesion to the endothelium, perpetuating the inflammatory response and promoting coagulation through uncontrolled activation of the complement system.17
Decreased placental perfusion and endothelial damage promote platelet aggregation and coagulation, resulting in an imbalance between vasoactive prostaglandins. Prostacyclin, a potent vasodilator and inhibitor of platelet aggregation, is normally produced by the vascular endothelium and renal cortex. In preeclampsia, a deficiency in prostacyclin is accompanied by an increase in thromboxane A2 (TXA2), a potent vasoconstrictor and platelet aggregator, which is produced by platelets and trophoblasts. The imbalance favoring TXA2 suggests an exacerbation of the pathophysiologic derangements of preeclampsia,11 leading to clinical trials examining the effects of low-dose aspirin in ameliorating the exaggerated inflammatory response by blocking the production of thromboxanes. Because of its protective effect, daily low-dose aspirin (60 to 80 mg) initiated in the late first trimester is recommended for women with significant risk for preeclampsia, primarily women with a medical history of early-onset preeclampsia and preterm birth at less than 34 0/7 weeks’ gestation or women with a history of preeclampsia in more than one prior pregnancy.2
Daily low-dose aspirin is recommended for women with significant risk for preeclampsia, such as those women with a prior pregnancy complicated by preeclampsia and preterm birth prior to 34 completed weeks or women with more than one prior pregnancy complicated by preeclampsia.2
Altered Coagulation
The hypercoagulable state of normal pregnancy is potentiated in preeclampsia. Procoagulant proteins, such as tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI-1), and von Willebrand are elevated while proteins that inhibit the coagulation cascade, including
anti-thrombin III, activated protein C, and protein S, are reduced. The compromise in placental perfusion may trigger fibrin deposition and formation of thrombi in the placental circulation, further worsening placental ischemia and resultant endothelial damage.7
anti-thrombin III, activated protein C, and protein S, are reduced. The compromise in placental perfusion may trigger fibrin deposition and formation of thrombi in the placental circulation, further worsening placental ischemia and resultant endothelial damage.7
What are the major pathophysiologic events in preeclampsia that compromise end-organ perfusion?
Understanding the pathophysiology underlying the diagnostic signs and symptoms in preeclampsia facilitates a greater comprehension of the clinical manifestations and rationale for interventions. The primary pathophysiologic process underlying the multiorgan system involvement in preeclampsia is illustrated in Figure 11.1.
 FIGURE 11.1 Pathophysiological alterations occurring in preeclampsia. (Source: Author) |
Remember the pathologic process precedes the development of diagnostic signs by several weeks or months. Fetal circulation can be compromised by vasospasm within the placental vascular bed long before warning signs are evident.
The rationale for nursing interventions and medical management is directly related to the pathophysiologic and anatomic changes that occur in preeclampsia.
In response to the increased demands of normal pregnancy, significant physiologic adaptations occur in order to maintain maternal and fetal oxygenation. Among these physiologic changes are an increase in circulating blood volume, increase in cardiac output, and relaxation and dilation of systemic blood vessels; all directed at maximizing blood flow to maternal end-organs and the uteroplacental circulation.18 There is decreased end-organ perfusion in preeclampsia arising from endothelial dysfunction which further propagates oxidative stress and systemic inflammation. The disease process is progressive, often resulting in:
Increased arterial pressure and vasospasm. Often a physiologic attempt at achieving hemostasis from vascular injury, it promulgates further endothelial injury.
Fluid or fluid components escape out of the blood vessel into the interstitial compartment. These components include protein substances (e.g., albumin), fluid, or both. Loss of albumin from the intravascular space decreases colloid osmotic pressure (COP), or the pressure exerted to “pull” fluid within the blood vessels. A further compromise in circulating intravascular blood volume ensues.
Platelets aggregate at the sites of endothelial injury, narrowing the blood vessel lumen further. The decline in platelet count reflects the consumption of platelets.
Arterial blood flow to end-organs is compromised. The flow of blood under high pressure through narrowed blood vessels may result in hemolysis, compounding the state of decreased oxygen delivery from reduced oxygen carrying capacity.
What clinical findings are associated with the pathophysiologic changes?
The spectrum of multisystem manifestations of preeclampsia include the following11:
Cardiovascular: hypertension, hypovolemia, dependent edema
Hematologic: thrombocytopenia, abnormal peripheral blood smear (schistocytes, burr cells, echinocytes), elevated lactate dehydrogenase (LDH), or significant decline in hemoglobin, unrelated to blood loss
Renal system: proteinuria, increased serum creatinine, increased serum uric acid, oliguria
Hepatic system: elevated serum bilirubin (serum bilirubin of 1.2 mg/dL or higher)—rarely increased, low-serum haptoglobin levels, elevated liver enzymes (AST and ALT) twice the upper level of normal or greater, right upper quadrant or epigastric pain (which may be indicative of subcapsular liver hematoma)19
Neurologic system: visual disturbances, cerebral disturbances, eclampsia
Uteroplacental unit: intrauterine fetal growth restriction, fetal surveillance findings that may indicate fetal hypoxemia (abnormal FHR, low biophysical profile score, abnormal Doppler velocimetry)
Pulmonary system: pulmonary edema from increased capillary permeability and resultant interstitial edema
Etiology of Preeclampsia
Most cases of preeclampsia occur in healthy nulliparous women and the ability to assess the risk for preeclampsia by socioeconomic and cultural factors has been difficult.2 Multiple factors that predispose the woman to the disease may further an understanding of what causes the disease. The etiology, however, remains unknown.
Paternal factors may play a significant role in the pathogenesis of preeclampsia. Long-term exposure to sperm from the same partner may offer protective effects against the physiologic events that lead to preeclampsia. This protective effect is lost when exposure to sperm from the same partner is of short duration, which might explain the increased incidence of preeclampsia in younger, nulliparous women less than 20 years of age, use of condoms, or conception with donor sperm. Conversely, a prior normal pregnancy with the same partner reduces the risk of preeclampsia. In addition, there are observations that demonstrate that the risks for preeclampsia are not entirely unique to women. A man who fathered a preeclamptic pregnancy is almost twice as likely to father another pregnancy in a new partner who develops preeclampsia, even if the woman herself has had a prior normal pregnancy with another partner.11
Genetic predisposition is thought to play a role based upon the observation that women whose mothers and sisters have had preeclampsia are more likely to have the disease compared to women without this family history.20
Women with pre-existing vascular disease or metabolic abnormalities are at increased risk for preeclampsia. The exact mechanism is not precisely understood. Some of the risk factors for preeclampsia are also associated with cardiovascular disease risk factors, such as maternal age older than 40 years, pregestational diabetes, pre-existing hypertension, and obesity.2,7 The “acute atherosis” of placental vessels encountered in preeclampsia closely resemble atherosclerotic plaques. In addition, levels of an adipocyte-derived hormone, leptin, are also observed in preeclampsia and coronary vascular disease. Obesity is also characterized by lipid abnormalities, which may explain why obese women are at higher risk for preeclampsia.7
Are certain pregnant women at risk for developing preeclampsia?
The prevailing risk factors for preeclampsia include the following2:
Primiparity
Prior pregnancy complicated by preeclampsia
Chronic hypertension
Chronic renal disease
History of thrombophilia
Multifetal pregnancy
Family history of preeclampsia
Type I or type II diabetes mellitus
Obesity
Collagen vascular disease, such as systemic lupus erythematosus (SLE)
Maternal age greater than 40, or maternal age greater than 35 with co-morbid conditions
Complications of Preeclampsia
Decreased end-organ perfusion contributes to organ system derangements in preeclampsia, which are observed on a continuum that extends from a presentation without severe features to catastrophic organ system failure. Signs and symptoms that may possibly indicate progression in severity of the disease and that potentially end with adverse outcomes necessitate vigilant assessment.
WATCH FOR SIGNS OF THE FOLLOWING21:
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