HYPERTENSIVE DISORDERS IN PREGNANCY

HYPERTENSIVE DISORDERS IN PREGNANCY

Prepared by assistant professor N.Petrenko, MD, PhD

 

LEARNING OBJECTIVES

Describe the pathophysiology of preeclampsia and eclampsia.

Differentiate the management of the woman with mild preeclampsia and the woman with severe preeclampsia.

Identify the priorities for management of eclamptic seizures.

Describe HELLP syndrome, including appropriate nursing actions.

 

KEY TERMS AND DEFINITIONS

Clonus Spasmodic alternation of muscular con­traction and relaxation; counted in beats

Eclampsia Severe complication of pregnancy of unknown cause and occurring more often in the primigravida; characterized by tonic and clonic convulsions, coma, high blood pressure, albu-minuria, and oliguria occurring during pregnancy or shortly after birth

HELLP syndrome Condition characterized by he-molysis, elevated liver enzymes, and low platelet count; a form of severe preeclampsia

Preeclampsia Disease encountered after 20 weeks of gestation or early in the puerperium; a vasospastic disease process characterized by increasing hypertension, proteinuria, and hemoconcentration

Pregnancy-induced hypertension (PIH) Hypertensive disorders of pregnancy including preeclamp-sia, eclampsia, and transient hypertension

 

Some women experience significant problems during the months of gestation that can greatly affect pregnancy outcome. Some of these conditions develop as a result of the pregnant state; others are problems that could happen to anyone, at any time of life, but occur in this woman during pregnancy. This chapter discusses a variety of disorders that did not exist before pregnancy, all of which have at least one thing in common: their occurrence in pregnancy puts the woman and fetus at risk. Hypertension in pregnancy, hyperemesis gravidarum, hemorrhagic complications of early and late pregnancy, surgery during pregnancy, trauma, and infections are discussed.


HYPERTENSION IN PREGNANCY

Significance and Incidence

Hypertension is the most common medical complication of pregnancy, with the incidence ranging from 1% to 5% (Ventura et al., 1999). A significant contributor to maternal and perinatal morbidity and mortality, preeclampsia complicates approximately 5% to 8% of all pregnancies not ending in first-trimester miscarriages (American College of Obstetricians and Gynecologists [ACOG], 1996; Sibai et al., 1997). In women with a history of chronic hypertension or renal disease predating pregnancy, the occurrence of preeclampsia is 25% (Jones & Hayslett, 1996). The prevalence rate for pregnancy-associated hypertension has risen in recent years. The rate has risen among all age, racial, and ethnic groups since the early 1990s (Ventura et al., 1999).

Preeclampsia predisposes the woman to potentially lethal complications, including eclampsia, abruptio placentae, disseminated intravascular coagulation (DIC), acute renal failure, hepatic failure, adult respiratory distress syndrome, and cerebral hemorrhage (ACOG, 1996; Cunningham et al., 2001; Roberts, 1999). Preeclampsia contributes significantly to intrauterine fetal death and perinatal mortality. Causes of perinatal death related to preeclampsia are uteroplacental insufficiency and abruptio placentae, which lead to intrauterine death, preterm birth, and low birth weight (Roberts, 1999).

Eclampsia (characterized by seizures) from profound cerebral effects of preeclampsia is the major maternal hazard. As a rule, maternal and perinatal morbidity and mortality rates are highest among cases in which eclampsia is seen early in gestation (before 28 weeks), maternal age is greater than 25 years, the woman is a multigravida, and chronic hypertension or renal disease is present (Mattar & Sibai, 2000). The fetus of the eclamptic woman is at increased risk from abruptio placentae, preterm birth, intrauterine growth restriction (IUGR), and acute hypoxia (Gilbert & Harmon, 1998).

 

Classification

The hypertensive disorders of pregnancy encompass a variety of conditions featuring an elevation of maternal blood pressure with a corresponding risk to maternal and fetal well-being. The two classification systems most commonly used in the United States today are based on reports from the American College of Obstetricians and Gynecologists (ACOG, 1996) and the Working Group on High Blood Pressure in Pregnancy (1990). These classification systems are summarized in Table 1.

Table 1 Classification of Hypertensive States of Pregnancy

TYPE

DESCRIPTION

Gestational Hypertensive Disorders: Pregnancy-Induced Hypertension (PIH)

Gestational hypertension

Development of mild hypertension during pregnancy in previously normotensive patient without proteinuria or pathologic edema

Gestational proteinuria

Development of proteinuria after 20 wk of gestation in previously nonproteinuric patient without hypertension

Preeclampsia

Development of hypertension and proteinuria in previously normotensive patient after 20 wk of gestation or in early postpartum period; in presence of trophoblastic disease it can develop before 20 wk of gestation

Eclampsia

Development of convulsions or coma in preeclamptic patient

 

CHRONIC HYPERTENSIVE DISORDERS

Chronic hypertension

Hypertension and/or proteinuria in pregnant patient with chronic hypertension

Superimposed preeclampsia/eclampsia

Development of preeclampsia or eclampsia in patient with chronic hypertension

Modified from Gilbert, E., & Harmon, J. (1998). Manual of high risk pregnancy and de­livery (2nd ed.). St. Louis: Mosby.

 

Clinically, there are two basic types of hypertension during pregnancy-chronic hypertension and pregnancy-induced hypertension-with the distinction based on the onset of hypertension in relation to pregnancy. Chronic hypertension is hypertension that predates the pregnancy or hypertension continuing beyond 42 days postpartum (ACOG, 1996). Pregnancy-induced hypertension (PIH) is the onset of hypertension, generally after the twentieth week of pregnancy, appearing as a marker of a pregnancy-specific vasospastic condition (ACOG, 1996; Roberts, 1999). Chronic hypertension and PIH may occur independently or simultaneously. PIH is further classified according to the maternal organ systems affected.

 

Preeclampsia

Preeclampsia, a pregnancy-specific condition in which hypertension develops after 20 weeks of gestation in a previously normotensive woman, is a multisystem, vasospastic disease process characterized by hemoconcentration, hypertension, and proteinuria. Preeclampsia is usually categorized as mild or severe in terms of management (Table 2).

 

Table 2 Differentiation Between Mild and Severe Preeclampsia

 

MILD PREECLAMPSIA

SEVERE PREECLAMPSIA

MATERNAL EFFECTS

Blood pressure

BP reading of 140/90 mm Hg x2, 4-6 hr apart

Rise to >160/110 mm Hg on two separate occasions 4-6 hr apart with pregnant woman on bed rest

Mean arterial pressure (MAP)

>105 mm Hg

>105 mm Hg

Weight gain

Weight gain of more than 0.5 kg/wk during the second and third trimesters or sudden weight gain of 2 kg/wk at any time

Same as mild preeclampsia

Proteinuria

— Qualitative dipstick

— Ouantitative 24 hr analysis

Proteinuria of 0.3 g/L in a 24 hr specimen or >0.1 g/L in a random day-time specimen on two or more occasions 6 hr apart (because protein loss is variable); with dipstick, values varying from 1+ to 2 +

Proteinuria of >0.5 g/L in 24 hr or >4+ protein on dipstick

Edema

Dependent edema, some puffiness of eyes, face, fingers; pulmonary edema absent

Generalized edema, noticeable puffiness; eyes, face, fingers; pulmonary edema possibly present

Reflexes

May be normal

Hyperreflexia 3+, possible ankle clonus

Urine output

Output matching intake, ≥30 ml/hr or <650 ml/24 hr

<20 ml/hr or <400 ml to 500 ml/24 hr

Headache

Absent/transient

Severe

Visual problems

Absent

Blurred, photophobia, blind spots on funduscopy

Irritability/changes in affect

Transient

Severe

Epigastric pain

Absent

Present

Serum creatinine

Normal

Elevated

Thrombocytopenia

Absent

Present

AST elevation

Normal or minimal

Marked

FETAL EFFECTS

Placental perfusion

Reduced

Decreased perfusion expressing as IUGR in fetus; FHR: late decelerations

Premature placental aging

Not apparent

At birth placenta appearing smaller than normal for duration of pregnancy, premature aging apparent with numerous areas of broken syncytia, ischemic necroses (white infarcts) numerous, intervillous fibrin deposition (red infarcts)

AST, Aspartate aminotransferase;

FHR, fetal heart rate.

 

An elevated blood pressure is often the first sign of preeclampsia to develop. Hypertension is a blood pressure greater than or equal to 140/90 mm Hg. ACOG's Committee on Terminology (ACOG, 1996) has defined hypertension as an increase in mean arterial pressure (MAP) of 105 mm Hg or more. The blood pressure elevation must be present on two occasions at least 4 to 6 hours apart (Fairlie & Sibai, 1999). One of the difficulties in diagnosing hypertension is a lack of standardization in blood pressure measurement. Box 1 presents recommendations for standardizing this procedure.

 

Box 1 Blood Pressure Measurement

1. Measure blood pressure with the woman seated (ambulatory) or in a 30-degree tilt on her left side.

2. After positioning, allow the woman at least 5 min utes of quiet rest before blood pressure measurement, to encourage relaxation.

3. Use the same arm each time for blood pressure measurement.

4. Hold the arm in a roughly horizontal position at heart level.

5. Use the proper-sized cuff (cuff should cover approximately 80% of the upper arm).

6. Maintain a slow, steady deflation rate.

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

8. Use Korotkoff phase V (disappearance of sound) for recording the diastolic value (some sources recommend recording both phase IV [the muffled sound] and phase V).

9. Use accurate equipment.

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

 

Proteinuria is a concentration of 0.1 g/L (1+ to 2+ on dipstick measurement) or more in at least two random urine specimens collected at least 6 hours apart. In a 24-hour spec­imen, proteinuria is a concentration of 0.3 g/L per 24 hours.

Pathologic edema is clinically evident, generalized accumulation of fluid of the face, hands, or abdomen that is not responsive to 12 hours of bed rest. It may also be manifested as a rapid weight gain of more than 2 kg in 1 week. The presence of edema is no longer considered necessary for the di­agnosis of preeclampsia (Sibai & Rodriguez, 1999).

Severe preeclampsia. Severe preeclampsia is the presence of any one of the following in the woman diagnosed with preeclampsia: (1) systolic blood pressure of at least 160 mm Hg or a diastolic blood pressure of at least 110 mm Hg; (2) proteinuria of greater than 0.5 g protein excreted in a 24-hour specimen, or greater than 3 + to 4 + on dipstick measurement; (3) oliguria, less than 400 to 500 ml of urine output over 24 hours; (4) cerebral or visual disturbances, such as altered level of consciousness, headache, scotomata, or blurred vision; (5) hepatic involvement; (6) thrombocytopenia with a platelet count less than 150,000/mm3; (7) pulmonary or cardiac involvement; or (8) epigastric pain, nausea, and vomiting (ACOG, 1996; Roberts, 1999; Sibai, 2002; Working Group on High Blood Pressure in Pregnancy, 1990).

HELLP syndrome. HELLP syndrome is a laboratory diagnosis for a variant of severe preeclampsia characterized by hemolysis (H), elevated liver enzymes (EL), and low platelets (LP).

 

Eclampsia

Eclampsia is the occurrence of seizures or coma in a patient with preeclampsia that cannot be attributed to other causes. Approximately half of all cases of eclampsia occur before labor begins, with the other half equally divided between the intrapartum and postpartum periods.

 

Chronic hypertension

Chronic hypertension is hypertension present before the pregnancy or diagnosed before the twentieth week of ges­tation. Hypertension that persists longer than 6 weeks postpartum is also classified as chronic hypertension.

 

Chronic hypertension with superimposed preeclampsia

Women with chronic hypertension may acquire preeclampsia or eclampsia. Superimposed preeclampsia is the development of proteinuria (0.5 g protein or more in a 24-hour specimen) and an increase in blood pressure (30 mm Hg systolic or 15 mm Hg diastolic) in women with chronic hypertension (Sibai, 2002).

 

Gestational hypertension

Gestational hypertension is the development of hypertension during pregnancy (often after 37 weeks of gestation) without other signs of preeclampsia or preexisting hypertension. It is the most common cause of hypertension in pregnancy. The incidence is higher in nulliparas and in twin gestations (Sibai, 2002).

 

 

Etiology

Preeclampsia is a condition unique to human pregnancy; signs and symptoms usually develop only during preg­nancy and disappear quickly after birth of the fetus and passage of placenta. The cause is unknown. No single patient profile identifies the woman who will have preeclampsia. Box 2 lists factors associated with increased incidence of PIH.

Box 2 Risk Factors Associated with the Development of Pregnancy-Induced Hypertension (PIH)

Chronic renal disease

Chronic hypertension

Family history of PIH

Twin gestation

Primigravidity

Maternal age <19 years; >40 years

Diabetes

Rh incompatibility

Obesity

 

Data from American College of Obstetricians and Gynecologists. (1996). Hypertension in pregnancy. ACOG Tech Bull219. Washington, DC: ACOG; Caritis, S. et al. (1998). Predictors of preeclampsia in women at high risk. Am J Obstet Gynecol, /73(4), 946-951; Gilbert, E., & Harmon, J. (1998). Manual of high risk pregnancy and delivery (2nd ed.). St. Louis: Mosby; and Sibai, B. et al. (1997). Risk factors associated with preeclampsia in healthy nulliparous women. Am J Obstet Gynecol, 777(5), 1003-1010.

 

Current theories regarding the etiology of PIH include increased vasoconstrictor tone (Gilstrap & Gant, 1990), abnormal prostaglandin action (Friedman, 1988), and endothelial cell activation (Dekker & Sibai, 1998). Immuno-logic factors may play an important role (Dekker & Sibai, 1999) (Fig. 1). Genetic disposition and diet may be other factors.

 

Fig. 1 Etiology of pregnancy-induced hypertension.

 

↑ BP—vasospasm

 

 

 

Decreased placental perfusion

 

 

 

Endothelial cell activation

 

 

Vasoconstriction

Activation of coagulation cascade

 

Intravascular fluid redistribution

 

Decreased organ perfusion

 

 

 

Pathophysiology

Preeclampsia progresses along a continuum from mild disease to severe preeclampsia, HELLP syndrome, or eclampsia. The pathophysiology of preeclampsia reflects alter­ations in the normal adaptations of pregnancy. Normal physiologic adaptations to pregnancy include increased blood plasma volume, vasodilation, decreased systemic vascular resistance, elevated cardiac output, and decreased colloid osmotic pressure (Box 3).

 

BOX 3 Normal Physiologic Adaptations to Pregnancy

CARDIOVASCULAR

↑ Blood volume; plasma volume expansion greater than red cell mass expansion, leading to physiologic anemia of pregnancy

Total peripheral resistance, decreases in blood pressure readings and mean arterial pressure

Cardiac output resulting from increased blood volume, slight increase in heart rate to compensate for peripheral relaxation

Oxygen consumption

Physiologic edema related to plasma colloid osmotic pressure and venous capillary hydrostatic pressure

HEMATOLOGIC

Clotting factors, predisposing to disseminated intravascular coagulation and clotting

Serum albumin resulting in decreases in colloid osmotic pressure, predisposing toward pulmonary edema

RENAL

Renal plasma flow and glomerular filtration rate

ENDOCRINE

Estrogen production resulting in T renin-angiotensin II-aldosterone secretion

Progesterone production blocking aldosterone effect (slight Na)

Vasodilator prostaglandins resulting in resistance to angiotensin II (slight blood pressure)

 

 

Pathologic changes in the endothelial cells of the glomeruli (glomeruloendotheliosis) are uniquely characteristic of preeclampsia, particularly in nulliparous women (85%). The main pathogenic factor is not an increase in blood pressure but poor perfusion as a result of vasospasm. Arteriolar vasospasm diminishes the diameter of blood vessels, which impedes blood flow to all organs and raises blood pressure (Working Group on High Blood Pressure in Pregnancy, 1990). Function in organs such as the placenta, kidneys, liver, and brain is depressed by as much as 40% to 60%. The pathophysiologic sequelae are shown in Fig. 2.

 

 

 

Generalized vasoconstriction

Hypertension

Decreased placental perfusion

Increased thromboxane to prostacyclin Increased sensitivity to angiotensin II

Uteroplacental arteriole lesions

IUGR

Abruptio placentae

Increased uterine contractility

Placental production of endothelin (a toxic substance to endothelial cells)

Fluid shifts from intravascular to intracellular space (Decreased plasma volume) (Increased hematocrit)

Glomerular damage

Proteinuria

Increased plasma uric acid and creatinine

Oliguria

Increased sodium retention

Vasospasms

Intravascular coagulation

Generalized edema

Visual edema of face, hands, and abdomen Pitting edema after 12 hours of bed rest

Endothelial cell damage

 

Cortical brain spasms

Headaches Hyperreflex

Seizure activity

 

 

Pulmonary edema

Dyspnea

 

 

Retinal arteriolar spasms

Blurred visi

Scotoma

 

 

Hemolysis of red blood cells (Torn RBCs)

Decreased hemoglobin

Maternal hyperbilirubinemia

 

 

Hepatic microemboli;

 liver damage

Elevated liver enzymes (AST and LDH)

Nausea/vomiting

Epigastric pain

Right upper quadrant pain

Decreased blood glucose

Liver rupture

 

 

Platelet aggregation and fibrin deposition

Low platelet count (thrombocytopenia] —DIC

 

Fig. 2 Pathophysiology of pregnancy-induced hypertension. (Modified from Gilbert, E., & Harmon, J. [1998]. Manual of high risk pregnancy and delivery [2nd ed.]. St. Louis: Mosby.)

 

 

HELLP Syndrome

HELLP syndrome appears in only 2% to 12% of severely preeclamptic women, or approximately 1 in 1000 pregnancies (Stone, 1998). Although the exact mechanism is unknown, HELLP syndrome is thought to arise as a result of changes occurring with preeclampsia. Arteriolar vasospasm, endothelial damage, and platelet aggregation with resultant tissue hypoxia are the underlying mechanisms for the pathophysiology of HELLP syndrome (Poole, 1993, 1997). A circulating immunologic component may be the underlying cause.

Most commonly, HELLP syndrome is seen in older Caucasian, multiparous women. Approximately 90% of patients report a history of malaise for several days. Many women (65%) experience epigastric or right upper quadrant abdominal pain (possibly related to hepatic ischemia), and approximately half develop nausea and vomiting.

 

NURSE ALERT! It is extremely important to understand that many patients with HELLP syndrome may not have signs or symptoms of severe preeclampsia. For example, many of these women are normotensive or have only slight elevations in blood pressure. Proteinuria also may be absent. As a result, women with HELLP syndrome are often misdiagnosed with a variety of other medical or surgical disorders (Sibai, 2002).

 

HELLP syndrome is a laboratory, not a clinical, diagnosis. To make a diagnosis of HELLP syndrome, a woman's platelet count must be less than 100,000/mm3, her liver enzyme levels (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]) must be elevated, and there must be some evidence of intravascular hemolysis (burr cells on peripheral smear or elevated bilirubin level) (Stone, 1998). A unique form of coagulopathy (not DIC) occurs with HELLP syndrome. The platelet count is low, but coagulation factor assays, prothrombin time (PT), partial thromboplastin time (FIT), and bleeding time remain normal (Stone, 1998).

Recognition of the clinical and laboratory findings associated with HELLP syndrome is important if early, aggressive therapy is to be initiated to prevent maternal and neonatal mortality. Complications reported with HELLP syndrome include renal failure, pulmonary edema, ruptured liver hematoma, DIC, and placental abruption (Sibai, 2002). African-American women with HELLP syndrome are at higher risk for eclampsia (Haddad et al., 2000).

 

CARE MANAGEMENT

Assessment and Nursing Diagnoses

Hypertensive disorders of pregnancy can occur without warning or with the gradual development of symptoms. Because currently the cause is unknown and proven methods to prevent the illness are nonexistent, a key goal is early detection of the disease to prevent the catastrophic maternal and fetal sequelae that can occur. One strategy to meet this goal is the identification of high risk individuals at the initial prenatal visit (see Box 2). During each subsequent visit the woman is assessed for signs or symptoms that suggest the onset or presence of preeclampsia.

 

Interview

The nurse begins the assessment process by complet­ing or reviewing the woman's prenatal record. Personal medical history is reviewed, especially the presence of di­abetes mellitus, renal disease, and hypertension. Family history is explored for occurrence of preeclamptic or hypertensive conditions, diabetes mellitus, and other chronic conditions. The social and experiential history provides information about the woman's marital status, nutritional status, cultural beliefs, activity level, and health habits (e.g., smoking, alcohol and illicit drug consumption).

A review of systems adds to the database for detecting blood pressure changes from baseline, abnormal weight gain and pattern of weight gain, increased signs of edema, and presence of proteinuria. Noting whether the woman is having unusual, frequent, or severe headaches; visual dis­turbances; or epigastric pain is also important.

 

Physical examination

Accurate and consistent blood pressure assessment is important for establishing a baseline and monitoring subtle changes throughout pregnancy. Many variables can influence blood pressure measurements, such as position, cuff size, arm used, and emotional state of the patient. Personnel caring for pregnant women need to be consistent in taking and recording blood pressure measurements in the standardized manner (see Box 1).

Observation of edema in addition to hypertension warrants additional investigation. Edema is assessed for distribution, degree, and pitting. If periorbital or facial edema is not obvious, the pregnant woman is asked whether it was present when she awoke. Edema may be described as dependent or pitting.

Dependent edema is edema of the lowest or most dependent parts of the body, where hydrostatic pressure is greatest. If a pregnant woman is ambulatory, this edema may first be evident in the feet and ankles. If the pregnant woman is confined to bed, the edema is more likely to occur in the sacral region.

Pitting edema is edema that leaves a small depression or pit after finger pressure is applied to the swollen area. The pit, which is caused by movement of fluid to adjacent tissue away from the point of pressure, normally disappears within 10 to 30 seconds. Although the amount of edema is difficult to quantitate, the method described in Fig. 3 may be used to record relative degrees of edema forma­tion in the lower extremities.

 

Fig. 3 Assessment of pitting edema of lower extremities. A, +1; B, +2; C, +3; D, +4.

 

Symptoms reflecting central nervous system (CNS) and visual system involvement usually accompany facial edema. Although it is not a routine assessment during the prenatal period, evaluation of the fundus of the eye yields valuable data. An initial baseline finding of normal eye grounds assists in differentiating preexisting disease from a new disease process.

Deep tendon reflexes (DTRs) are evaluated if preeclampsia is suspected. The biceps and patellar reflexes and ankle clonus are assessed and the findings recorded.

 

NURSE ALERT The evaluation of DTRs is especially important if the woman is being treated with magnesium sulfate; absence of DTRs is an early indication of impending magnesium toxicity.

 

To elicit the biceps reflex, the examiner strikes a downward blow over the thumb, which is situated over the biceps tendon (Fig. 4, A). Normal response is flexion of the arm at the elbow, described as a 2+ response (Table 3). The patellar reflex is elicited with the woman's legs hanging freely over the end of the examining table or with the woman lying on her left side with the knee slightly flexed. A blow with a percussion hammer is dealt directly to the patellar tendon, inferior to the patella. Normal response is the extension or kicking out of the leg (Fig. 4, B). To assess for hyperactive reflexes (clonus) at the ankle joint, the examiner supports the leg with the knee flexed (Fig. 4, C). With one hand, the examiner sharply dorsi-flexes the foot, maintains the position for a moment, and then releases the foot. Normal (negative clonus) response is elicited when no rhythmic oscillations (jerks) are felt while the foot is held in dorsiflexion. When the foot is released, no oscillations are seen as the foot drops to the plantar flexed position. Abnormal (positive clonus) response is recognized by rhythmic oscillations of one or more "beats" felt when the foot is in dorsiflexion and seen as the foot drops to the plantar flexed position.

 

Fig. 4 A, Biceps reflex. B, Patellar reflex with patient's legs hanging freely over end of examining table. C, Test for ankle clonus. (From Seidel, H. et al. [1999]. Mosby's guide to physical examination [4th ed.]. St. Louis: Mosby.)

 

Tabl 3 Assessing Deep Tendon Reflexes

GRADE

DEEP TENDON REFLEX RESPONSE

0

No response

1+

Sluggish or diminished

2+

Active or expected response

3+

More brisk than expected, slightly hyperactive

4+

Brisk, hyperactive, with intermittent or transient clonus

 

An important assessment is determination of fetal status. Uteroplacental perfusion is decreased in women with preeclampsia, placing the fetus in jeopardy. The fetal heart rate (FHR) is assessed for baseline rate and variability and accelerations, which indicate an intact, oxygenated fetal CNS. Abnormal baseline rate, decreased or absent variability, and late decelerations are indications of fetal intolerance to the intrauterine environment. Biophysical or biochemical monitoring such as nonstress testing, contraction stress testing, biophysical profile (BPP), and serial ultrasonography are all used to assess fetal status.

Dopler flow velocimetry studies also may be used to evaluate maternal and fetal well-being. Uteroplacental perfusion is assessed by measuring the velocity of blood flow through the uterine artery, umbilical artery, or both. A systolic/diastolic ratio greater than 3 after 30 weeks of gestation is considered abnormal and is associated with IUGR, usually resulting from uteroplacental insufficiency (Miller, 1998).

Uterine tonicity is evaluated for signs of labor and abruptio placentae. If labor is suspected, a vaginal examination for cervical changes is indicated.

During the physical examination, the pregnant woman is examined for signs of progression of mild preeclampsia to severe preeclampsia or eclampsia. Signs of worsening liver involvement, renal failure, worsening hypertension, cerebral involvement, and developing coagulopathies must be assessed and documented. Respirations are assessed for crackles or diminished breath sounds, which may indicate pulmonary edema. Eclampsia is usually preceded by various premonitory symptoms and signs, including headache, severe epigastric pain, hyperreflexia, and hemoconcentration.

 

Laboratory tests

Blood and urine specimens are collected to aid in the diagnosis and treatment of preeclampsia, HELLP syndrome, and chronic hypertension. Baseline laboratory test information is useful in cases of early diagnosis of preeclampsia because it can be compared with later results to evaluate progression and severity of disease (Table 4). An initial blood specimen is obtained for the following tests to assess the disease process and its effect on renal and hepatic functioning:

  Complete blood cell count (including a platelet count)

  Clotting studies (including bleeding time, FT, PTT, and fibrinogen)

  Liver  enzymes   (lactate   dehydrogenase   [LDH],  AST, ALT)

  Chemistry panel (blood urea nitrogen [BUN], creatinine, glucose, uric acid)

  Type and screen, possible crossmatch

 

Table 4 Common Laboratory Changes in Preeclampsia

 

NORMAL

PIH

HELLP

Hemoglobin/hematocrit

12 to 16 gm/dl/37% to 47%

May ↑

Platelets

150,000 to 400,000/mm3

Unchanged

<100,000/mm3

PT/PTT

12 to 14 sec/60 to 70 sec

Unchanged

Unchanged

Fibrinogen

150 to 400 mg/dl

300 to 600 mg/dl

Present

Fibrin split products (FSP)

Absent

Absent

Blood urea nitrogen (BUN)

10 to 20 mg/dl

<10 mg/dl

Creatinine

0.5 to 1.1 mg/dl

<1 mg/dl

Lactate dehydrogenase (LDH)

45 to 90 U/L

Unchanged

Aspartate aminotransferase (AST)

4 to 20 U/L

Unchanged

Alanine aminotransferase (ALT)

3 to 21 U/L

Unchanged

Creatinine clearance

80 to 125 ml/min

130 to 180 ml/min

Burr cells/schistocytes

Absent

Absent

Present

Uric acid

2 to 6.6 mg/dl

4.5 to 6 mg/dl

>10 mg/dl

Bilirubin (total)

0.1 to 1 mg/dl

Unchanged or

 

The hematocrit, hemoglobin, and platelet levels are monitored closely for changes indicating a worsening of patient status. Because hepatic involvement is a possible complication, serum glucose levels are monitored if liver function tests indicate elevated liver enzymes. Once the platelet count drops below 100,000/mm3, coagulation profiles are needed to identify developing DIC.

Proteinuria is determined from dipstick testing of a clean-catch or catheterized urine specimen. A reading of 2+ on two or more occasions at least 6 hours apart should be followed by a 24-hour urine collection (Gilbert & Harmon, 1998). A 24-hour collection for protein and creatinine clearance is more reflective of true renal status. Proteinuria is usually a late sign in the course of preeclampsia. Protein readings are designated as follows:

0           negative

Trace    trace

1 +      30 mg/dl (equivalent to 0.3 g/L)

2+      100 mg/dl

3+     300 mg/dl

4+     1000 mg (1 g)/dl

 

Urine output is assessed for volume of at least 30 ml/hr or 120 ml/4 hr. Renal laboratory assessments include mon­itoring trends in serum creatinine and BUN levels. As re­nal function becomes compromised, renal excretion of creatinine and other waste products, including magnesium sulfate, decreases. As renal excretion decreases, serum levels for creatinine, BUN, uric acid, and magnesium rise.

Nursing diagnoses for the woman with hypertensive disorders in pregnancy may include the following:

•        Anxiety related to

- preeclampsia and its effect on woman and infant

•        Deficient knowledge related to

-management (diet, medications, activity restrictions)

•        Ineffective individual/family coping related to

-woman's restricted activity and concern over a complicated pregnancy

-woman's inability to work outside the home

-transfer of woman to tertiary care center for more intensive management

•        Powerlessness related to

-inability to prevent or control condition and outcomes

•        Ineffective tissue perfusion related to

-hypertension

-cyclic vasospasms

-cerebral edema

-hemorrhage

•        Risk for injury to fetus related to

-uteroplacental insufficiency

-preterm birth

-abruptio placentae

•        Risk for injury to mother related to

-CNS irritability secondary to cerebral edema, vasospasm, decreased renal perfusion

-magnesium sulfate and antihypertensive therapies

-abruptio placentae

 

Expected Outcomes of Care

Expected outcomes for care of women with hypertensive disorders of pregnancy include that the woman will do the following:

  Recognize and immediately report signs and symptoms indicative of worsening condition

  Adhere to the medical regimen to minimize risk to herself and her fetus

  Identify and use available support systems

  Verbalize her fears and concerns to cope with the condition and situation

  Develop no signs of eclampsia and its complications

  Give birth to a healthy infant

  Develop no sequelae to her condition or its management

 

Plan of Care and Interventions

Preeclampsia

Nursing actions are derived from medical management, health care provider directives, and nursing diagnoses. The most effective therapy is prevention. Early prenatal care, identification of pregnant women at risk for preeclampsia, and recognition and reporting of physical warning signs are essential components in the optimization of maternal and perinatal outcomes. The role of the nurse's skills in assess­ing the woman for factors and symptoms of preeclampsia cannot be overestimated.

The goals of therapy are to ensure maternal safety and to deliver a healthy newborn as close to term as possible. At or near term, the plan of care for a woman with preeclampsia is most likely to be induction of labor, pre­ceded, if necessary, by cervical ripening. When preeclampsia is diagnosed in a woman who is less than 37 weeks of gestation, however, immediate delivery may not be in the best interest of the fetus. In this situation, the initial intervention is usually a thorough evaluation of both the maternal and fetal condition. This evaluation may be done in the high risk clinic or the physician's office, or the woman may be hospitalized.

Emotional and psychologic support is essential in assisting the woman and her family to cope. Their perception of the disease process, the reasons for it, and the care received will affect their compliance with and participa­tion in therapy. The family needs to use coping mecha­nisms and support systems to help them through this crisis. A plan of care specifically designed for the woman with preeclampsia must be superimposed on the nursing care all women need during labor and the birth process.

 

Mild preeclampsia and home care

If the woman has mild preeclampsia (e.g., blood pressure is stable, urine protein is less than 500 mg in a 24-hour collection, and no subjective complaints), she may be managed expectantly, usually at home. The maternal-fetal condition must be assessed two to three times per week. Many agencies are available to provide this assessment in the home. Arrangements for this service may be made, depending on the woman's insurance coverage. If home nursing care is not an option, the woman may be asked to perform self-assessment daily, including weight, urine dipstick protein determinations, blood pressure measurement, and fetal movement counting (Lowdermilk & Grohar, 1998). She will be instructed to report the develop­ment of any subjective symptoms immediately to her health care provider (see Self-Care box) and to return to the physician's office or high risk clinic for assessment as scheduled.

The only reason for expectant management of preeclampsia is to allow additional time for fetal growth and maturation. The fetal condition is closely monitored. An evaluation of fetal growth by ultrasound should be obtained every 3 weeks. Fetal movement is counted daily. Other fetal assessment tests include a nonstress test (NST) or BPP once or twice a week as needed. Fetal jeopardy as evidenced by inappropriate growth or abnormal test results necessitates immediate delivery (Sibai, 2002).

Activity restriction. Bed rest in the lateral recumbent position is a standard therapy for preeclampsia and maximizes uteroplacental blood flow during pregnancy. It has been shown to be beneficial in decreasing blood pressure and promoting diuresis. However, recommendations for bed rest for all high risk pregnant women are becoming more controversial. Maloni (1994) documented adverse physiologic outcomes related to complete bed rest, including cardiovascular deconditioning; diuresis with accompanying fluid, electrolyte, and weight loss; muscle atrophy; and psychologic stress. These changes begin on the first day of bed rest and continue for the duration of therapy. Sibai (2002) recommends rest at home and no activ­ity limits for patients hospitalized with mild preeclampsia.

Women with mild preeclampsia feel reasonably well; boredom from activity restriction is therefore common. Diversionary activities, visits from friends, telephone con­versations, and creation of a comfortable and convenient environment are just a few ways of coping with this boredom (see Self-Care box). Gentle exercise (e.g., range of motion, stretching, Kegel exercises, pelvic tilts) is important in maintaining muscle tone, blood flow, regularity of bowel function, and a sense of well-being (Maloni, 1998). Relaxation techniques can help reduce the stress associated with the high risk condition and prepare the woman for labor and birth.

Diet. Diet and fluid recommendations are much the same as for healthy pregnant women. The efficacies of a high-protein diet, avoidance of foods high in sodium, and forgoing additional salt at the table have not been proven. Therefore Sibai (2002) recommends a regular diet with no salt restriction. Because pregnant women with hypertension have a lower plasma volume than do normotensive women, sodium restriction is not neces­sary. Women need salt for maintenance of blood volume and placental perfusion. The exception may be the woman with chronic hypertension that was successfully controlled with a low-salt diet before the pregnancy. Adequate fluid intake helps maintain optimum fluid volume and aids in renal perfusion and filtration. The nurse uses assessment data regarding the woman's diet to counsel her as needed in areas of deficiency (see Self-Care box).

Successful home care requires the woman to be well educated about preeclampsia and motivated to follow the plan of care. She must also be reliable about keeping appointments. The effects of illness, language, age, culture, beliefs, and support systems must be considered. The woman's support systems must be mobilized and involved in planning and implementing her care (see Plan of Care).

 

Patient Instructions for Self-Care

1. Assessing and Reporting Clinical Signs of Preeclampsia

Report immediately any increase in your blood pressure, protein in urine, weight gain greater than 1 lb/wk, or edema.

Take your blood pressure on the same arm in a sitting position each time for consistent and accurate readings. Support arm on a table in a horizontal position at heart level.

Use the same scale, wearing the same clothes, at the same time each day, after voiding, before breakfast, for reliable daily weights.

Dipstick test your clean-catch urine sample to assess proteinuria; report frequency or burning on urination.

Report to your health care provider if proteinuria is +2 or more or if you have a decrease in urine output.

Assess your baby's activity daily. Decreased activity (three or fewer movements per hour) may indicate fetal compromise and should be reported.

It is important to keep your scheduled prenatal appointments so that any changes in you or your baby's condition can be detected.

Keep a daily log or diary of your assessments for your home health care nurse, or bring it with you to your next prenatal visit.

 

2. Coping with Bed Rest

In bed, lie on your side. This allows more blood to get to your uterus (womb) and baby. The bed or sofa should be near a window and a bathroom.

Increase your fluid intake to 8 glasses/day and add roughage (bran, fruits, leafy vegetables) to your diet to decrease constipation. Keep a bowl of fruit and a large container full of water close by.

Include diversionary activities, such as puzzles, reading, and crafts, to reduce boredom. Place a box or table within reach to store magazines, books, telephone, etc.

Do gentle exercises, such as circling your hands and feet or gently tensing and relaxing arm and leg muscles. This improves muscle tone, circulation, and sense of well-being.

Encourage family participation in your care.

Have significant others assist you with care of the house, children, etc.

Use relaxation to help cope with stress. Relax your body one muscle at a time, or imagine some pleasant scene, word, or image. Soothing music can also help you relax.

 

3. Nutrition

Eat a nutritious, balanced diet (60 to 70 g protein, 1200 mg calcium, and adequate zinc, magnesium, and vitamins). Consult with registered dietitian on the diet best suited for you as an individual.

There is no sodium restriction; however, consider limiting excessively salty foods (luncheon meats, pretzels, potato chips, pickles, sauerkraut).

Eat foods with roughage (whole grains, raw fruits, and vegetables).

Drink six to eight 8-oz glasses of water per day.

Avoid alcohol and limit caffeine intake.

 

 

Severe preeclampsia and HELLP syndrome

If the woman's condition worsens or she already has severe preeclampsia or HELLP syndrome and is critically ill, she should receive appropriate management (usually in a tertiary care center), ranging from immediate birth to conservative management of the pregnancy (Leicht & Harvey, 1999). Important components of management include the administration of magnesium sulfate as prophylaxis against seizures and an antihypertensive agent if diastolic blood pressure is higher than 100 to 110 mm Hg.

Antepartum care focuses on stabilization and preparation for birth. The woman may be admitted to an antepartum or a labor and birth unit, depending on the hospital. If the woman's condition is severe, she may be placed in an obstetric critical care unit or a medical intensive care unit (if an obstetric critical care unit is not available) for any necessary hemodynamic monitoring. Maternal and fetal surveillance, patient education regarding the disease process, and supportive measures directed toward the woman and her family are initiated. Assessments include review of the cardiovascular system, pulmonary system, renal system, hematologic system, and CNS. Fetal assessments for well-being (e.g., NST, BPP, Doppler velocimetry) are important because of the potential for hypoxia related to uteroplacental insufficiency. Baseline laboratory assessments include metabolic studies for liver enzyme (AST, ALT, LDH) determination, complete blood count with platelets, coagulation profile to assess for DIC, and electrolyte studies to establish renal functioning.

Weight is measured on admission and every day thereafter. An indwelling urinary catheter facilitates monitoring of renal function and effectiveness of therapy. If appropriate, vaginal examination may be done to check for cervical changes. Abdominal palpation establishes uterine tonicity and fetal size, activity, and position. Electronic monitoring to determine fetal status is initiated at least once a day. The nurse's skill in implementing the techniques described here can be reassuring to the woman and her family. The woman's room must be close to staff and emergency drugs, supplies, and equipment. Noise and external stimuli must be minimized. Seizure precautions are taken (Box 4).

BOX 4 Hospital Precautionary Measures

·        Environment

- Quiet

- Nonstimulating

- Lighting subdued

·        Seizure precautions

- Suction equipment tested and ready to use

- Oxygen administration equipment tested and ready to use

·        Call button within easy reach

·        Emergency medication tray immediately accessible

- Hydralazine and magnesium sulfate in or adjacent to woman's room

- Calcium gluconate immediately available

·        Emergency birth pack accessible

 

 

Bed rest is commonly ordered. The nurse's ingenuity may be called on to help the woman cope physically and psychologically with the side effects of immobility and an environment limited in stimuli and support. Thromboembolic events, a risk factor during normal pregnancy, pose an even greater risk with preeclampsia (see Plan of Care).

Intrapartum nursing care of the woman with severe preeclampsia or HELLP syndrome involves continuous monitoring of maternal and fetal status as labor progresses. The assessment and prevention of tissue hypoxia and hemorrhage, both of which can lead to permanent compromise of vital organs, continue throughout the intrapartum and postpartum periods (Leicht & Harvey, 1999).

Magnesium sulfate. One of the important goals of care for the woman with severe preeclampsia is prevention or control of convulsions. Magnesium sulfate (MgSO4) is the drug of choice in the prevention and treatment of convulsions caused by preeclampsia or eclampsia (ACOG, 1996). Benefits of magnesium sulfate therapy include an increase in uterine blood flow to protect the fetus and an increase in prostacyclins to prevent uterine vasoconstriction (Gilbert & Harmon, 1998).

Magnesium sulfate is administered as a secondary infusion to the main intravenous (IV) line (e.g., piggybacked) by volumetric infusion pump. An initial loading dose of 4 to 6 g of magnesium sulfate per protocol or physician's order is infused over 20 to 30 minutes. This dose is followed by a maintenance dose of magnesium sulfate that is diluted in an IV solution per physician's order (e.g., 40 g of magnesium sulfate in 1000 ml of lactated Ringer's solution) and administered by infusion pump at 1 to 3 g/hr (Gilbert & Harmon, 1998; Mandeville & Troiano, 1999). This dose should maintain a therapeutic serum magne­sium level of 4 to 8 g/dl. Serum magnesium levels are obtained after the patient has received magnesium sulfate for 4 to 6 hours. The infusion rate is adjusted to maintain the therapeutic level (Sisson & Sauer, 1996) (Box 5).

 

BOX 5 Care of Patient with Preeclampsia Receiving Magnesium Sulfate

Magnesium Sulfate Administration

PATIENT AND FAMILY TEACHING

Explain technique, rationale, and reactions to expect

  Route and rate

  Purpose of "piggyback"

Reasons for use

  Tailor information to patient's readiness to learn

  Explain it is to prevent disease progression

  Explain it is to prevent seizures

Reactions to expect from medication

  Initially patient will feel flushed, hot, sedated, nauseated, especially during the bolus

  Sedation will continue

Monitoring to anticipate

  Maternal: blood pressure, pulse, DTRs, level of consciousness, urine output (indwelling catheter), presence of headache, visual disturbances, epigastric pain

  Fetal: FHR and activity

 

ADMINISTRATION

  Verify physician order

  Position woman in side-lying position

  Prepare solution and administer with an infusion control device (pump)

  Piggyback a solution of 40 g magnesium sulfate in 1000 ml lactated Ringer's solution with an infusion control device at the ordered rate: loading dose—initial bolus of 4 to 6 g over 15 to 30 min; maintenance dose—1 to 3 g/hr

 

MATERNAL AND FETAL ASSESSMENTS

  Monitor blood pressure, pulse, respiratory rate, FHR, and contractions every 15 to 30 min, depending on patient condition

  Monitor intake and output, proteinuria, DTRs, presence of headache, visual disturbances, level of consciousness and epigastric pain at least hourly

  Restrict hourly fluid intake to a total of 100 to 125 ml/hr; urinary output should be at least 30 ml/hr

 

REPORTABLE CONDITIONS

  Blood pressure: systolic >160 mm Hg, diastolic >110 mm Hg, or both

  Respiratory rate: <12 breaths/min

  Urinary output <30 ml/hr

  Presence of headache, visual disturbances, or epigastric pain

  Increasing severity or loss of DTRs; increasing edema, proteinuria

  Any abnormal laboratory values (magnesium levels, platelet count, creatinine clearance, levels of uric acid, AST, ALT, prothrombin time, partial  thromboplastin time, fibrinogen, fibrin split products)

  Any other significant change in maternal or fetal status

 

EMERGENCY MEASURES

  Keep emergency drug tray at bedside with calcium gluconate and intubation equipment

  Keep side rails up

  Keep lights dimmed and maintain a quiet environment

 

DOCUMENTATION

  All of the above

 

Intramuscular (IM) magnesium sulfate is seldom used because absorption rate cannot be controlled, injections are painful, and tissue necrosis may occur. However, the IM route may be used with some women who are being transported to a tertiary care center. The IM dose is 4 to 5 g given in each buttock, a total of 10 g (with 1% procaine possibly being added to the solution to reduce injection pain), and can be repeated at 4-hour intervals. Z-track technique should be used for the deep IM injection, followed by gentle massage at the site.

Magnesium sulfate interferes with the release of acetylcholine at the synapses, decreasing neuromuscular irritability, depressing cardiac conduction, and decreasing CNS irritability. Because magnesium circulates free and unbound to protein and is excreted in the urine, accurate recordings of maternal urine output must be obtained. Diuresis is an excellent prognostic sign; however, if renal function declines, all of the magnesium sulfate will not be excreted and can cause magnesium toxicity.

Serum magnesium levels are obtained on the basis of the woman's response and if any signs of toxicity are pre­sent. Early symptoms of toxicity include nausea, a feeling of warmth, flushing, muscle weakness, decreased reflexes, and slurred speech.

 

NURSE ALERT Loss of patellar reflexes, respiratory depression, oliguria, and decreased level of consciousness are signs of magnesium toxicity. Actions are needed to prevent respiratory or cardiac arrest. If magnesium toxicity is suspected, the infusion should be discontinued immediately. Calcium gluconate, the antidote for magnesium sulfate, may also be ordered (10 ml of a 10% solution, or 1 g) and given by slow IV push (usually by the physician) over at least 3 minutes (Sibai, 2002) to avoid undesirable reactions such as arrhythmias, bradycardia, and ventricular fibrillation.

 

NURSE ALERT Because magnesium sulfate is also a tocolytic agent, its use may increase the duration of labor. A preeclamptic woman receiving magnesium sulfate may need augmentation with oxytocin during labor. The amount of oxytocin needed to stimulate labor may be more than that needed for a woman who is not on magnesium sulfate.

 

Control of blood pressure. For the severely hypertensive preeclamptic woman, antihypertensive medications may be ordered to lower the diastolic blood pressure. Initiation of antihypertensive therapy reduces maternal morbidity and mortality rates associated with left ventricular failure and cerebral hemorrhage. Because a degree of maternal hypertension is necessary to maintain uteroplacental perfusion, antihypertensive therapy must not decrease the arterial pressure too much or too rapidly. The target range for the diastolic pressure is therefore 90 to 100 mm Hg (Leicht & Harvey, 1999).

IV hydralazine remains the antihypertensive agent of choice for the treatment of hypertension in severe preeclampsia. IV labetalol hydrochloride and oral methyldopa and nifedipine are also used (Cunningham et al., 2001; Sisson & Sauer, 1996). The choice of agent used depends on patient response and physician preference. Table 5 compares antihypertensive agents used to treat hypertension in pregnancy.

 

Table 5 Pharmacologic Control of Hypertension in Pregnancy

ACTION

TARGET TISSUE

EFFECTS

NURSING ACTIONS

MATERNAL

FETAL

HYDRALAZINE (APRESOLINE, NEOPRESOL)

Arteriolar vasodilator

Peripheral arterioles: to decrease muscle tone, decrease peripheral resistance; hypothalamus and medullary vasomotor center for minor decrease in sympathetic tone

Headache, flushing, palpitation, tachycardia, some decrease in uteroplacental blood flow, increase in heart rate and cardiac output, increase in oxygen consumption, nausea and vomiting

Tachycardia; late decelerations and bradycardia if maternal diastolic pressure <90 mm Hg

Assess for effects of medications, alert mother (family) to expected effects of medications, assess blood pressure frequently because precipitous drop can lead to shock and perhaps abruption placentae; assess urinary output; maintain bed rest in a lateral position with side rails up; use with caution in presence of maternal tachycardia

LABETALOL HYDROCHLORIDE (NORMODYNE)

 

 

Peripheral arterioles (see hydralazine)

 

 

β-blocking agent causing vasodilation without significant change in cardiac output

 

Minimal: flushing, tremulousness; minimal change in pulse rate

Minimal, if any

See hydralazine; less likely to cause excessive hypotension and tachycardia; less rebound hypertension than hydralazine

METHYLDOPA (ALDOMET)

Maintenance therapy if needed: 250-500 mg orally every 8 hr (a2-receptor agonist)

Postganglionic nerve endings: interferes with chemical neurotransmission to reduce peripheral vascular resistance, causes CNS sedation

Sleepiness, postural hypotension, constipation; rare: drug-induced fever in 1% of women and positive Coombs' test result in 20%

After 4 mo maternal therapy, positive Coombs' test result in infant

See hydralazine

NIFEDIPINE (PROCARDIA)

Calcium channel blocker

Arterioles: to reduce systemic vascular resistance by relaxation of arterial smooth muscle

Headache, flushing; possible potentiation of effects on CNS if administered concurrently with magnesium sulfate, may interfere with labor

Minimal

See hydralazine; use caution if patient also getting magnesium sulfate

 

 

Eclampsia

The convulsions that occur in eclampsia are frightening to observe. Increased hypertension and tonic contraction of all body muscles (seen as arms flexed, hands clenched, legs inverted) precede the tonic-clonic convulsions (Fig. 5). During this stage, muscles alternately relax and contract. Respirations are halted and then begin again with long, deep, stertorous inhalations. Hypotension follows, and coma ensues. Nystagmus and muscular twitching persist for a time. Disorientation and amnesia cloud the immediate recovery. Oliguria and anuria are notable. Seizures may recur within minutes of the first convulsion, or the woman may never have another. Eclamptic seizures can result in tissue damage to the woman during the convulsion, especially if she is in a bed with unpadded side rails. During the convulsion the pregnant woman and fetus are not receiving oxygen, so eclamptic seizures produce a marked metabolic insult to both the woman and the fetus.

 

Fig. 5 Eclampsia (convulsions or seizures)

 

Immediate care. The immediate care during a convulsion is to ensure a patent airway (see Emergency box). When convulsions occur, the woman is turned onto her side to prevent aspiration of vomitus and supine hypoten­sion syndrome. After the convulsion ceases, food and fluid are suctioned from the glottis or trachea, and oxygen is administered by face mask. Magnesium sulfate (e.g., 2 g IV push over 3 minutes) or other anticonvulsant is given as ordered (Leicht & Harvey, 1999). If an IV infusion is not in place, one is begun with a large-bore needle. Time, duration, and description of convulsions are recorded, and any urinary or fecal incontinence is noted. The fetus is monitored for adverse effects. Transient fetal bradycardia and decreased FHR variability are common.

Aspiration is a leading cause of maternal morbidity and mortality after eclamptic seizure. After initial stabilization and airway management, the nurse should anticipate orders for a chest radiograph and possibly arterial blood gases to rule out the possibility of aspiration.

A rapid assessment of uterine activity, cervical status, and fetal status is performed after a convulsion. During the convulsion, membranes may have ruptured; the cervix may have dilated because the uterus becomes hypercontractile and hypertonic; birth may be imminent. If not, once a woman's seizure activity and blood pressure are controlled, a decision should be made regarding whether birth should take place. The more serious the condition of the woman, the greater the need to proceed to birth. The route of birth—induction of labor versus cesarean birth—depends on maternal and fetal condition. If fetal lungs are not mature and the birth can be delayed for 48 hours, steroids such as betamethasone may be given to the woman.

The woman may have been incontinent of urine and stool during the convulsion; she will need assistance with hygiene and a change of gown. Oral care with a soft toothbrush may be of comfort.

Immediately after a seizure, the woman may be confused and can be combative, necessitating the temporary use of restraints. It may take several hours for the woman to regain her usual level of mental functioning. The health care provider explains procedures briefly and quietly. The woman is never left alone. The family is also kept informed of management, rationale for treatment, and the woman's progress.

Laboratory tests are ordered to assess for HELLP syndrome and to have blood typed and crossmatched for administration of packed red blood cells as needed. Blood must be available for emergency transfusion because abruptio placentae, with accompanying hemorrhage and shock, often occurs in women with eclampsia. Other tests include determination of electrolyte levels, liver function battery, and complete hemogram and clotting profile, including platelet count and fibrin split product levels (to assess for DIC).

 

EMERGENCY Eclampsia

TONIC-CLONIC CONVULSION SIGNS

Stage of invasion: 2 to 3 sec, eyes are fixed, twitching of facial muscles occurs

Stage of contraction: 15 to 20 sec, eyes protrude and are bloodshot, all body muscles are in tonic contraction

Stage of convulsion: muscles relax and contract alternately (clonic), respirations are halted and then begin again with long, deep, stertorous inhalation, coma ensues

INTERVENTION

Keep airway patent: turn head to one side, place pillow under one shoulder or back if possible Call for assistance Protect with side rails up Observe and record convulsion activity

AFTER CONVULSION OR SEIZURE

Do not leave unattended until fully alert

Observe for postconvulsion coma, incontinence

Use suction as needed

Administer oxygen via face mask at 10 L/min

Start IV fluids and monitor for potential fluid overload

Give magnesium sulfate or other anticonvulsant drug as ordered

Insert indwelling urinary catheter

Monitor blood pressure

Monitor fetal and uterine status

Expedite laboratory work as ordered to monitor kidney function, liver function, coagulation system, and drug levels

Provide hygiene and a quiet environment

Support and keep woman and family informed

Be prepared for delivery when woman is in stable condition

 

 

Postpartum nursing care

After birth the symptoms of preeclampsia or eclampsia resolve quickly, usually within 48 hours. The hematopoi-etic and hepatic complications of HELLP syndrome may persist longer. These patients often show an abrupt de­crease in platelet count, with a concomitant increase in LDH and AST levels, after a trend toward normalization of values has begun. Generally the laboratory abnormali­ties seen with HELLP syndrome resolve in 72 to 96 hours.

The nursing care of the woman with hypertensive disease differs from that required in the usual postpartum period in a number of respects. The following variations in the nursing process are described.

Careful assessment of the woman with a hypertensive disorder continues throughout the postpartum period. Blood pressure is measured at least every 4 hours for 48 hours or more frequently as the woman's condition warrants. Even if no convulsions occurred before the birth, they may occur within this period. Magnesium sulfate infusion may be continued 12 to 24 hours after the birth. As­sessments for effects and side effects continue until the medication is discontinued.

 

NURSE ALERT! The woman is at risk for a boggy uterus and a large lochial flow as a result of the magnesium sulfate therapy. Uterine tone and lochial flow must be monitored closely.

 

The preeclamptic woman is unable to tolerate excessive postpartum blood loss because of hemoconcentration. Oxytocin or prostaglandin products are used to control bleeding. Ergot products (e.g., Ergotrate, Methergine) are contraindicated because they can increase blood pressure.

The woman is asked to report symptoms such as headaches and blurred vision. The nurse assesses affect, level of con­sciousness, blood pressure, pulse, and respiratory status before an analgesic is given for headache. Magnesium sulfate potentiates the action of narcotics, CNS depressants, and calcium-channel blockers; these drugs must be administered with caution. The woman may need to continue an antihypertensive medication regimen if her diastolic blood pressure exceeds 100 mm Hg at discharge.

The woman's and family's responses to labor, birth, and the neonate are monitored. Interactions and involvement in the care of the neonate are encouraged to the extent that the woman and her family desire. In addition, the woman and her family need opportunities to discuss their emotional response to complications. The nurse provides information concerning the prognosis. Preeclampsia and eclampsia do not necessarily recur in subsequent pregnancies (recurrence rate is approximately 30%), but prenatal care is essential.

 

Prevention

Early prenatal care for identification of women at risk and early detection of development of preeclampsia is the best prevention because there is no known etiology for preeclampsia. There have been numerous clinical trials studying various methods for prevention. These interventions included the use of calcium, magnesium, zinc, fish oil dietary supplementation, and possibly exercise (see Research box). Antihypertensive agents, diuretics, and low-salt diets have also been studied (Mattar & Sibai, 1999; Sibai, 1998). None of these interventions demonstrated a benefit in reducing the incidence or severity of preeclampsia in healthy pregnant women. Nurses should be aware of what strategies are being studied and use the most reliable evidence about the results so that they can counsel pregnant women about interventions that are likely to be beneficial. One resource is the Cochrane Pregnancy and Childbirth Database (Enkin et al., 1995).

 

RESEARCH

Exercise and Blood Pressure in Pregnancies with Risk of Hypertension

Regular exercise during pregnancy may reduce nausea and fatigue and may improve ease of labor and birth outcomes. Moderate exercise is encouraged in low risk pregnancies, but it is still customary to limit exercise when there is a risk of hypertensive disorder of pregnancy. The rationale behind this restriction has been that vascular function is disrupted by inflammation, which decreases perfusion to the placenta and to maternal kidneys, and that exercise would increase the blood pressure and the inflammation. However, there is evidence that exercise by at risk pregnant women may enhance vasodilation and perfusion and tend to decrease the likelihood of preeclampsia.

To prospectively study whether moderate exercise during pregnancy lowers blood pressure, a research team recruited 16 pregnant women before 14 weeks of gestation. All the women had a history of mild hypertension, gestational hypertension, or family history of hypertension and were thus at risk for pregnancy-induced hypertension. Researchers randomly assigned half of the women to a group that engaged in supervised 45-minute treadmill sessions, three times a week, from gestational weeks 18 to 28; the other half were placed in a control group. Results showed that both groups had similar body fat and similar daily total energy expenditures. Systolic and diastolic blood pressures decreased in the treat­ment group and increased in the control group, al­though none of the changes achieved significance. The trend was strongest for diastolic pressures. One subject in each group developed gestational hypertension, and both delivered at term. Other outcomes were not noted.

IMPLICATIONS FOR PRACTICE

Regular, moderate exercise appears to be acceptable, possibly even desirable, in pregnancies of women at risk for pregnancy-induced hypertension. Exercise appears to have more influence on lowering blood pressure than either body fat composition or overall daily physical activity. Until research provides more evidence about exercise in these high risk women, nurses should ask all women at risk for pregnancy-induced hypertension about their exercise habits, encourage them to discuss an acceptable level of exercise with the physician or nurse-midwife, and mon­itor them closely for signs of hypertension at each prenatal visit.

Source: Yeo, S., et al. (2000). Effect of exercise in pregnant women with a risk of gestational hypertensive disorders. J Reprod Med, 45(4), 293-298.

 

Evaluation

Evaluation of the effectiveness of care of the woman with preeclampsia is based on the expected outcomes.


PLAN OF CARE

Mild Preeclampsia: Home Care

NURSING DIAGNOSIS Risk for injury related to signs of preeclampsia

Expected Outcomes Patient will demonstrate ability to assess self and fetus for signs of worsening preeclampsia; no adverse sequelae will occur as result of preeclamptic condition.

Nursing Interventions/Rationales

Review warning signs/symptoms of preeclampsia to ensure adequate knowledge base exists for decision making.

Assess home environment, including woman's ability to assume self-care responsibilities, support systems, language, age, culture, beliefs, and effects of illness, to determine if home care is viable option.

Teach woman how to do a self-assessment for clinical signs of preeclampsia (take and record blood pressure, measure urine protein, maintain daily weight log, assess edema formation, assess fetal activity) to provide immediate evidence of a worsening condition.

Teach woman to report any increases in blood pressure, +2 proteinuria, weight gain greater than 1 lb per week, presence of edema, and decreased fetal activity to her health care provider immediately to prevent worsening of preeclamptic condition.

Teach woman about use of rest and relaxation as palliative treatment options to decrease blood pressure and promote diuresis.

 

NURSING DIAGNOSIS Fear/anxiety related to preeclampsia and its effect on the fetus

Expected Outcome Patient's feelings and symptoms of fear/anxiety will decrease/ease.

Nursing Interventions/Rationales

Provide a calm, soothing atmosphere and teach family to provide emotional support to facilitate coping.

Encourage verbalization of fears to decrease intensity of emotional response.

Involve woman and family in the management of her preeclamptic condition to promote a greater sense of control.

Help woman identify and use appropriate coping strategies and support systems to reduce fear/anxiety.

Explore use of desensitization strategies such as progres­sive muscle relaxation, visual imagery, or thought stopping to reduce fear-related emotions and related physical symptoms.

 

NURSING DIAGNOSIS Deficient diversional activity related to imposed bed rest.

Expected Outcome Patient will verbalize diminished feelings of boredom.

Nursing Interventions/Rationales

Assist woman to explore creatively personally meaningful activities that can be pursued from the bed to ensure activities that have meaning, purpose, and value to the individual.

Maintain emphasis on personal choices of woman to promote control and minimize imposition of routines by others.

Evaluate what support and system resources are available in the environment to assist in providing diversional activities.

Explore ways for woman to remain an active participant in home management and decision making to promote control.

Engage support of family and friends in carrying out chosen activities and making necessary environmental alterations to ensure success.

Teach woman about stress management and relaxation tech­niques to help manage tension of confinement

 

PLAN OF CARE

Severe Preeclampsia: Hospital Care

NURSING DIAGNOSIS Risk for injury to woman and fetus related to CNS irritability

Expected Outcome Patient will show diminished signs of CNS irritability (e.g., DTRs 2+, absence of clonus) and have no convulsions.

Nursing Interventions/Rationales

Establish baseline data (e.g., DTRs, clonus) to use as basis for evaluating effectiveness of treatment.

Administer IV MgS04 per physician's orders to decrease hy-perreflexia and minimize risk of convulsions.

Monitor maternal vital signs, FHR, urine output, DTRs, IV flow rate, and serum levels of MgSO4 to assess for and prevent MgSO4 toxicity (e.g., depressed respirations, oliguria, sudden drop in blood pressure, hyporeflexia, fetal distress).

Have calcium gluconate at bedside if needed as antidote for MgSO4 toxicity.

Maintain a quiet, darkened environment to avoid stimuli that may precipitate seizure activity.

 

NURSING DIAGNOSIS Ineffective tissue perfusion related to preeclampsia secondary to arteriolar vasospasm

Expected Outcome Patient will exhibit signs of increased vasodilation (i.e., diuresis, decreased edema, weight loss).

Nursing Interventions/Rationales

Establish baseline data (i.e., weight, degree of edema) to use as basis for evaluating effectiveness of treatment.

Administer intravenous magnesium sulfate per physician order, which serves to relax vasospasms and increase renal perfusion.

Place woman on bed rest in a side-lying position to maximize uteroplacental blood flow, reduce blood pressure, and promote diuresis.

Monitor intake and output, edema, and weight to assess for evidence of vasodilation and increased tissue perfusion.

 

NURSING DIAGNOSES Risk for

excess fluid volume to increased sodium retention secondary to administration of MgSO4

impaired gas exchange related to pulmonary edema secondary to increased vascular resistance

decreased cardiac output related to use of antihypertensive drugs

injury to fetus related to uteroplacental insufficiency secondary to use antihypertensive medications

Expected Outcomes Patient will exhibit signs of normal fluid volume (i.e., balanced intake and output, normal serum creatinine levels, normal breath sounds); adequate oxygenation (i.e., normal respirations, fully oriented to person, time, and place); normal range of cardiac output (i.e., normal pulse rate and rhythm); and fetal well-being (i.e., adequate fetal movement, normal FHR).

Nursing Interventions/Rationales

Monitor woman for signs of fluid volume excess (increased edema, decreased urine output, elevated serum creatinine level, weight gain, dyspnea, crackles) to detect potential complications.

Monitor woman for signs of impaired gas exchange (i.e., increased respirations, dyspnea, altered blood gases, hypox-emia) to detect potential complications.

Monitor woman for signs of decreased cardiac output (i.e., altered pulse rate and rhythm) to detect potential complications.

Monitor fetus for signs of difficulty (i.e., decreased fetal activity, decreased FHR) to prevent complications.

Record findings and report signs of increasing problems to physician to enable timely interventions


GESTOSIS OF EARLY TERMS OF PREGNANCY

Ptyalism in pregnancy, or excessive salivation, is especially annoying for a small number of patients, sometimes approaching 1 liter production per day. Medical treatment with tincture of belladonna or atropine alter ptyalism only slightly so that reassurance of the time-limited nature of the problem is a mainstay of management.

At least 66 % of women experience nausea and 50 % emesis in the first  trimester, with the frequency of these symptoms lessening as the second and third trimesters ensue. Classically, symptoms are predominantly present in the morning (“morning sickness”), but they may occur throughout the day and evening.

The genesis of pregnancy-induced nausea and vomiting is not clear. It may be that the hormonal changes of pregnancy are responsible. Chorionic gonadotropin, for instance, has been implicated on the basis that its levels are rather high at the same time that nausea and vomiting are  most common.

Light, moderate and severe degrees of vomiting are distinguished.

Light degree of vomiting accompanying with 2-4 times per day episodes of vomiting after taking meals. general state of the woman is satisfactory, light tachycardia may be present.

Moderate degree of vomiting accompanying with 10 times and more per day episodes of vomiting which don’t from taking meals. Weight loss, ketosis, increased temperature are present.

Frequent small feedings and avoidance of foods that are unpleasant to the patient usually relieve symptoms to a manageable level. A variety of antiemetics can be prescribed if the above measures fail to provide adequate relief, but unfortunately, none is completely effective and all carry risks (Metoclopramide, Meclizine, Promethazine). Of historical interest is the compound medication Bendectin, a combination of the antihistamine doxylamine and vitamin B6 (pyrodoxine), which was reasonable effective as an antiemetic in pregnancy. 

   Severe degree of vomiting is also called as Hyperemesis gravidarum (intractable emesis during pregnancy) is a more severe form of nausea and vomiting, occurring in approximately 4 out of 1000 pregnancies.

         Fortunately, hyperemesis gravidarum has become uncommon. This syndrome is defined as vomiting sufficiently pernicious to produce weight loss, dehydration, acidosis from starvation, alkalosis from loss of hydrochloric acid in vomitus, and hypokalemia. It appears to be related to high or rapidly rising serum levels of chorionic gonadotropin or estrogens. Goodwin and associates (1994) described significantly higher total as well as free b-subunits of chorionic gonadotropin concentrations in women with hyperemesis compared with asymptomatic controls.  Hyperemesis may lead to transient hepatic dysfunction.

      Dehydration is corrected as well as fluid and electrolyte deficits and acidosis or alkalosis. This requires appropriate amounts of sodium, potassium, chloride, lactate or bicarbonate, glucose, and water, all of which should be administered parenterally until vomiting has been controlled. Vomiting may be frequent and severe. Schwartz and Rossoff (1994) described a woman whose retching led to bilateral pneumothoraces and pneumomediastinum. A number of anti-emetics may be given to alleviate nausea and vomiting such as promethazine, prochlorperazine, and chlorpromazine. Nageotte and colleagues (1996) reported success with intravenous droperidol-diphenhydramine. For severe disease,  metoclopramide may be given parenterally. This stimulates motility of the upper intestinal tract without stimulating gastric, biliary, or pancreatic secretions. Its anti-emetic properties apparently result from central antagonism of dopamine receptors. With persistent vomiting, appropriate steps should be taken to diagnose other diseases, such as gastroenteritis, cholecystitis, pancreatitis, hepatitis, peptic ulcer, pyelonephritis, and fatty liver of pregnancy.

In many instances, social and psychological factors contribute to the illness (Deuchar, 1995). With correction of these circumstances, the woman usually improves remarkably while hospitalized, only to relapse after discharge. Positive assistance with psychological and social problems is beneficial.

Godsey and Newman (1991) studied 140 women admitted for hyperemesis to the Medical University of South Carolina Hospital. In 27 percent of these women, multiple admissions were necessary. In some women with persistent and severe disease, parenteral nutrition is used (Levine and Esser, 1988). Enteral nutrition also has been successfully used after acute nausea and vomiting subside (Boyce, 1992).

firmed at surgery.

Rare forms of gestosis in pregnancy:

1.              dermatosis gravidarum, clinic, diagnosis, treatment;

2.              tetania gravidarum, clinic, diagnosis, treatment;

3.              osteomalacia gravidarum, clinic, diagnosis, treatment;

4.              acute fatty liver of pregnancy, clinic, diagnosis, differential diagnosis (viral hepatitis, cholestasis),  treatment;

5.                 bronchial asthma of pregnancy, clinic, diagnosis, differential diagnosis,  treatment.

Acute fatty liver of pregnancy  is a rare complication of pregnancy, but its severity and maternal mortality rate of 30 % make its timely diagnosis and treatment of importance. It is usually occurs late in pregnancy in primagravidas and characterized by vague gastrointestinal symptoms becoming worse over several days’ time. Thereafter headache, mental confusion, and epigastric pain may ensue, and if untreated, there may be rapid development of coagulopathy, coma, multiple organ failute and death. Laboratory findings include an initial modest elevation in bilirubin and an elevation of transaminase levels. Treatment of this serious complication is correction of coagulopathy and electrolyte imbalances, cardiorespiratory support, and delivery as feasible by the vaginal route, if possible.

Fig.1 Fatty liver of pregnancy. Electron photomicrograph of two hepatocytes containing numerus microvesicular fat droplets (*). The nuclei (N) remain centered within the cells, unlike with the case of macrovesicular fat deposition. (Courtesy of Dr. Don Wheeler.)

 

Fig.2 Computerized tomograph in severely preeclamptic woman at term shows intrahepatic and subcapsular hemorrhage in right lobe of liver. (From Howard and Jones, 1993, with permission.)