Medicine

# UNIT TEST II

UNIT TEST II

Prepared by assistant professor N.Petrenko, MD, PhD

LEARNING OBJECTIVES

Summarize knowledge about normal and complicated pregnancies

to 24 weeks since last menstrual period, or weight of fetus is greater than 500 g

Gravidity and parity information is obtained during history-taking interviews and may be recorded in patient records in several ways. One abbreviation commonly used in maternity centers consists of five digits separated with hyphens. The first digit represents the total number of pregnancies, including the present one (gravidity); the second digit represents the total number of term births; the third indicates the number of preterm births; the fourth identifies the number of abortions (miscarriage or elective termination of pregnancy before viability); and the fifth is the number of children currently living. The acronym GTPAL (gravidity, term, preterm, abortions, living children) may be helpful in remembering this system of notation. For example, if a woman pregnant only once with twins gives birth at the thirty-fifth week and the babies survive, the abbreviation that represents this information is "1-0-1-0-2." During her next pregnancy the abbreviation is "2-0-1-0-2." Additional examples are given in Table 1.

Others prefer a four-digit system. The first digit of the five-digit system, which signifies gravidity, is dropped. The acronym TPAL may be useful in remembering what the four digits stand for.

 Table 1 Gravidity and Parity Using  Five-Digit (GTPAL) System GRAVIDITY PREGNANCIES TERM BIRTH PRETERM BIRTH ABORTIONS LIVING CHILDREN Sarah is pregnant for the first time. 1 0 0 0 0 She carries the pregnancy to term, and the neonate survives. 1 1 0 0 1 She is pregnant again. 2 1 0 0 1 Her second pregnancy ends in abortion. 2 1 0 1 1 During her third pregnancy, she gives birth to preterm twins. 3 1 1 1 3

PREGNANCY TESTS

Early detection of pregnancy allows for early initiation of care. Human chorionic gonadotropin (hCG) is the biologic marker on which pregnancy tests are based. Production of hCG begins as early as the day of implantation and can be detected in the blood as early as 6 days after conception, or approximately 20 days since the last menstrual period (LMP), and in urine approximately 26 days after conception (Cunningham et al., 2001). The level of hCG rises until it peaks at approximately 60 to 70 days of gestation and then begins to decline. The lowest level is reached between 100 and 130 days of pregnancy and remains constant until birth (Varney, 1997).

Serum and urine pregnancy tests are performed in clinics, offices, women's health centers, and laboratory settings. Both serum and urine tests provide accurate results. A 7- to 10-ml sample of venous blood is collected for serum testing. Most urine tests require a first-voided morning urine specimen because it contains levels of hCG approximately the same as those in serum. Random urine samples usually have lower levels. Urine tests are less expensive and provide more immediate results than serum tests (Hatcher et al., 1998).

Many different pregnancy tests are available, but they all depend on recognition of hCG or a beta subunit of hCG. The wide variety of tests precludes discussion of each; however, several categories of tests are described here. The nurse should read the manufacturer's directions for the test to be used.

Immunoassoys, or agglutination inhibition tests, depend on an antigen-antibody reaction between hCG and an antiserum. Usually, the antiserum is mixed with urine, and hCG-coated particles (e.g., latex or blood cells) are added. If hCG is present in the urine, agglutination does not occur because the hCG neutralizes the hCG antibody, and the test is considered positive (Cunningham et al., 2001). Although immunologic tests are accurate from 4 to 10 days after a missed period, they are most appropriate for confirming a pregnancy at or after the sixth week of gestation (Hatcher et al., 1998).

Radioimmunoassay pregnancy tests for the beta subunit of hCG in serum or urine samples use radioactively labeled markers and are usually performed in a laboratory. These tests are accurate with low hCG levels and can confirm pregnancy 1 week after conception (Hatcher et al., 1998).

Radioreceptor assay is a serum test that measures the ability of a blood sample to inhibit the binding of radiolabeled hCG to receptors. The test is 90% to 95% accurate from 6 to 10 days after conception (Pagana & Pagana, 2001).

Enzyme-linked immunosorbent assay (ELISA) testing is the most popular method of testing for pregnancy. It uses a specific monoclonal antibody (anti-hCG) with enzymes to bond with hCG in urine. Depending on the specific test, levels of hCG as low as 5 to 50 mlU/ml can be detected as early as 4 days after implantation (Hatcher et al., 1998). As an office or home procedure it requires minimal time and offers results in 5 minutes. A positive test is indicated by a simple color-change reaction.

ELISA technology is the basis for most over-thecounter home pregnancy tests. With these one-step tests, the woman usually applies urine to a strip and reads the results. The test kits come with directions for collection of the specimen, the testing procedure, and reading of the results. Most manufacturers of the kits provide a toll-free telephone number to call if users have concerns and questions about test procedures or results (see Teaching Guidelines box). The most common error in performing home pregnancy tests is doing the test too early in pregnancy (Hatcher et al., 1998).

 TEACHING GUIDELINES Home Pregnancy Testing • Follow the manufacturer's instructions carefully. Do not omit steps. • Review the manufacturer's list of foods, medications, and other substances that can affect the test results. • Use a first-voided morning urine specimen. • If the test done at the time of your missed period is negative, repeat the test in 1 week if you still have not had a period. • If you have questions about the test, contact the manufacturer. • Contact your health care provider for follow-up if the test is positive or if the test is negative and you still have not had a period

Interpreting the results of pregnancy tests requires some judgment. The type of pregnancy test and its degree of sensitivity (ability to detect low levels of a substance) and specificity (ability to discern the absence of a substance) have to be considered in conjunction with the woman's history. This includes the date of her last normal menstrual period (LNMP), her usual cycle length, and results of previous pregnancy tests. It is important to know if the woman is a substance abuser and what medications she is taking, because medications such as anticonvulsants and tranquilizers can cause false-positive results and diuretics and promethazine can cause false-negative results (Pagana & Pagana, 2001). Improper collection of the specimen, hormone-producing tumors, and laboratory errors also may cause false results. Whenever there is any question, further evaluation or retesting may be appropriate.

Maternal physiologic adaptations are attributed to the hormones of pregnancy and to mechanical pressures arising from the enlarging uterus and other tissues. These adaptations protect the woman's normal physiologic functioning, meet the metabolic demands pregnancy imposes on her body, and provide a nurturing environment for fetal development and growth. Although pregnancy is a normal phenomenon, problems can occur.

SIGNS OF PREGNANCY

Some of the physiologic adaptations are recognized as signs and symptoms of pregnancy. Three commonly used categories ofsigns and symptoms of pregnancy are presumptive, those changes felt by the woman (e.g., amenorrhea, fatigue, nausea and vomiting, breast changes);probable, those changes observed by an examiner (e.g., Hegar sign, ballottement, pregnancy tests); and positive, those signs that are attributed only to the presence of the fetus (e.g., hearing fetal heart tones, visualization of the fetus, and palpating fetal movements). Table 2 summarizes the signs of pregnancy in relation to when they might occur and other causes for their occurrence.

 Table 2 Sign and Pregnancy TIME OF OCCURRENCE (GESTATIONAL AGE) SIGN OTHER POSSIBLE CAUSE PRESUMPTIVE SIGNS 3-4 wk Breast changes Premenstrual changes, oral contraceptives 4 wk Amenorrhea Stress, vigorous exercise, early menopause, endocrine problems, malnutrition 4-14 wk Nausea, vomiting Gastrointestinal virus, food poisoning 6-12 wk Urinary frequency Infection, pelvic tumors 12 wk Fatigue Stress, illness 16-20 wk Quickening Gas, peristalsis PROBABLE SIGNS 5 wk Goodell sign Pelvic congestion 6-8 wk Chadwick sign Pelvic congestion 6-12 wk Hegar sign Pelvic congestion 4-12 wk Positive pregnancy test (serum) Hydatidiform mole, choriocarcinoma 6-12 wk Positive result to pregnancy test (urine) False-positive results may be caused by pelvic infection, tumors 16 wk Braxton Hicks contractions Myomas, other tumors 16-28 wk Ballottement Tumors, cervical polyps POSITIVE SIGNS 5-6 wk Visualization of fetus by real-time ultrasound examination No other causes 16wk Visualization of fetus by x-ray study 6 wk Fetal heart tones detected by ultrasound examination 8-17 wk Fetal heart tones detected by Doppler ultrasound stethoscope 17-19 wk Fetal heart tones detected by fetal Stethoscope 19-22 wk Fetal movements palpated Late pregnancy Fetal movements visible

REPRODUCTIVE SYSTEM AND BREASTS

Uterus

The phenomenal uterine growth in the first trimester is stimulated by high levels of estrogen and progesterone. Early uterine enlargement results from increased vascularity and dilation of blood vessels, hyperplasia (production of new muscle fibers and fibroelastic tissue) and hypertrophy (enlargement of preexisting muscle fibers and fibroelastic tissue), and development of the decidua. By 7 weeks of gestation, the uterus is the size of a large hen's egg; by 10 weeks of gestation, it is the size of an orange (twice its nonpregnant size); and by 12 weeks of gestation, it is the size of a grapefruit. After the third month, uterine enlargement is primarily the result of mechanical pressure of the growing fetus (Varney, 1997).

As the uterus enlarges, it also changes in shape and position. At conception the uterus is shaped like an upsidedown pear. During the second trimester, as the muscular walls strengthen and become more elastic, the uterus becomes spherical or globular. Later, as the fetus lengthens, the uterus becomes larger and more ovoid and rises out of the pelvis into the abdominal cavity.

The pregnancy may "show" after the fourteenth week, although this depends to some degree on the woman's height and weight. Abdominal enlargement may be less apparent in the nulipara with good abdominal muscle tone (Fig. 1). Posture also influences the type and degree of abdominal enlargement that occurs. In normal pregnancies the uterus enlarges at a predictable rate. As the uterus grows, it may be palpated above the symphysis pubis some time between the twelfth and fourteenth weeks of pregnancy (Fig. 2). The uterus rises gradually to the level of the umbilicus at 22 to 24 weeks of gestation and nearly reaches the xiphoid process at term. Between weeks 38 and 40, fundal height drops as the fetus begins to descend and engage in the pelvis (lightening) (Fig. 2, dashed line). Generally, lightening occurs in the nullipara approximately 2 weeks before the onset of labor and at the start of labor in the multipara.

Fig. 1 Comparison of abdomen, vulva, and cervix in nullipara

(A) and multipara (B) at the same stage of pregnancy.

Fig. 2 Height of fundus by weeks of normal gestation with a single fetus. Dashed line indicates height after lightening. (From Seidel, H. et al. [1999]. Mosby's guide to physical examination [4th ed.]. St. Louis: Mosby.)

Uterine enlargement is determined by measuring fundal height, a measurement commonly used to estimate the duration of pregnancy. However, variation in the position of the fundus or the fetus, variations in the amount of amniotic fluid present, the presence of more than one fetus, maternal obesity, and variation in examiner techniques can reduce the accuracy of this estimation of the duration of pregnancy.

The uterus normally rotates to the right as it elevates, probably because of the presence of the rectosigmoid colon on the left side. However, the extensive hypertrophy (enlargement) of the round ligaments keeps the uterus in the midline. Eventually, the growing uterus touches the anterior abdominal wall and displaces the intestines to either side of the abdomen (Fig. 3). When a pregnant woman is standing, most of her uterus rests against the anterior abdominal wall, and this contributes to altering her center of gravity.

Fig. 3 Displacement of internal abdominal structures and diaphragm by the enlarging uterus at 4, 6, and 9 months of gestation.

At approximately 6 weeks of gestation, softening and compressibility of the lower uterine segment (the uterine isthmus) occur (Hegar sign). This results in exaggerated uterine anteflexion during the first 3 months of pregnancy (Fig. 4). In this position the uterine fundus presses on the urinary bladder, causing the woman to experience urinary frequency.

Fig. 4 Hegar sign. Bimanual examination for assessing compressibility, softening of isthmus (lower uterine segment) while the cervix is still firm.

Early uterine enlargement may not be symmetric, depending on the site of implantation. For example, if corneal implantation occurred, a soft, irregular bulge (Piskacek sign) may be detected during a pelvic examination (Varney, 1997).

Changes in contractility. Soon after the fourth month of pregnancy, uterine contractions can be felt through the abdominal wall. These contractions are referred to as the Braxton Hicks sign. Braxton Hicks contractions are irregular, painless contractions that occur intermittently throughout pregnancy. These contractions facilitate uterine blood flow through the intervillous spaces of the placenta and thereby promote oxygen delivery to the fetus. Although Braxton Hicks contractions are not painful, some women do complain that they are annoying. After the twenty-eighth week, these contractions become much more definite, but they usually cease with walking or exercise. Braxton Hicks contractions can be mistaken for preterm and true labor; however, they do not increase in intensity or frequency or cause cervical dilation.

Uteroplacental blood flow. Placental perfusion depends on the maternal blood flow to the uterus. Blood flow increases rapidly as the uterus increases in size. Although uterine blood flow increases twentyfold, the fetoplacental unit grows more rapidly. Consequently, more oxygen is extracted from the uterine blood during the latter part of pregnancy (Cunningham et al., 2001). In a normal term pregnancy, one sixth of the total maternal blood volume is within the uterine vascular system. The rate of blood flow through the uterus averages 500 ml/min, and oxygen consumption of the gravid uterus increases to meet fetal needs. A low maternal arterial pressure, contractions of the uterus, and maternal supine position are three factors known to decrease blood flow. Estrogen stimulation may increase uterine blood flow. Doppler ultrasound can be used to measure uterine blood flow velocity, especially in pregnancies at risk because of conditions associated with decreased placental perfusion such as hypertension, intrauterine growth restriction, diabetes mellitus, and multiple gestation (Creasy & Resnik, 1999). Using an ultrasound device or a fetal stethoscope, the health care provider may hear the uterine soufflé or the funic souffle.

Cervical changes. A softening of the cervical tip called Goodell sign may be observed at approximately the beginning of the sixth week in a normal, unscarred cervix. This sign is brought about by increased vascularity, slight hypertrophy, and hyperplasia (increase in number of cells) of the muscle and its collagen-rich connective tissue, which becomes loose, edematous, highly elastic, and increased in volume. The glands near the external os proliferate beneath the stratified squamous epithelium, giving the cervix the velvety appearance characteristic of pregnancy. Friability is increased and may cause slight bleeding after coitus with deep penetration or after vaginal examination. Pregnancy can also cause the squamocolumnar junction, the site for obtaining cells for cervical cancer screening, to be located away from the cervix. Because of all these changes, evaluation of abnormal Papanicolaou tests during pregnancy can be complicated. However, careful assessment of all pregnant women is important because approximately 3% of all cervical cancers are diagnosed during pregnancy (Creasy & Resnik, 1999).

The cervix of the nullipara is rounded. Lacerations of the cervix almost always occur during the birth process. With or without lacerations, however, after childbirth the cervix becomes more oval in the horizontal plane, and the external os appears as a transverse slit (see Fig. 1).

Changes related to the presence of the fetus. Passive movement of the unengaged fetus is called ballottement and can be identified generally between the sixteenth and eighteenth week. Ballottement is a technique of palpating a floating structure by bouncing it gently and feeling it rebound. In the technique used to palpate the fetus, the examiner places a finger in the vagina and taps gently upward, causing the fetus to rise. The fetus then sinks, and a gentle tap is felt on the finger (Fig. 5).

Fig. 5 Internal ballottement (18 weeks).

The first recognition of fetal movements, or "feeling life," by the multiparous woman may occur as early as the fourteenth to sixteenth week. The nulliparous woman may not notice these sensations until the eighteenth week or later. Quickening is commonly described as a flutter and is difficult to distinguish from peristalsis. Gradually, fetal movements increase in intensity and frequency. The week when quickening occurs provides a tentative clue in dating the duration of gestation.

Vagina and vulva

Pregnancy hormones prepare the vagina for stretching during labor and birth by causing the vaginal mucosa to thicken, connective tissue to loosen, smooth muscle to hypertrophy, and the vaginal vault to lengthen. Increased vascularity results in a violet-bluish color of the vaginal mucosa and cervix. The deepened color, termed Chadwick sign, may be evident as early as the sixth week, but is easily noted at the eighth week of pregnancy (Creasy & Resnik, 1999).

Leukorrhea is a white or slightly gray mucoid discharge with a faint musty odor. This copious mucoid fluid occurs in response to cervical stimulation by estrogen and progesterone. The fluid is whitish because of the presence of many exfoliated vaginal epithelial cells caused by hyperplasia of normal pregnancy. This vaginal discharge is never pruritic or blood stained. Because of the progesterone effect, ferning usually does not occur in the dried cervical mucous smear, as it would in a smear of amniotic fluid. Instead, a beaded or cellular crystallizing pattern formed in the dried mucus is seen (Cunningham et al., 2001). The mucus fills the endocervical canal, resulting in the formation of the mucous plug (operculum) (Fig. 6). The operculum acts as a barrier against bacterial invasion during pregnancy

Fig. 6 A, Cervix in nonpregnant woman. B, Cervix during pregnancy.

During pregnancy, the pH of vaginal secretions ranges from approximately 3.5 to 6. The increased production of lactic acid in the vaginal epithelium, probably caused by increased estrogen levels, produces a more acid environment. However, the pregnant woman is more vulnerable to some vaginal infections, especially yeast infections (Bennett & Brown, 1999).

The increased vascularity of the vagina and other pelvic viscera results in a marked increase in sensitivity. The increased sensitivity may lead to a high degree of sexual interest and arousal, especially during the second trimester of pregnancy. The increased congestion plus the relaxed walls of the blood vessels and the heavy uterus may result in edema and varicosities of the vulva. The edema and varicosities usually resolve during the postpartum period.

External structures of the perineum are enlarged during pregnancy because of an increase in vasculature, hypertrophy of the perineal body, and deposition of fat (Fig. 7). The labia majora of the nullipara approximate and obscure the vaginal introitus; those of the parous woman separate and gape after childbirth and perineal or vaginal injury. Fig. 1 compares the perineum of the nullipara and the multipara in relation to the pregnant abdomen, vulva, and cervix.

Fig. 7 A, Pelvic floor in nonpregnant woman. B, Pelvic floor at end of pregnancy. Note marked hypertrophy and hyperplasia below dashed line joining tip of coccyx and inferior margin of symphysis. Note elongation of bladder and urethra as a result of compression. Fat deposits are increased.

Breasts

Fullness, heightened sensitivity, tingling, and heaviness of the breasts begins in the early weeks of gestation in response to increased levels of estrogen and progesterone. Breast sensitivity varies from mild tingling to sharp pain. Nipples and areolae become more pigmented; secondary pinkish areolae develop, extending beyond the primary areolae; and nipples become more erectile. Hypertrophy of the sebaceous (oil) glands embedded in the primary areolae, called Montgomery tubercles , may be seen around the nipples. These sebaceous glands may have a protective role in that they keep the nipples lubricated for breastfeeding.

The richer blood supply causes the vessels beneath the skin to dilate. Once barely noticeable, the blood vessels become visible, often appearing in an intertwining blue network beneath the surface of the skin. Venous congestion in the breasts is more obvious in primigravidas. Striae gravidarum may appear at the outer aspects of the breasts.

During the second and third trimesters, growth of the mammary glands accounts for the progressive breast enlargement. The high levels of luteal and placental hormones in pregnancy promote proliferation of the lactiferous ducts and lobule-alveolar tissue, so palpation of the breasts reveals a generalized, coarse nodularity. Glandular tissue displaces connective tissue, and as a result the tissue becomes softer and looser.

Although development of the mammary glands is functionally complete by midpregnancy, lactation is inhibited until a drop in estrogen level occurs after the birth. A thin, clear, viscous secretory material (precolostrum) can be found in the acini cells by the third month of gestation.

Colostrum, the creamy, white/yellowish to orange premilk fluid, may be expressed from the nipples as early as 16 weeks of gestation (Lawrence, 1999). See Chapter 20 for discussion of lactation.

GENERAL BODY SYSTEMS

Cardiovascular system

Maternal adjustments to pregnancy involve extensive changes in the cardiovascular system, both anatomic and physiologic. Cardiovascular adaptations protect the woman's normal physiologic functioning, meet the metabolic demands pregnancy imposes on her body, and provide for fetal developmental and growth needs.

Slight cardiac hypertrophy (enlargement) is probably secondary to the increased blood volume and cardiac output that occurs. The heart returns to its normal size after childbirth. As the diaphragm is displaced upward by the enlarging uterus, the heart is elevated upward and rotated forward to the left (Fig. 8). The apical impulse, a point of maximum intensity, is shifted upward and laterally approximately 1 to 1.5 cm. The degree of shift depends on the duration of pregnancy and the size and position of the uterus.

Fig. 8 Changes in position of heart, lungs, and thoracic cage in pregnancy. Dashed line, nonpregnant; solid line, change that occurs in pregnancy.

The changes in heart size and position and increases in blood volume and cardiac output contribute to auscultatory changes common in pregnancy. There is more audible splitting of Sx and S2, and S, may be readily heard after 20 weeks of gestation. In addition, systolic and diastolic murmurs may be heard over the pulmonic area. These are transient and disappear shortly after the woman gives birth (Cunningham et al., 2001).

Between 14 and 20 weeks of gestation, the pulse increases approximately 10 to 15 beats per minute (beats/ min), which then persists to term. Palpitations may occur. In twin gestations, the maternal heart rate increases significantly in the third trimester (Creasy & Resnik, 1999).

The cardiac rhythm may be disturbed. The pregnant woman may experience sinus arrhythmia, premature atrial contractions, and premature ventricular systole. In the healthy woman with no underlying heart disease, no therapy is needed; however, women with preexisting heart disease will need close medical and obstetric supervision during pregnancy.

Blood pressure. Arterial blood pressure (brachial artery) is affected by age, activity level, and presence of health problems. Additional factors must be considered during pregnancy. These factors include maternal anxiety, maternal position, and size and type of blood pressure apparatus.

Maternal anxiety can elevate readings. If an elevated reading is found, the woman is given time to rest, and the reading is repeated.

Maternal position affects readings. Brachial blood pressure is highest when the woman is sitting, lowest when she is lying in the lateral recumbent position, and intermediate when she is supine, except for some women who experience supine hypotensive syndrome (see following discussion). Therefore, at each prenatal visit, the reading should be obtained in the same arm and with the woman in the same position. The position and arm used should be recorded along with the reading.

The proper size cuff is absolutely necessary for accurate readings. The cuff should be 20% wider than the diameter of the arm around which it is wrapped, or approximately 12 to 14 cm for average-sized individuals and 18 to 20 cm for obese persons. Too small a cuff yields a false-high reading; too large a cuff yields a false-low reading. Caution should also be used when comparing auscultatory and oscillatory blood pressure readings because discrepancies can occur (Green & Froman, 1996).

In the first trimester, blood pressure usually remains the same as the prepregnancy level. During the second trimester, there is a decrease in both systolic and diastolic pressure of 5 to 10 mm Hg. This decrease is probably the result of peripheral vasodilation caused by hormonal changes that occur during pregnancy. During the third trimester, maternal blood pressure should return to the first-trimester levels.

Calculating the mean arterial pressure (MAP) (mean of the blood pressure in the arterial circulation) can increase the diagnostic value of the findings. Normal MAP readings in the nonpregnant woman are 86.4 ± 7.5 mm Hg. MAP readings for a pregnant woman are slightly higher (Creasy 6 Resnik, 1999). One way to calculate MAP is illustrated in Box 1

 Box 1 Calculation of Mean Arterial Pressure (MAP)

Some degree of compression of the vena cava occurs in all women who lie flat on their backs during the second half of pregnancy . Some women experience a fall in their systolic blood pressure of more than 30 mm Hg. After 4 to 5 minutes a reflex bradycardia is noted, cardiac output is reduced by half, and the woman feels faint. This condition is termed supine hypotensive syndrome (Cunningham et al., 2001).

Compression of the iliac veins and inferior vena cava by the uterus causes increased venous pressure and reduced blood flow in the legs (except when the woman is in the lateral position). These alterations contribute to the dependent edema, varicose veins in the legs and vulva, and hemorrhoids that develop in the latter part of term pregnancy (Fig. 9).

Fig. 9 Hemorrhoids. (Courtesy Marjorie Pyle, RNC, Lifecircle, Costa Mesa, CA.)

Blood volume and composition. The degree of blood volume expansion varies considerably. Blood volume increases by approximately 1500 ml, or 40% to 45% above nonpregnancy levels (Cunningham et al., 2001). This increase consists of 1000 ml of plasma plus 450 ml of red blood cells (RBCs). The blood volume starts to increase at approximately the tenth to twelfth week, peaks at approximately the thirty-second to thirty-fourth week, then decreases slightly at the fortieth week. The increase in volume of a multiple gestation is greater than that for a pregnancy with a single fetus (Creasy & Resnik, 1999). Increased volume is a protective mechanism. It is essential for meeting the blood volume needs of the hypertrophied vascular system of the enlarged uterus, adequately hydrating fetal and maternal tissues when the woman assumes an erect or a supine position, and providing a fluid reserve to compensate for blood loss during birth and the puerperium. Peripheral vasodilation maintains a normal blood pressure despite the increased blood volume in pregnancy.

During pregnancy there is an accelerated production of RBCs (normal 4.2 to 5.4 million/mm3). The percentage of increase depends on the amount of iron available. The RBC mass increases by approximately 17% (Creasy & Resnik, 1999).

Because the plasma increase exceeds the increase in RBC production, there is a decrease in normal hemoglobin values (12 to 16 g/dl blood) and hematocrit values (37% to 47%). This state of hemodilution is referred to as physiologic anemia. The decrease is more noticeable during the second trimester, when rapid expansion of blood volume takes place faster than RBC production. If the hemoglobin value drops to 10 g/dl or less or if the hematocrit drops to 35% or less, the woman is considered anemic.

The total white cell count increases during the second trimester and peaks during the third trimester. This increase is primarily in the granulocytes; the lymphocyte count stays approximately the same throughout pregnancy. See Table 3 for laboratory values during pregnancy.

 Table 3 Laboratory values for Pregnant and Nonpregnant Women HEMATOLOGIC VALUES Complete Blood Count (CBC) Hemoglobin (g/dl) 12-16* >11* Hematocrit, packed cell volume (%) 37-47 >33* Red blood cell (RBC) volume (per ml) 1600 1500-1900 Plasma volume (per ml) 2400 3700 RBC count (million/mm3) 4.2-5.4 5-6.25 White blood cells (total per mm3) 5000-10,000 5000-15,000 Neutophils (%) 55-70 60-85 Lymphocytes (%) 20-40 15-40 Erythrocyte sedimentation rate (mm/hr) 20 Elevated second and third trimesters Mean corpuscular hemoglobin concentration (MCHC) (g/dl packed RBCs) 32-36 No change hemoglobin concentration Mean corpuscular hemoglobin (MCH) (pg) 27-31 No change per picogram (less than a nanogram) Mean corpuscular volume (MCV) (yu.m3) 80-95 No change per cubic micrometer Blood Coagulation and Fibrinolytic Activityt Factor 65-140 Increase in pregnancy, return to normal in early puerperium; factor VIII increases during and immediately after birth Factor 55-145 Factor 60-140 Factor 45-155 Factor 65-135 Decrease in pregnancy Factor 50-150 Prothrombin time (PT) (sec) 11-12.5 Slight decrease in pregnancy Partial thromboplastin time (PTT) (sec) 60-70 Slight decrease in pregnancy, and decreases further during second and third stages of labor (indicates clotting at placental site) Bleeding time (min) 1-9 (Ivy) No appreciable change Coagulation time (min) 6-10 (Lee/White) No appreciable change Platelets (per mm3) 150,000-400,000 No significant change until 3-5 days after birth and then a rapid increase (may predispose woman to thrombosis) and gradual return to normal Fibrinolytic activity Decreases in pregnancy and then abrupt return to normal (protection against thromboembolism) Fibrinogen (mg/dl) 200-400 Increased levels late in pregnancy Mineral/Vitamin Concentrations Vitamin B12, folic acid, ascorbic acid Serum proteins Total (g/dl) Albumin (g/dl) Globulin, total (g/dl) 6.4-8.3 3.5-5.0 2.3-3.4 5.5-7.5 Slight increase 3-4 Blood glucose Fasting (mg/dl) 2-Hour postprandial (mg/dl) 70-105 <140 Decreases <140 after a 100-g carbohydrate meal is considerednormal Acid-Base Values in Arterial Blood Po2 80-100 104-108 (increased) Pco2 35-45 27-32 (decreased) Sodium bicarbonate (HCO3) (mEq/L) 21-28 18-31 (decreased) Blood 7.35-7.45 7.40-7.45 (slightly increased —more alkaline) HEPATIC VALUES Bilirubin total (mg/dl) Not more than 1 mg/dl Unchanged Serum cholesterol (mg/dl) 120-200 Increases from 16-32 weeks of pregnancy; remains at this level until after birth Serum alkaline phosphatase (U/L) 30-120 Increases from week 12 of pregnancy to 6 weeks after birth Serum albumin (g/dl) 3.5-5 Slight increase RENAL VALUES Bladder capacity (ml) 1300 1500 Renal plasma flow (RPF) (ml/min 490-700 Increase by 25%-30% Glomerular filtration rate (GFR) (ml/min) 88-128 Increase by 30%-50% Nonprotein nitrogen (NPN) (mg/dl) 25-40 Decreases Blood urea nitrogen (BUN) (mg/dl) 10-20 Decreases Serum creatinine (mg/dl) 0.5-1.1 Decreases Serum uric acid (mg/dl) 2.7-7.3 Decreases Urine glucose Negative Present in 20% of pregnant women Intravenous pyelogram (IVP) Normal Slight to moderate hydroureter and hydronephrosis; right kidney larger than left kidney

Cardiac output. Cardiac output increases from 30% to 50% over the nonpregnant rate by the thirty-second week of pregnancy; it declines to approximately a 20% increase at 40 weeks of gestation. This elevated cardiac output is largely a result of increased stroke volume and heart rateand occurs in response to increased tissue demands for oxygen (Creasy & Resnik, 1999). Cardiac output in late pregnancy is appreciably higher when the woman is in the lateral recumbent position than when she is supine. In the supine position, the large, heavy uterus often impedes venous return to the heart and affects blood pressure. Cardiac output increases with any exertion, such as labor and birth. (Table 4 summarizes cardiovascular changes in pregnancy.)

 TABLE 4 Cardiovascular Changes in Pregnancy Heart rate Increases 10-15 beats/min Blood pressure Remains at prepregnancy levels in first trimester Slight decrease in second trimester Returns to prepregnancy levels in third trimester Blood volume Increases by 1500 ml or 40%-45% above prepregnancy level Red blood cell mass Increases 17% Hemoglobin Decreases Hematocrit Decreases White blood cell count Increases in second and third trimester Cardiac output Increases 30%-50%

Circulation and coagulation times. The circulation time decreases slightly by week 32. It returns to near normal near term. There is a greater tendency for blood to coagulate (clot) during pregnancy because of increases in various clotting factors (factors VII, VIII, IX, X, and fibrinogen). This, combined with the fact that fibrinolytic activity (the splitting up or the dissolving of a clot) is depressed during pregnancy and the postpartum period, provides a protective function to decrease the chance of bleeding but also makes the woman more vulnerable to thrombosis, especially after cesarean birth.

Respiratory system

Structural and ventilatory adaptations occur during pregnancy to provide for maternal and fetal needs. Maternal oxygen requirements increase in response to the acceleration in the metabolic rate and the need to add to the tissue mass in the uterus and breasts. In addition, the fetus requires oxygen and a way to eliminate carbon dioxide.

Elevated levels of estrogen cause the ligaments of the rib cage to relax, permitting increased chest expansion (see Fig. 8). The transverse diameter of the thoracic cage increases by approximately 2 cm, and the circumference increases by 6 cm (Cunningham et al., 2001). The costal angle increases and the lower rib cage appears to flare out. The chest may not return to its prepregnant state after birth (Seidel et al., 1999).

The diaphragm is displaced by as much as 4 cm during pregnancy. As pregnancy advances, thoracic (costal) breathing replaces abdominal breathing, and it becomes less possible for the diaphragm to descend with inspiration. Thoracic breathing is primarily accomplished by the diaphragm rather than by the costal muscles (Creasy & Resnik, 1999).

The upper respiratory tract becomes more vascular in response to elevated levels of estrogen. As the capillaries become engorged, edema and hyperemia develop within the nose, pharynx, larynx, trachea, and bronchi. This congestion within the tissues of the respiratory tract gives rise to several conditions commonly seen during pregnancy. These conditions include nasal and sinus stuffiness, epistaxis (nosebleed), changes in the voice, and a marked inflammatory response that can develop into a mild upper respiratory infection.

Increased vascularity of the upper respiratory tract also can cause the tympanic membranes and eustachian tubes to swell, giving rise to symptoms of impaired hearing, earaches, or a sense of fullness in the ears.

Pulmonary function. Respiratory changes in pregnancy are related to the elevation of the diaphragm and chest wall changes (Creasy & Resnik, 1999). Changes in the respiratory center result in a lowered threshold for carbon dioxide. The actions of progesterone and estrogen are presumed responsible for the increased sensitivity of the respiratory center to carbon dioxide. In addition, pregnant women become more aware of the need to breathe; some may even complain of dyspnea at rest. (See Table 5 for respiratory changes in pregnancy.)

 Table 5 Respiratory Changes in Pregnancy Respiratory rate Unchanged or slightly increased Tidal volume Increased 30%-40% Vital capacity Unchanged Inspiratory Increased Expiratory Decreased Total Unchanged to slightly decreased Oxygen consumption Increased 15%-20%

Although pulmonary function is not impaired by pregnancy, diseases of the respiratory tract may be more serious during this time (Cunningham et al., 2001). One important factor responsible for this may be the increased oxygen requirement.

Basal metabolism rate. The basal metabolism rate (BMR) varies considerably in women at the beginning of and during pregnancy, although it usually increases by 15% to 20% at term (Worthington-Roberts & Williams, 1997). The BMR returns to nonpregnant levels by 5 to 6 days postpartum. The elevation in BMR during pregnancy reflects increased oxygen demands of the uterineplacental-fetal unit and greater oxygen consumption because of increased maternal cardiac work (Chamberlain & Pipkin, 1998). Peripheral vasodilation and acceleration of sweat gland activity help dissipate the excess heat resulting from the increased BMR during pregnancy. Pregnant women may experience heat intolerance, which is annoying to some women. Lassitude and fatigability after only slight exertion are experienced by many women in early pregnancy. These feelings, along with a greater need for sleep, may persist and may be caused in part by the increased metabolic activity.

Acid-base balance. Around the tenth week of pregnancy, there is a decrease of approximately 5 mm Hg in the partial pressure of carbon dioxide (PCO2). Progesterone may be responsible for increasing the sensitivity of the respiratory center receptors so that tidal volume is increased and PCO2 falls, the base excess (HCO3, or bicarbonate) falls, and pH increases slightly. These alterations in acidbase balance indicate that pregnancy is a state of respiratory alkalosis compensated by mild metabolic acidosis (Chamberlain & Pipkin, 1998). These changes also facilitate the transport of CO2 from the fetus and O2 release from the mother to the fetus (see Table 3).

Renal system

The kidneys are responsible for maintaining electrolyte and acid-base balance, regulating extracellular fluid volume, excreting waste products, and conserving essential nutrients.

Anatomic changes. Changes in renal structure during pregnancy result from hormonal activity (estrogen and progesterone), pressure from an enlarging uterus, and an increase in blood volume. As early as the tenth week of pregnancy, the renal pelves and the ureters dilate. Dilation of the ureters is more pronounced above the pelvic brim, in part because they are compressed between the uterus and the pelvic brim. In most women the ureters below the pelvic brim are of normal size. The smooth muscle walls of the ureters undergo hyperplasia and hypertrophy and muscle tone relaxation. The ureters elongate, become tortuous, and form single or double curves. In the latter part of pregnancy, the renal pelvis and ureter are dilated more on the right side than on the left because the heavy uterus is displaced to the right by the sigmoid colon.

Because of these changes, a larger volume of urine is held in the pelves and ureters, and urine flow rate is slowed. The resulting urinary stasis or stagnation has the following consequences:

• There is a lag between the time urine is formed and when it reaches the bladder. Therefore clearance test results may reflect substances contained in glomerular filtrate several hours before.

• Stagnated urine is an excellent medium for the growth of microorganisms. In addition, the urine of pregnant women contains more nutrients, including glucose, thereby increasing the pH (making the urine more alkaline). This makes pregnant women more susceptible to urinary tract infection.

Bladder irritability, nocturia, and urinary frequency and urgency (without dysuria) are commonly reported in early pregnancy. Near term, bladder symptoms may return, especially after lightening occurs.

Urinary frequency results initially from increased bladder sensitivity and later from compression of the bladder (see Fig. 7). In the second trimester the bladder is pulled up out of the true pelvis into the abdomen. The urethra lengthens to 7.5 cm as the bladder is displaced upward. The pelvic congestion that occurs in pregnancy is reflected in hyperemia of the bladder and urethra. This increased vascularity causes the bladder mucosa to be traumatized and bleed easily. Bladder tone may decrease, which increases the bladder capacity to 1500 ml. At the same time the bladder is compressed by the enlarging uterus, resulting in the urge to void even if the bladder contains only a small amount of urine.

Functional changes. In normal pregnancy, renal function is altered considerably. Glomerular filtration rate (GFR) and renal plasma flow increase early in pregnancy (Cunningham et al., 2001). These changes are caused by pregnancy hormones, an increase in blood volume, the woman's posture, physical activity, and nutritional intake. The woman's kidneys must manage the increased metabolic and circulatory demands of the maternal body and also excretion of fetal waste products. Renal function is most efficient when the woman lies in the lateral recumbent position and least efficient when the woman assumes a supine position. A side-lying position increases renal perfusion, which increases urinary output and decreases edema. When the pregnant woman is lying supine, the heavy uterus compresses the vena cava and the aorta, and cardiac output decreases. As a result, blood flow to the brain and heart is continued at the expense of other organs, including the kidneys and uterus.

Fluid and electrolyte balance. Selective renal tubular reabsorption maintains sodium and water balance regardless of changes in dietary intake and losses through sweat, vomitus, or diarrhea. From 500 to 900 mEq of sodium is normally retained during pregnancy to meet fetal needs. To prevent excessive sodium depletion, the maternal kidneys undergo a significant adaptation by increasing tubular reabsorption. Because of the need for increased maternal intravascular and extracellular fluid volume, additional sodium is needed to expand fluid volume and to maintain an isotonic state. As efficient as the renal system is, it can be overstressed by excessive dietary sodium intake or restriction or by use of diuretics. Severe hypovolemia and reduced placental perfusion are two consequences of using diuretics during pregnancy.

The capacity of the kidneys to excrete water during the early weeks of pregnancy is more efficient than later in pregnancy. As a result, some women feel thirsty in early pregnancy because of the greater amount of water loss. The pooling of fluid in the legs in the latter part of pregnancy decreases renal blood flow and GFR. This pooling of blood in the lower legs is sometimes referred to as physiologic edema or dependent edema and requires no treatment. The normal diuretic response to the water load is triggered when the woman lies down, preferably on her side, and the pooled fluid reenters general circulation.

Normally, the kidney reabsorbs almost all of the glucose and other nutrients from the plasma filtrate. In pregnant women, however, tubular reabsorption of glucose is impaired so that glucosuria occurs at varying times and to varying degrees. Normal values range from 0 to 20 mg/dl, meaning that during any one day the urine is sometimes positive and sometimes negative. In nonpregnant women, blood glucose levels must be at 160 to 180 mg/dl before glucose is "spilled" into the urine (not reabsorbed). During pregnancy, glycosuria occurs when maternal glucose levels are lower than 160 mg/dl. Why glucose, as well as other nutrients such as amino acids, is wasted during pregnancy is not understood, nor has the exact mechanism been discovered. Although glycosuria may be found in normal pregnancies (2 + levels may be seen with increased anxiety states), the possibility of diabetes mellitus and gestational diabetes must be kept in mind.

Proteinuria usually does not occur in normal pregnancy except during labor or after birth (Cunningham et al., 2001). However, the increased amount of amino acids that must be filtered may exceed the capacity of the renal tubules to absorb it, so small amounts of protein are then lost in the urine. Values of trace to +1 protein (dipstick assessment) or less than 300 mg/24 hr are acceptable during pregnancy (Creasy & Resnik, 1999). The amount of protein excreted is not an indication of the severity of renal disease, nor does an increase in protein excretion in a pregnant woman with known renal disease necessarily indicate a progression in her disease. However, a pregnant woman with hypertension and proteinuria must be carefully evaluated because she may be at greater risk for an adverse pregnancy outcome (see Table 3).

Integumentary system

Alterations in hormonal balance and mechanical stretching are responsible for several changes in the integumentary system during pregnancy. Hyperpigmentation is stimulated by the anterior pituitary hormone melanotropin, which is increased during pregnancy. Darkening of the nipples, areolae, axillae, and vulva occurs at approximately the sixteenth week of gestation. Facial melasma, also called chloasma or "mask of pregnancy," is a blotchy, brownish hyperpigmentation of the skin over the cheeks, nose, and forehead, especially in dark-complexioned pregnant women. Chloasma appears in 50% to 70% of pregnant women, beginning after the sixteenth week and increasing gradually until term. The sun intensifies this pigmentation in susceptible women. Chloasma caused by normal pregnancy usually fades after birth.

The linea nigra (Fig. 10) is a pigmented line extending from the symphysis pubis to the top of the fundus in the midline; this line is known as the linea alba before hormoneinduced pigmentation. In primigravidas the extension of the linea nigra, beginning in the third month, keeps pace with the rising height of the fundus; in multigravidas the entire line often appears earlier than the third month. Not all pregnant women develop linea nigra.

Fig. 10 Linea nigra. (From Seidel, H. et al. [1999]. Mosby's guide to physical examination [4th ed.]. St. Louis: Mosby.)

Striae gravidarum, or stretch marks (seen over lower abdomen in Fig. 11), which appear in 50% to 90% of pregnant women during the second half of pregnancy, may be caused by action of adrenocorticosteroids. Striae reflect separation within the underlying connective (collagen) tissue of the skin. These slightly depressed streaks tend to occur over areas of maximum stretch (i.e., abdomen, thighs, and breasts). The stretching sometimes causes a sensation that resembles itching. The tendency to develop striae may be familial. After birth they usually fade, although they never disappear completely. Color of striae varies depending on the pregnant woman's skin color. The striae appear pinkish on a woman with light skin and are lighter than surrounding skin in dark-skinned women. In the multipara, in addition to the striae of the present pregnancy, glistening silvery lines (in light-skinned women) or purplish lines (in dark-skinned women) are commonly seen. These represent the scars of striae from previous pregnancies.

Fig. 11 Striae gravidarum, or "stretch marks." (Courtesy Michael S. Clement, MD, Mesa, AZ.)

Angiomas are commonly referred to as vascular spiders.They are tiny, star-shaped or branched, slightly raised and pulsating end-arterioles usually found on the neck, thorax, face, and arms. They occur as a result of elevated levels of circulating estrogen. The spiders are bluish in color and do not blanch with pressure. Vascular spiders appear during the second to the fifth month of pregnancy in 65% of Caucasian women and 10% of African-American women. The spiders usually disappear after birth.

Pinkish red, diffuse mottling or well-defined blotches are seen over the palmar surfaces of the hands in approximately 60% of Caucasian women and 35% of African-American women during pregnancy (Cunningham et al., 2001). These color changes, called palmar erythema, are related primarily to increased estrogen levels.

Pruritus is a relatively common dermatologic symptom in pregnancy, with cholestasis of pregnancy being the most common cause of pruritic rash. The goal of management is to relieve the itching. Topical steroids are the usual treatment, although systemic steroids may be needed. The problem usually resolves in the postpartum period (Gordon & Landon, 1996).

Gum hypertrophy may occur. An epulis (gingival granuloma gravidarum) is a red, raised nodule on the gums that bleeds easily. This lesion may develop around the third month and usually continues to enlarge as pregnancy progresses. It is usually managed by avoiding trauma to the gums (e.g., using a soft toothbrush). An epulis usually regresses spontaneously after birth.

Nail growth may be accelerated. Some women may notice thinning and softening of the nails. Oily skin and acne vulgaris may occur during pregnancy. For some women the skin clears and looks radiant. Hirsutism, the excessive growth of hair or growth of hair in unusual places, is commonly reported. An increase in fine hair growth may occur but tends to disappear after pregnancy. However, growth of coarse or bristly hair does not usually disappear after pregnancy.

Increased blood supply to the skin leads to increased perspiration. Women feel hotter during pregnancy, possibly related to a progesterone-induced increase in body temperature and the increased BMR.

Musculoskeletal system

The gradually changing body and increasing weight of the pregnant woman cause noticeable alterations in her posture (Fig. 12) and the way she walks. The great abdominal distention that gives the pelvis a forward tilt, decreased abdominal muscle tone, and increased weight bearing require a realignment of the spinal curvature late in pregnancy. The woman's center of gravity shifts forward. An increase in the normal lumbosacral curve (lordosis) develops, and a compensatory curvature in the cervicodorsal region (exaggerated anterior flexion of the head) develops to help her maintain her balance. Aching, numbness, and weakness of the upper extremities may result. Large breasts and a stoop-shouldered stance will further accentuate the lumbar and dorsal curves. Walking is more difficult, and the waddling gait of the pregnant woman, called "the proud walk of pregnancy" by Shakespeare, is well known. The ligamentous and muscular structures of the middle and lower spine may be severely stressed. These and related changes often cause musculoskeletal discomfort, especially in older women or those with a back disorder or a faulty sense of balance.

Fig. 12 Postural changes during pregnancy. A, Nonpregnant. B, Incorrect posture during pregnancy. C, Correct posture during pregnancy.

Slight relaxation and increased mobility of the pelvic joints are normal during pregnancy. They are secondary to the exaggerated elasticity and softening of connective and collagen tissue caused by increased circulating steroid sex hormones, especially estrogen. Relaxin, an ovarian hormone, assists in this relaxation and softening. These adaptations permit enlargement of pelvic dimensions to facilitate labor and birth. The degree of relaxation varies, but considerable separation of the symphysis pubis and the instability of the sacroiliac joints may cause pain and difficulty in walking. Obesity and multifetal pregnancy tend to increase the pelvic instability. Peripheral joint laxity also increases as pregnancy progresses, but the cause is not known (Schauberger et al., 1996).

The muscles of the abdominal wall stretch and ultimately lose some tone. During the third trimester the rectus abdominis muscles may separate (Fig. 13), allowing abdominal contents to protrude at the midline. The umbilicus flattens or protrudes. After birth, the muscles gradually regain tone. However, separation of the muscles (diastasis recti abdominis) may persist.

Fig. 13 Possible change in rectus abdominis muscles during pregnancy. A, Normal position in nonpregnant woman. B, Diastasis recti abdominis in pregnant woman.

Neurologic system

Little is known regarding specific alterations in function of the neurologic system during pregnancy, aside from hypothalamic-pituitary neurohormonal changes. Specific physiologic alterations resulting from pregnancy may cause the following neurologic or neuromuscular symptoms:

• Compression of pelvic nerves or vascular stasis caused by enlargement of the uterus may result in sensory changes in the legs.

• Dorsolumbar lordosis may cause pain because of traction on nerves or compression of nerve roots.

• Edema involving the peripheral nerves may result in carpal tunnel syndrome during the last trimester. The syndrome is characterized by paresthesia (abnormal sensation such as burning or tingling) and pain in the hand, radiating to the elbow. The sensations are caused by edema that compresses the median nerve beneath the carpal ligament of the wrist. The dominant hand is usually affected most, although as many as 80% of women experience symptoms in both hands. Symptoms usually regress after pregnancy. In some cases, surgical treatment may be necessary (Cunningham et al., 2001).

• Acroesthesia (numbness and tingling of the hands) is caused by the stoop-shouldered stance (see Fig. 12, B) assumed by some women during pregnancy. The condition is associated with traction on segments of the brachial plexus.

• Tension headache is common when anxiety or uncertainty complicates pregnancy. However, vision problems, sinusitis, or migraine may also be responsible for headaches.

• Light-headedness, faintness, and even syncope (fainting) are common during early pregnancy. Vasomotor instability, postural hypotension, or hypoglycemia may be responsible.

• Hypocalcemia may cause neuromuscular problems such as muscle cramps or tetany.

Gastrointestinal system

Appetite. During pregnancy, the pregnant woman's appetite and food intake fluctuate. Early in pregnancy, some women experience "morning sickness" in response to increasing levels of hCG and altered carbohydrate metabolism (see Research box). Morning sickness refers to nausea with or without vomiting. It appears at approximately 4 to 6 weeks of gestation and usually subsides by the end of the third month (first trimester) of pregnancy. Severity varies from mild distaste for certain foods to more severe vomiting. The condition may be triggered by the sight or odor of various foods. Fatigue may also be responsible for severe nausea, but further research is needed to determine the role of this factor (O'Brien & Zhou, 1995). By the end of the second trimester, the appetite increases in response to increasing metabolic needs. Rarely does morning sickness have harmful effects on the embryo/fetus or the woman. Whenever the vomiting is severe or persists beyond the first trimester, or when it is accompanied by fever, pain, or weight loss, further evaluation is necessary and medical intervention is likely.

Women may also experience changes in their sense of taste, leading to cravings and changes in dietary intake. Some women have nonfood cravings (pica) such as ice, clay, and laundry starch (Cunningham et al., 2001).

 RESEARCH ACUPRESSURE INTERVENTION FOR NAUSEA AND VOMITING OF PREGNANCY Up to 70% of all pregnant women experience nausea and vomiting of pregnancy (NVP), typically between weeks 5 through 12 of gestation.This may lead to nutritional deficits, dehydration, and electrolyte imbalances. Employment and family functioning may be affected. Pharmacologic treatment for NVP may cause teratogenic effects to the fetus. Nonpharmacologic treatments, including vitamin B6 (pyridoxine); acupressure; certain eating and drinking patterns; and vitamin, herbal, and homeopathic remedies, are not well researched. This clinical study investigated the use of acupressure as a treatment of NVR A total of 110 first-trimester pregnant women with NVP were randomly assigned to wearing Sea-Bands or placebo wrist bands. Sea-Bands are an acupressure device consisting of an elastic band worn at the wrist that holds a button against a point 3 fingerbreadths below the wrist crease and between the two flexor tendons on the medial forearm. The placebos had no button. Days 1 through 4, the women wore their Sea-Band or placebo, then removed them for days 5 through 7, keeping seven daily logs of nausea and vomiting. Results showed that the Sea-Band group had significantly less nausea and vomiting than the placebo group while wearing the device.The Sea-Band group also had a significant rise in nausea and vomiting after the device was discontinued. In addition, women in the Sea-Band group who used vitamin B6 during the treatment had significantly more relief from nausea and vomiting than did nontakers, but this effect disappeared when the device was removed. IMPLICATION FOR PRACTICE Alternative and complementary treatments for women's health, including pregnancy, are numerous. Nurses need to be informed about the most current treatments for discomforts of pregnancy that are effective and at the same time safe, noninvasive, and inexpensive. This study suggests that acupressure can be recommended for relief of NVR   Source: Steel, N. et al. (2001). Effect of acupressure by Sea-Bands on nausea and vomiting of pregnancy. J Obstet Gyncol Neonatal Nurs, 30(1), 61-70.

Mouth. The gums become hyperemic, spongy, and swollen during pregnancy. They tend to bleed easily because the rising levels of estrogen cause selective increased vascularity and connective tissue proliferation (a nonspecific gingivitis). Epulis (discussed in the section on the integumentary system) may develop at the gumline. Some pregnant women complain of ptyalism (excessive salivation), which may be caused by the decrease in unconscious swallowing by the woman when nauseated or from stimulation of salivary glands by eating starch (Cunningham et al., 2001).

Esophagus, stomach, and intestines. Herniation of the upper portion of the stomach (hiatal hernia) occurs after the seventh or eighth month of pregnancy in approximately 15% to 20% of pregnant women. This condition results from upward displacement of the stomach, which causes the hiatus of the diaphragm to widen. It occurs more often in multiparas and older or obese women.

Increased estrogen production causes decreased secretion of hydrochloric acid. Therefore peptic ulcer formation or flare-up of existing peptic ulcers is uncommon during pregnancy.

Increased progesterone production causes decreased tone and motility of smooth muscles, resulting in esophageal regurgitation, slower emptying time of the stomach, and reverse peristalsis. As a result, the woman may experience "acid indigestion" or heartburn (pyrosis).

Iron is absorbed more readily in the small intestine in response to increased needs during pregnancy. Even when the woman is deficient in iron, it will continue to be absorbed in sufficient amounts for the fetus to have a normal hemoglobin level.

Increased progesterone (causing loss of muscle tone and decreased peristalsis) results in an increase in water absorption from the colon and may cause constipation. Constipation can also result from hypoperistalsis (sluggishness of the bowel), food choices, lack of fluids, iron supplementation, decreased activity level, abdominal distention by the pregnant uterus, and displacement and compression of the intestines. If the pregnant woman has hemorrhoids (see Fig. 9) and is constipated, the hemorrhoids may become everted or may bleed during straining at stool. A mild ileus (sluggishness and lack of movement resulting in obstruction) that follows birth, as well as postbirth fluid loss and perineal discomfort, contributes to continuing constipation.

Gallbladder and liver. The gallbladder is often distended because of its decreased muscle tone during pregnancy. Increased emptying time and thickening of bile caused by prolonged retention are typical changes. These features, together with slight hypercholesterolemia from increased progesterone levels, may account for the development of gallstones during pregnancy.

Hepatic function is difficult to appraise during pregnancy. However, only minor changes in liver function develop. Occasionally, intrahepatic cholestasis (retention and accumulation of bile in the liver, caused by factors within the liver) occurs late in pregnancy in response to placental steroids and may result in pruritus gravidarum (severe itching) with or without jaundice. These distressing symptoms subside soon after birth.

Abdominal discomfort. Intraabdominal alterations that can cause discomfort include pelvic heaviness or pressure, round ligament tension, flatulence, distention and bowel cramping, and uterine contractions. In addition to displacement of intestines, pressure from the expanding uterus causes an increase in venous pressure in the pelvic organs. Although most abdominal discomfort is a consequence of normal maternal alterations, the health care provider must be constantly alert to the possibility of disorders such as bowel obstruction or an inflammatory process.

Appendicitis may be difficult to diagnose in pregnancy because the appendix is displaced upward and laterally, high and to the right, away from McBurney's point (Fig. 14).

Fig. 14 Change in position of appendix in pregnancy. Note McBurney's point.

Endocrine system

Profound endocrine changes are essential for pregnancy maintenance, normal fetal growth, and postpartum recovery.

Pituitary and placental hormones. During pregnancy, the elevated levels of estrogen and progesterone (produced first by the corpus luteum in the ovary until approximately 14 weeks of gestation and then by the placenta) suppress secretion of follicle-stimulating hormone and luteinizing hormone by the anterior pituitary. The maturation of a follicle and ovulation do not occur. Although the majority of women experience amenorrhea (absence of menses), at least 20% have some slight, painless spotting during early gestation. Implantation bleeding and bleeding following intercourse related to cervical friability can occur. Most of the women experiencing slight gestational bleeding continue to full term and have normal infants. However, all instances of bleeding should be reported and evaluated.

After implantation, the fertilized ovum and the chorionic villi produce hCG, which maintains the corpus luteum's production of estrogen and progesterone until the placenta takes over their production (Creasy & Resnik, 1999).

Progesterone is essential for maintaining pregnancy by relaxing smooth muscles, resulting in decreased uterine contractility and prevention of miscarriage. Progesterone and estrogen cause fat to deposit in subcutaneous tissues over the maternal abdomen, back, and upper thighs. This fat serves as an energy reserve for both pregnancy and lactation. Estrogen also promotes the enlargement of the genitals, uterus, and breasts and increases vascularity, causing vasodilation. Estrogen causes relaxation of pelvic ligaments and joints. It also alters metabolism of nutrients by interfering with folic acid metabolism, increasing the level of total body proteins, and promoting retention of sodium and water by kidney tubules. Estrogen may decrease secretion of hydrochloric acid and pepsin, which may be responsible for digestive upsets such as nausea.

Serum prolactin produced by the anterior pituitary begins to rise early in the first trimester and increases progressively to term. It is responsible for initial lactation; however, the high levels of estrogen and progesterone inhibit lactation by blocking the binding of prolactin to breast tissue until after birth (Guyton & Hall, 1997).

Oxytocin is produced by the posterior pituitary in increasing amounts as the fetus matures. This hormone can stimulate uterine contractions during pregnancy, but high levels of progesterone prevent contractions until near term. Oxytocin also stimulates the let-down or milk-ejection reflex after birth in response to the infant sucking at the mother's breast.

Human chorionic somatomammotropin (hCS), previously called human placental lactogen, is produced by the placenta, acts as a growth hormone, and contributes to breast development. It decreases the maternal metabolism of glucose and increases the amount of fatty acids for metabolic needs (Alsat et al., 1997; Guyton & Hall, 1997).

Thyroid gland. During pregnancy there is an increase in gland activity and hormone production. The increased activity is reflected in a moderate enlargement of the thyroid gland caused by hyperplasia of the glandular tissue and increased vascularity (Cunningham et al., 2001). Thyroxine-binding globulin increases as a result of increased estrogen levels. This increase begins at approximately 20 weeks of gestation. The level of total (free and bound) thyroxine (T4) increases between 6 and 9 weeks of gestation and plateaus at 18 weeks of gestation. Free T4 and free triiodothyronine (T3) return to nonpregnant levels after the first trimester. Despite these changes in hormone production, the pregnant woman usually does not develop hyperthyroidism (Cunningham et al., 2001).

Parathyroid gland. Parathyroid hormone controls calcium and magnesium metabolism. Pregnancy induces a slight hyperparathyroidism, a reflection of increased fetal requirements for calcium and vitamin D. The peak level of parathyroid hormone occurs between 15 and 35 weeks of gestation when the needs for growth of the fetal skeleton are greatest. Levels return to normal after birth.

Pancreas. The fetus requires significant amounts of glucose for its growth and development. To meet its need for fuel, the fetus not only depletes the store of maternal glucose but also decreases the mother's ability to synthesize glucose by siphoning off her amino acids. Maternal blood glucose levels fall. Maternal insulin does not cross the placenta to the fetus. As a result, in early pregnancy, the pancreas decreases its production of insulin.

As pregnancy continues, the placenta grows and produces progressively larger amounts of hormones (i.e., hCS, estrogen, and progesterone). Cortisol production by the adrenals also increases. Estrogen, progesterone, hCS, and cortisol collectively decrease the mother's ability to use insulin. Cortisol stimulates increased production of insulin but also increases the mother's peripheral resistance to insulin (i.e., the tissues cannot use the insulin). Decreasing the mother's ability to use her own insulin is a protective mechanism that ensures an ample supply of glucose for the needs of the fetoplacental unit. The result is an added demand for insulin by the mother that continues to increase at a steady rate until term. The normal beta cells of the islets of Langerhans in the pancreas can meet this demand for insulin.

Adrenal glands. The adrenal glands change little during pregnancy. Secretion of aldosterone is increased, resulting in reabsorption of excess sodium from the renal tubules. Cortisol levels are also increased (Chamberlain & Pipkin, 1998).

Nursing Care During Pregnancy

The prenatal period is a time of physical and psychologic preparation for birth and parenthood. Becoming a parent is a time of intense learning both for par­ents and for those close to them. The prenatal period provides  a unique  opportunity for nurses  and  other members of the health care team to influence family health. During this period, essentially healthy women seek regular care and guidance. The nurse's health pro­motion interventions can affect the well-being of the woman, her unborn child, and the rest of her family for many years.

Regular prenatal visits, ideally beginning soon after the first missed menstrual period, offer opportunities to en­sure the health of the expectant mother and her infant. Prenatal health care permits diagnosis and treatment of maternal disorders that may have preexisted or may de­velop during the pregnancy. Care is designed to monitor the growth and development of the fetus and to identify abnormalities that may interfere with the course of normal labor. The woman and her family can seek support for stress and learn parenting skills.

Pregnancy lasts 9 calendar months, but health care providers use the concept of lunar months, which last 28 days, or 4 weeks. Thus normal pregnancy lasts approxi­mately 10 lunar months, or 40 weeks. Health care providers also refer to early, middle, and late pregnancy as trimesters. The first trimester lasts from weeks 1 through 13; the sec­ond, from weeks 14 through 26; and the third, from weeks 27 through 40. A pregnancy is considered at term if it ad­vances to 38 to 40 weeks. The focus of this chapter is on meeting the health needs of the expectant family over the course of pregnancy, which is known as the prenatal period.

DIAGNOSIS OF PREGNANCY

Women may suspect pregnancy when they miss a menstrual period. Many women come to the first prenatal visit after a positive home pregnancy test. However, the clinical diagno­sis of pregnancy before the second missed period may be difficult in some women. Physical variability, lack of relax­ation, obesity, or tumors, for example, may confound even the experienced obstetrician or midwife. Accuracy is impor­tant, however, because emotional, social, medical, or legal consequences of an inaccurate diagnosis, either positive or negative, can be extremely serious. A correct date for the last (normal) menstrual period (LMP), the date of intercourse, and a basal body temperature record may be of great value in the accurate diagnosis of pregnancy.

SIGNS AND SYMPTOMS

Great variability is possible in the subjective and objective symptoms of pregnancy. Therefore the diagnosis of preg­nancy may be uncertain for a time. Many of the indicators of pregnancy are clinically useful in the diagnosis of preg­nancy, and they are classified as presumptive, probable, or positive (see Table 8-2).

ESTIMATING DATE OF BIRTH

Following the diagnosis of pregnancy, the woman's first question usually concerns when she will give birth. This date has traditionally been termed the estimated date of confinement (EDC). To promote a more positive percep­tion of both pregnancy and birth, however, the term esti­mated date of birth (EDB) is usually used. Because the pre­cise date of conception generally is unknown, several formulas or rules of thumb have been suggested for cal­culating the EDB. None of these guides are infallible, but

Nagele's rule is reasonably accurate and is the method usually used.

Nagele's rule is as follows: add 7 days to the first day of the LMP, subtract 3 months, and add 1 year. For exam­ple, if the first day of the LMP was July 10, 2002, the EDB is April 17, 2003. In simple terms, add 7 days to the LMP and count forward 9 months. Nagele's rule assumes that the woman has a 28-day cycle and that the pregnancy oc­curred on the fourteenth day. An adjustment is in order if the cycle is longer or shorter than 28 days. Approximately 4% to 10% of pregnant women give birth spontaneously on the EDB; however, most women give birth during the period extending from 7 days before to 7 days after the EDB.

Antepartal Hemorrhagic disorders

HEMORRHAGIC COMPLICATIONS

Bleeding in pregnancy may jeopardize both maternal and fetal well-being. Maternal blood loss decreases oxygencarrying capacity, which predisposes the woman to increased risk for hypovolemia, anemia, infection, preterm labor, and preterm birth and adversely affects oxygen delivery to the fetus. Fetal risks from maternal hemorrhage include blood loss or anemia, hypoxemia, hypoxia, anoxia, and preterm birth. Antepartal hemorrhage is a leading cause of maternal death, with ectopic pregnancy rupture and abruptio placentae being responsible for most maternal deaths (Koonin et al., 1997).

EARLY PREGNANCY BLEEDING

Bleeding during early pregnancy is alarming to the woman and of concern to the health care provider and nurse. The common bleeding disorders of early pregnancy include miscarriage, incompetent cervix, ectopic pregnancy, and hydatidiform mole (molar pregnancy).

Miscarriage

Miscarriage is a pregnancy that ends before 20 weeks of gestation. The 20-week marker is considered the point of viability, or when the fetus is able to survive in an extrauterine environment. A fetal weight less than 500 g may also be used to define miscarriage (Cunningham et al., 2001). A miscarriage results from natural causes. Induced abortion (intentional interruption of pregnancy) is discussed in Chapter 6.

Incidence and etiology. Approximately 10% to 15% of all clinically recognized pregnancies end in miscarriage (Simpson, 2002). An early miscarriage is one that occurs before 12 weeks of gestation. At least 50% of all clinically recognized pregnancy losses result from chromosomal abnormalities (Simpson, 2002). The majority (over 90%) of miscarriages occur early, before 8 weeks of gestation (Simpson, 2002). Possible causes of early miscarriage include endocrine imbalance (as in women who have luteal phase defects or insulin-dependent diabetes mellitus with high blood glucose levels in the first trimester), immunologic factors (such as antiphospholipid antibodies), infections (such as bacteriuria and Chlamydia trachomatis), systemic disorders (such as lupus erythematosus), and genetic factors (ACOG, 1995; Gilbert & Harmon, 1998).

A late miscarriage is one that occurs between 12 and 20 weeks of gestation. Late miscarriages usually result from maternal causes, such as advancing maternal age and parity, chronic infections, premature dilation of the cervix and other anomalies of the reproductive tract, chronic debilitating diseases, nutrition, and recreational drug use (Cunningham et al., 2001). Little can be done to avoid genetically caused pregnancy loss, but correction of maternal disorders, immunization against infectious diseases, adequate early prenatal care, and treatment of pregnancy complications can do much to prevent miscarriage.

Types. The types of miscarriage include threatened, inevitable, incomplete, complete, and missed. Miscarriages (both early and late) can recur; all but the threatened miscarriage can lead to infection (Fig. 6).

Clinical manifestations. Signs and symptoms of miscarriage depend on the duration of pregnancy. Once pregnancy has been diagnosed, the presence of uterine bleeding, uterine contractions, and uterine pain are ominous signs that must be considered a threatened miscarriage until proven otherwise.

If miscarriage occurs before the sixth week of pregnancy, the woman may report a heavy menstrual flow. Miscarriage that occurs between the sixth and twelfth weeks of pregnancy causes moderate discomfort and blood loss. After the twelfth week, miscarriage is typified by more severe pain, similar to that of labor, because the fetus must be expelled. Diagnosis of the type of miscarriage is based on the signs and symptoms present (Table 6).

 TABLE 6 Assessing Miscarriage and the Usual Management TYPE OF MISCARRIAGE AMOUNT OF BLEEDING UTERINE CRAMPING PASSAGE OF TISSUE CERVICAL DILATION MANAGEMENT Threatened Slight, spotting Mild No No Bed rest, sedation, and avoidance of stress and orgasm usually recommended. Further treatment depends on woman's response to treatment. Inevitable   Incomplete Moderate   Heavy, profuse Mild to severe Severe No   Yes Yes   Yes, with tissue in cervix Prompt termination of pregnancy is accomplished, usually by  dilation and curettage. Complete Slight Mild Yes No No further intervention may be needed if uterine contractions are adequate to prevent hemorrhage and there is no infection. Missed None, spotting None No No If spontaneous evacuation of the uterus does not occur within 1 month, pregnancy is terminated by method appropriate to duration of pregnancy. Blood clotting factors are monitored until uterus is empty. DIC and incoagulability of blood with uncontrolled hemorrhage may develop in cases of fetal death after the twelfth week, if products of conception are retained for longer than 5 weeks. Septic Varies, usually malodorous Varies Varies Yes, usually Immediate termination of pregnancy by method appropriate to duration of pregnancy. Cervical culture and sensitivity studies are done, and broad-spectrum antibiotic therapy (e.g., ampicillin) is started. Treatment for septic shock is initiated if  necessary. Recurren Varies Varies Yes Yes, usually Varies, depends on type. Prophylactic cerclage may be done if premature cervical dilation is the cause.

Symptoms of a threatened miscarriage (see Fig. 6, A) include spotting of blood but with the cervical os closed. Mild uterine cramping may be present. Inevitable (see Fig. 6, B) and incomplete (see Fig. 6, C) miscarriages involve a moderate to heavy amount of bleeding with an open cervical os. Tissue may be present with the bleeding. Mild to severe uterine cramping may be present. An inevitable miscarriage is often accompanied by rupture of membranes (ROM) and cervical dilation; passage of the products of conception is a certainty.

An incomplete miscarriage involves the expulsion of the fetus with retention of the placenta (Cunningham et al., 2001).

In a complete miscarriage (see Fig. 6, D), all fetal tissue is passed, the cervix is closed, and there may be slight bleeding. Mild uterine cramping may be present. The term missed miscarriage (see Fig. 6, E) refers to a pregnancy in which the fetus has died but the products of conception are retained in utero for several weeks. It may be diagnosed by ultrasonic examination after the uterus stops increasing in size or even decreases in size. There may be no bleeding or cramping, and the cervical os remains closed.

Recurrent early (habitual) miscarriage is the loss of three or more previable pregnancies. Women having three or more miscarriages are at increased risk for preterm birth, placenta previa, and fetal anomalies in subsequent pregnancies (Cunningham et al., 2001).

Miscarriages can become septic, although this is not a common occurrence. Symptoms of a septic miscarriage include fever and abdominal tenderness. Vaginal bleeding, which may be slight to heavy, is usually malodorous.

CARE MANAGEMENT

Whenever a woman with vaginal bleeding early in pregnancy seeks treatment, a thorough assessment should be performed (Box 6). Information to be obtained includes chief complaint, type and location of pain, quantity and nature of bleeding, and date of last menstrual period (LMP) to determine approximate gestational age. The initial database should also include vital signs, previous pregnancies, previous pregnancy losses, allergies, and emotional status. Frequently the woman is anxious and fearful of what may happen to her and to her pregnancy.

 BOX 6 Assessment of Bleeding in Pregnancy INITIAL DATABASE Chief complaint Vital signs Gravidity, parity LMP/estimated date of birth Pregnancy history (previous and current) Allergies Nausea and vomiting Pain (onset, quality, precipitating event location) Bleeding or coagulation problems Level of consciousness Emotional status EARLY PREGNANCY Confirmation of pregnancy Bleeding (bright or dark, intermittent or continuous) Pain (type, intensity, persistence) Vaginal discharge LATE PREGNANCY Estimated date of birth Bleeding (quantity, associated pain) Vaginal discharge Amniotic membrane status Uterine activity Abdominal pain Fetal status/viability

Various laboratory findings are characteristic of miscarriage. Evaluation of hCG, a placental hormone, is used in the diagnosis of pregnancy and pregnancy loss. The beta subunit of hCG (/3-hCG) can be detected in maternal plasma and urine 8 to 9 days after ovulation if the woman  is pregnant. In early pregnancy, the concentration of /3-hCG before 20 weeks of gestation should double every 1.4 to 2 days until approximately 60 or 70 days of gestation (Cunningham et al., 2001). Before 8 weeks of gestation, if miscarriage is suspected, two serum quantitative /3-hCG levels are drawn 48 hours apart. If a normal pregnancy is present, the /3-hCG level doubles in this time frame. Ultrasonography can then be used to determine the presence of a viable gestational sac. With considerable or persistent blood loss, anemia is likely (hemoglobin level less than 11 g/dl). If infection is present, the white blood cell (WBC) count is greater than 12,000 cells/mm3.

The following nursing diagnoses are appropriate for the woman experiencing miscarriage:

Anxiety/fear related to

-unknown outcome and unfamiliarity with medical procedures

Deficient fluid volume related to

-excessive bleeding secondary to miscarriage

Anticipatory grieving related to

-unexpected pregnancy outcome

Situational low self-esteem related to

-inability to successfully carry a pregnancy to term gestation

Risk for infection related to

-surgical treatment

-dilated cervix

Immediate nursing care focuses on physiologic stabilization. Typical orders to be followed would be initiation of an IV line, request for blood testing of hemoglobin and hematocrit, blood type and Rh, and indirect Coombs' screen. An ultrasound is performed for diagnostic confirmation.

Medical management. Medical management (see Table 6) depends on the classification and on signs and symptoms. Traditionally, threatened miscarriages have been managed with bed rest and supportive care. Followup treatment depends on whether the threatened miscarriage progresses to actual miscarriage or symptoms subside and the pregnancy remains intact. Dilation and curettage (D&C) is a surgical procedure in which the cervix is dilated and a curette is inserted to scrape the uterine walls and remove uterine contents. A D&C is commonly performed to treat inevitable and incomplete miscarriage. The nurse reinforces explanations, answers any questions or concerns, and prepares the woman for surgery.

Dilation and evacuation, performed after 16 weeks of gestation, consists of wide cervical dilation followed by instrumental removal of the uterine contents.

Before either surgical procedure is performed, a full history should be obtained and general and pelvic examinations should be performed. General preoperative and postoperative care are appropriate for the woman requiring surgical intervention for miscarriage. Analgesics or anesthesia appropriate to the procedure are used.

For late incomplete or inevitable miscarriages (16 to 20 weeks) and missed miscarriages, prostaglandins may be administered into the amniotic sac or by vaginal suppository to induce or augment labor and cause the products of conception to be expelled. IV oxytocin may also be used.

Nursing care is similar to the care for any woman whose labor is being induced (see Chapter 24). Special care may be needed for management of side effects of prostaglandin, such as nausea and vomiting and diarrhea. If the products of conception are not passed in entirety, the woman may be prepared for manual or surgical evacuation of the uterus.

After evacuation of the uterus, 10 to 20 U of oxytocin in 1000 ml of IV fluids may be given to prevent hemorrhage. For excessive bleeding after the miscarriage, ergot products such as ergonovine or a prostaglandin derivative such as carboprost tromethamine may be given to contract the uterus. Three or four doses of ergonovine, 0.2 mg orally or intramuscularly every 4 hours, may be given if the woman is normotensive. A 25-mg dose of carboprost may be given intramuscularly every 15 to 90 minutes for as many as eight doses (Cunningham et al., 2001). Antibiotics are given as necessary. Analgesics, such as antiprostaglandin agents, may decrease discomfort from cramping. Transfusion therapy may be required for shock or anemia. The woman who is Rh negative and is not isoimmunized is given an intramuscular injection of Rho(D) immune globulin within 72 hours of the miscarriage.

Psychosocial aspects of care focus on what the pregnancy loss means to the woman and her family. Hutti, de-Pacheco, and Smith (1998) found that women's responses to miscarriage ranged from no grief to intense, long-lasting grief. Explanations are provided regarding the nature of the miscarriage, expected procedures, and possible future implications for childbearing.

As with the other fetal or neonatal losses, the woman should be offered the option of seeing the products of conception. She may also want to know what the hospital does with the products of conception or whether she needs to make a decision about final disposition of fetal remains.

Home care. The woman will likely be discharged home within a few hours of undergoing D&C or as soon as her vital signs are stable, vaginal bleeding is minimal, and she has recovered from anesthesia. Discharge teaching should emphasize the need for rest. If significant blood loss has occurred, iron supplementation may be ordered. Teaching includes information about normal physical findings, such as cramping, type and amount of bleeding, resumption of sexual activity, and family planning. Follow-up care should assess the woman's physical and emotional recovery. Referrals to local support groups should be provided as needed (see Teaching Guidelines box).

Follow-up phone calls after a loss are important. The woman may appreciate a phone call on what would have been her due date. These calls provide opportunities for the woman to ask questions, seek advice, and receive information to help process her grief.

 TEACHING GUIDELINES Discharge Teaching for t h e Woman After Early Miscarriage • Advise woman to report any heavy, profuse, or bright red bleeding to health care provider. • Reassure woman that a scant, dark discharge may persist for 1 to 2 weeks. • To reduce the risk of infection, remind the woman not to put anything into the vagina until bleeding has stopped (e.g., no tampons, no vaginal intercourse). She should take antibiotics as prescribed. • Acknowledge that the woman has experienced a loss and that time is required for recovery. She may have mood swings and depression. • Refer the woman to support groups, clergy, or professional counseling as needed. • Advise woman that attempts at pregnancy should be postponed for at least 2 months to allow body to recover

Recurrent premature dilation of the cervix (incompetent cervix)

Another cause of late miscarriage is incompetent cervix, which has traditionally been defined as passive and painless dilation of the cervix during the second trimester. This definition assumes an "all or nothing" role for the cervix; it is either "competent" or "incompetent." Newer thinking contends that cervical competence is variable and exists as a continuum that is determined in part by cervical length. Other related factors include composition of the cervical tissue and the individual circumstances associated with the pregnancy in terms of maternal stress and lifestyle. Lams (2002) refers to this condition as abnormal or reduced cervical competence. Freda (1999) suggests the term recurrent premature dilation of the cervix.

Etiology. Etiologic factors include a history of previous cervical lacerations during childbirth, excessive cervical dilation for curettage or biopsy, or ingestion of diethylstilbestrol by the woman's mother while being pregnant with the woman. Other instances may result from a congenitally short cervix or cervical or uterine anomalies. Reduced cervical competence is a clinical diagnosis, based on history. Short labors and recurring loss of pregnancy at progressively earlier gestational ages are characteristics of reduced cervical competence. Ultrasound is used to diagnose this condition objectively. A short cervix (less than 20 mm in length) is indicative of reduced cervical competence. Often, but not always, the short cervix is accompanied by cervical fanneling, or effacement of the internal cervical os (lams, 2002).

CARE MANAGEMENT

The nurse assesses the woman's feelings about her pregnancy and her understanding of reduced cervical competence. It is also important to evaluate the woman's support systems. Because the diagnosis of reduced cervical competence is usually not made until the woman has lost one or two pregnancies, she may feel guilty or responsible for this impending loss. It is therefore important to assess for previous reactions to stresses and appropriateness of coping responses. The woman needs the support of her health care providers, as well as that of her family.

Medical management. Conservative management consists of bed rest, hydration, and tocolysis (inhibition of uterine contractions). A cervical cerclage may be performed. During gestation, a McDonald cerclage, band of homologous fascia, or nonabsorbable ribbon (Mersilene) may be placed around the cervix beneath the mucosa to constrict the internal os of the cervix (Fig. 7). Prophylactic cerclage is placed at 10 to 14 weeks of gestation, after which the woman is told to refrain from intercourse, prolonged (more than 90 minutes) standing, and heavy lifting. She is followed during the course of her pregnancy with ultrasound scans to assess for cervical shortening and funneling. The cerclage is electively removed (usually an office or a clinic procedure) when the woman reaches 37 weeks of gestation, or it may be left in place and a cesarean birth performed. If removed, cerclage placement must be repeated with each successive pregnancy.  Approximately 80% to 90% of pregnancies treated with cerclage result in live, viable births (lams, 2002).

Fig. 7 A, Cerclage correction of premature dilation of the cervical os. B, Cross-sectional view of closed internal os.

A woman whose reduced cervical competence is diagnosed during the current pregnancy may undergo emergency cerclage placement. Risks of the procedure include premature rupture of membranes, preterm labor, and chorioamnionitis. Because of these risks, and because bed rest and tocolytic therapy can be used to prolong the pregnancy, cerclage is rarely performed after 25 weeks of gestation (lams, 2002).

Nursing management. If a cerclage is performed, the nurse monitors the woman postoperatively for contractions, ROM, and signs of infection. Discharge teaching focuses on continued monitoring of these aspects at home. Home uterine monitoring may be indicated with followup from a home health agency.

Home care. The woman must understand the importance of activity restriction at home and the need for close observation and supervision. Instruction includes the rationale for bed rest or activity restriction and warning signs of preterm labor, ROM, and infection to report (Lowdermilk & Grohar, 1998). The woman must be instructed on the importance of taking oral tocolytic medication if prescribed, the expected response, and possible side effects. Tocolytics may be given prophylactically to prevent uterine contractions and further dilation of the cervix. If home uterine monitoring is implemented, the woman is taught how to apply a uterine contraction monitor and transmit the monitor tracing by telephone to the monitoring center. Nurses at the monitoring center assess the tracing for contractions, answer questions, provide emotional support and education, and report information to the woman's physician or nurse-midwife. The woman should know the signs that would warrant immediate transfer to the hospital, including strong contractions less than 5 minutes apart, rupture of membranes, severe perineal pressure, and an urge to push (Health Care Resources, 1997). If management is unsuccessful and the fetus is born before viability, appropriate grief support should be provided. If the fetus is born prematurely, appropriate anticipatory guidance and support will be necessary.

Ectopic pregnancy

Incidence and etiology. Ectopic pregnancy is one in which the fertilized ovum is implanted outside the uterine cavity (Fig. 8). Approximately 95% of ectopic pregnancies occur in the uterine (fallopian) tube, with most located on the ampullar or largest portion of the tube. Other sites include the abdominal cavity (3% to 4%), ovary (1%), and cervix (1%).

Fig. 8 Sites of implantation of ectopic pregnancies. Order of frequency of occurrence is ampulla, isthmus, interstitium, fimbria, tuboovarian ligament, ovary, abdominal cavity, and cervix (external os).

Ectopic pregnancy is responsible for 10% of all maternal deaths, and it is the leading pregnancy-related cause of firsttrimester maternal death (Powell & Spellman, 1996). Moreover, ectopic pregnancy is a leading cause of infertility. Approximately 60% of women who have been treated for ectopic pregnancy are able to conceive afterward, and approximately 40% of those pregnancies are ectopic (Powell & Spellman, 1996).

The reported incidence of ectopic pregnancy is rising as a result of improved diagnostic techniques, such as more sensitive /3-hCG assays, and the availability of transvaginal ultrasound. An increased incidence of sexually transmitted infections, better treatment of pelvic inflammatory disease (PID) (which formerly would have caused sterility), increased numbers of tubal sterilizations, and surgical reversal of tubal sterilizations also have resulted in more ectopic pregnancies (Simpson, 2002).

Ectopic pregnancy is classified according to site of implantation (e.g., tubal or ovarian). The uterus is the only organ capable of containing and sustaining a term pregnancy. However, abdominal pregnancy with birth by laparotomy may result in a living infant (Fig. 9) in 5% to 25% of such pregnancies; however, the risk of deformity is as high as 40% (Gilbert & Harmon, 1998).

Fig. 9 Ectopic pregnancy, abdominal.

Clinical manifestations. A missed period, adnexal fullness, and tenderness may suggest an unruptured tubal pregnancy. The tenderness can progress from a dull pain to a colicky pain when the tube stretches. Pain may be unilateral, bilateral, or diffuse over the abdomen. Abnormal vaginal bleeding that is dark red or brown occurs in 50% to 80% of women. If the ectopic pregnancy ruptures, pain increases. This pain may be generalized, unilateral, or acute deep lower quadrant pam caused by blood irritating the peritoneum. Referred shoulder pain can occur as a result of diaphragmatic irritation caused by blood in the peritoneal cavity. The woman may exhibit signs of shock related to the amount of bleeding in the abdominal cavity and not necessarily related to obvious vaginal bleeding. An ecchymotic blueness around the umbilicus (Cullen sign), indicating hematoperitoneum, may develop in a neglected ruptured intraabdominal ectopic pregnancy.

CARE MANAGEMENT

The differential diagnosis of ectopic pregnancy involves consideration of numerous disorders that share many signs and symptoms. The physician, nurse-midwife, or nurse practitioner must consider miscarriage, ruptured corpus luteum cyst, appendicitis, salpingitis, ovarian cysts, torsion of the ovary, and urinary tract infection (Table 7). The key to early detection of ectopic pregnancy is having a high index of suspicion for this condition. Any woman with abdominal pain, vaginal spotting or bleeding, and a positive pregnancy test should undergo screening for ectopic pregnancy, especially if she has any of the risk factors previously mentioned. Laboratory screening includes determination of serum progesterone and /3-hCG levels. If either of these values is lower than would be expected for a normal pregnancy, the woman is asked to return within 48 hours for serial measurements. At this time, the woman will also undergo transvaginal ultrasound to confirm intrauterine or tubal pregnancy (Gracia & Barnhart, 2001).

 Table 7 Differential Diagnosis of Ectopic Pregnancy ECTOPIC PREGNANCY APPENDICITIS SALPINGITIS RUPTURED OVARIAN CYST MISCARRIAGE Pain Unilateral cramps and Tenderness before rupture May be colicky after rupture Sudden sharp abdominal pelvic pain Abdominal tenderness Epigastric, periumbilical, then right lower quadrant pain, tenderness localizing at McBurney's point, rebound tenderness Usually in both lower quadrants with or without rebound Mild to severe pelvic pressure Unilateral, becoming general with progressive bleeding, dull cramping Mild uterine cramps to severe uterine pain Nausea and vomiting Occasionally before, frequently after rupture Usual, precedes shift of pain to right lower quadrant Infrequent Rare Almost never Menstruation Some aberration, missed period, Unrelated to menses Hypermenorrhea, metrorrhagia. or both Period delayed, then bleeding, often with pain Amenorrhea then spotting, then brisk bleeding Temperature pulse, and blood pressure 37.2°-37.8° C, pulse variable normal before and rapid after rupture, 4 BP after rupture 37.2°-37.8° C, pulse rapid 37.2°-40° C: pulse elevated in proportion to fever Not over 37.2° C, pulse normal unless blood loss marked, then rapid To 37.2° C Signs of shock related to obvious bleeding Pelvic examination Unilateral tenderness. especially on movement of cervix, crepitant mass on one side or in culde-sac; dark red or brown vaginal discharge No masses, rectal tenderness high on right side No vaginal discharge Bilateral tenderness on movement of cervix Purulent discharge Tenderness over affected ovary, no masses Cervix open or closed, uterus slightlyenlarged. Irregularly softened, tender with infection, vaginal bleeding Laboratory findings WBC to 15,000/mm3 Pregnancy test positive Ultrasound to rule out pregnancyafter 6 weeks WBC 10,000-18,000/mm3 (rarely normal) Pregnancy test negative WBC 15,000-30,000/mm3 Pregnancy test negative WBC normal to 10,000/mm3 Pregnancy test negative unless also pregnant Ultrasound will show ovarian cyst WBC normal Pregnancy test positive

The woman should also be assessed for the presence of active bleeding, associated with tubal rupture. If internal bleeding is present, assessment may reveal vertigo, shoulder pain, hypotension, and tachycardia. A vaginal examination should be performed only once, and then with great caution. Approximately half of patients with a tubal pregnancy have a palpable mass on examination. It is possible to rupture the mass during a bimanual examination, so gentleness is critical (Simpson, 2002).

Removal of the ectopic pregnancy by salpingostomy is possible before rupture. Residual tissue is dissolved with a dose of methotrexate postoperatively. Methotrexate is a folk acid analog that destroys the rapidly dividing cells (DeLoia, Stewart-Akers, & Creinin, 1998). It may also be used in a single-dose IM injection to treat unruptured pregnancies (Lipscomb et al., 1998). It has been shown to produce results similar to those of surgical therapy, in terms of high success rate, low complication rate, and good reproductive potential (Buster & Heard, 2000).

Advanced ectopic abdominal pregnancy requires laparotomy as soon as the woman has been stabilized for operation. If the placenta of a second- or third-trimester abdominal pregnancy is attached to a vital organ, such as the liver, separation is usually not attempted because of the risk of hemorrhage. The cord is cut flush with the placenta and the abdomen is closed, with the placenta left in place. Degeneration and absorption of the placenta usually occur without complication, although infection and intestinal obstruction may occur. Methotrexate may be given to dissolve the residual tissue (Cunningham et al., 2001).

If surgery is planned, general preoperative and postoperative care is appropriate for the woman with an ectopic pregnancy. Before surgery, vital signs (pulse, respirations, and blood pressure) are assessed every 15 minutes or as needed, according to severity of the bleeding and the woman's condition. Preoperative laboratory tests include determination of blood type and Rh factor, complete blood cell count, and serum quantitative /3-hCG assay. Blood replacement may be necessary. Postoperatively, the nurse needs to verify the woman's Rh and antibody status and administer Rho(D) immune globulin if appropriate. The woman should be encouraged to verbalize her feelings related to the loss. Referral to community resources may be appropriate.

Hemodynamically stable women with ectopic pregnancies are eligible for methotrexate therapy if the mass is unruptured and measures less than 4 cm in diameter by ultrasound (Simpson, 2002). Management is almost always accomplished on an outpatient basis. The woman is informed how the medication works, what adverse effects are possible, whom to call if she has concerns or problems develop, and the importance of follow-up care. After receiving the methotrexate injection, the woman will need to return at least weekly for follow-up laboratory studies and possibly another dose for an average of 2 to 8 weeks until /3-hCG level drops. During that time, she is instructed to put nothing in her vagina (no tampons, douches, or intercourse) and to avoid sun exposure because the drug will make her more photosensitive (Powell & Spellman, 1996).

NURSE ALERT The woman on methotrexate therapy who drinks alcohol and takes vitamins containing folic acid (such as prenatal vitamins) increases her risk of experiencing side effects of the drug or exacerbating the ectopic rupture.

Future fertility should be discussed. Any woman who has been diagnosed with an ectopic pregnancy should be told to contact her health care provider as soon as she suspects that she might be pregnant, because of the increased risk for recurrent ectopic pregnancy. These women may need referral to grief or infertility support groups. In addition to the loss of the current pregnancy, they are faced with the possibility of future pregnancy losses or infertility.

Hydatidiform mole

Hydatidiform mole (molar pregnancy) is a gestational trophoblastic disease. There are two distinct types of hydatidiform moles: complete (or classic) mole and partial mole.

Incidence and etiology. Hydatidiform mole occurs in 1 in 1200 pregnancies in the United States and Europe, but a higher incidence has been reported in Asian countries (Berman, DiSaia, & Brewster, 1999). The etiology is unknown, although there may be an ovular defect or a nutritional deficiency. Women at higher risk for hydatidiform mole formation are those who have undergone ovulation stimulation with clomiphene (Clomid) and those who are in their early teens or older than 40 years of age. The risk of a second mole is 1% to 2%.

Types. The complete mole results from fertilization of an egg whose nucleus has been lost or inactivated (Fig. 10, A). The mole resembles a bunch of white grapes (Fig. 10, B). The fluid-filled vesicles grow rapidly, causing the uterus to be larger than expected for the duration of the pregnancy. Usually the complete mole contains no fetus, placenta, amniotic membranes, or fluid. Maternal blood has no placenta to receive it; hemorrhage into the uterine cavity and vaginal bleeding therefore occur. In approximately 20% of cases of complete mole, progression toward choriocarcinoma occurs.

Fig. 10 A, Chromosomal origin of complete mole. Single sperm (color) fertilizes an "empty" ovum. Reduplication of sperm's 23,X set gives completely homozygous diploid 46,XX. Similar process follows fertilization of empty ovum by two sperm with two independently drawn sets of 23,X or 23,Y; both karyotypes of 46,XX and 46,XY can therefore result. B, Uterine rupture with hydatidiform mole. 1, Evacuation of mole through cervix. 2, Rupture of uterus and spillage of mole into peritoneal cavity (rare).

A partial mole often has embryonic or fetal parts and an amniotic sac present. Congenital anomalies are usually present. The potential for malignant transformation is much less (less than 6%) than that associated with the complete hydatidiform mole (Copeland & Landon, 2002).

Clinical manifestations. The signs and symptoms of a complete hydatidiform mole in the early stages cannot be distinguished from those of normal pregnancy. Later, vaginal bleeding occurs in almost 95% of cases. The vaginal discharge may be dark brown (resembling prune juice) or bright red and either scant or profuse. It may continue for only a few days or intermittently for weeks. Early in pregnancy the uterus in approximately half of affected women is significantly larger than expected from menstrual dates. The percentage of women with an excessively enlarged uterus increases as length of time since LMP increases. Approximately 25% of affected women have a uterus smaller than would be expected from menstrual dates.

Anemia from blood loss, excessive nausea and vomiting (hyperemesis gravidarum), and abdominal cramps caused by uterine distention are relatively common findings. Preeclampsia occurs in approximately 15% of cases, usually between 9 and 12 weeks of gestation, but any symptoms of PIH before 20 weeks of gestation may suggest hydatidiform mole. Hyperthyroidism and pulmonary embolization of trophoblastic elements occur infrequently but are serious complications of hydatidiform mole. Partial moles cause few of these symptoms and may be mistaken for an incomplete or missed miscarriage.

CARE MANAGEMENT

Nursing assessments during prenatal visits should include observation for signs of molar pregnancy during the first 24 weeks. If hydatidiform mole is suspected, ultrasonography and serial /3-hCG immunoassays are used to confirm the diagnosis. The sonographic pattern of a molar pregnancy is characterized by a diffuse "snowstorm" pattern. A /3-hCG titer will remain high or rise above normal peak after the time at which it normally drops (70 to 100 days) (Cunningham et al., 2001).

Although most moles abort spontaneously, suction curettage offers a safe, rapid, and effective method of evacuation of hydatidiform mole if necessary (Gilbert & Harman, 1998). Induction of labor with oxytocic agents or prostaglandins is not recommended because of the increased risk of embolization of trophoblastic tissue (Copeland & Landon, 2002). Administration of Rho(D) immune globulin to women who are Rh negative is necessary to prevent isoimmunization.

The nurse provides the woman and her family with information about the disease process, the necessity for a long course of follow-up, and the possible consequences of the disease. Follow-up management includes frequent physical and pelvic examinations and biweekly measurements of /3-hCG level until the level drops to normal and remains normal for 3 weeks. Monthly measurements are taken for 6 months and then every 2 months for a total of 1 year. A rising titer and an enlarging uterus may indicate choriocarcinoma. The nurse helps the woman understand and cope with pregnancy loss and recognize that the pregnancy was abnormal. Explanations about the importance of the need to postpone a subsequent pregnancy and contraceptive counseling are provided to emphasize the importance of consistent and reliable use of the method chosen. To avoid confusion with signs of pregnancy, pregnancy should be avoided for 1 year. Any contraceptive method except an intrauterine device is acceptable. Oral contraceptives are highly effective. The woman and her family are encouraged to express their feelings, and information is provided about support groups or counseling resources
if needed.

LATE PREGNANCY BLEEDING

Late pregnancy bleeding disorders include placenta previa, premature separation of placenta (abruptio placentae), and cord insertion and placental variations. Expedient assessment for and diagnosis of the cause of bleeding is essential to reduce risk of maternal and perinatal morbidity and mortality (Fig. 11).

Fig. 11 Bleeding during late pregnancy. CBC, Complete blood count; IV, intravenous.

Placenta previa

Fig. 12 Types of placenta previa after onset of labor. A, Complete, or total. B, Incomplete, or partial. C, Marginal, or low lying

In placenta previa, the placenta is implanted in the lower uterine segment near or over the internal cervical os. The degree to which the internal cervical os is covered by the placenta has traditionally been used to classify three types of placenta previa (Fig. 12). Placenta previa often is described as total or complete if the internal os is entirely covered by the placenta when the cervix is fully dilated. Partial placenta previa implies incomplete coverage of the internal os. Marginal placenta previa indicates that only an edge of the placenta extends to the internal os but may extend onto the os during dilation of the cervix during labor. The term low-lying placenta is used when the placenta is implanted in the lower uterine segment but does not reach the os.

Incidence and etiology. The incidence of placenta previa is approximately 0.5% of births (Clark, 1999). The most important risk factors are previous placenta previa, previous cesarean birth, and induced abortion, possibly related to endometrial scarring (Ananth et al., 1997). The risk also increases with multiple gestation (because of the larger placental area), closely spaced pregnancies, advanced maternal age (older than 35 years), African or Asian ethnicity, smoking, and cocaine use (Clark, 1999).

Clinical manifestations. Approximately 70% of women with placenta previa have painless vaginal bleeding; 20% have vaginal bleeding associated with uterine activity. Previa should be suspected whenever vaginal bleeding occurs after 24 weeks of gestation. This bleeding is associated with the stretching and thinning of the lower uterine segment that occurs during the third trimester. Placental attachment is gradually disrupted, and bleeding occurs when the uterus is not able to adequately contract and stop blood flow from open vessels (Benedetti, 2002). The initial bleeding is usually a small amount and stops as clots form; however, it can recur at any time (Table 8). It is bright red in color.

 ABRUPTIO PLACENTAE PLACENTA PREVIA GRADE 1 MILD SEPARATION (10% TO 20%) GRADE 2 MODERATE SEPARATION (20% TO 50%) GRADE 3 SEVERE SEPARATION (>50%) Bleeding, external, vaginal Minimal Absent or moderate Absent to moderate Minimal to severe and life-threatening Total amount of blood loss <500 ml 1000-1500 ml >1500 ml Varies Color of blood Dark red Dark red Dark red Bright red Shock Rare; none Mild shock Common, often sudden, profound Uncommon Coagulopathy Rare; none Occasional DIC Frequent DIC None Uterine tonicity Normal Increased, may be localized to one region or diffuse over uterus, uterus fails to relax between contractions Tetanic, persistent uterine contraction, boardlike uterus Normal Tenderness (pain) Usually absent Present Agonizing, unremitting uterine pain Absent Ultrasonographic findings Location of placenta Normal, upper uterine segment Normal, upper uterine segment Normal, upper uterine segment Abnormal, lower uterine segment Station of presenting part Variable to engaged Variable to engaged Variable to engaged High, not engaged Fetal position Usual distribution* Usual distribution* Usual distribution* Commonly transverse, breech, or oblique Pregnancy-induced or chronic hypertension Usual distribution* Commonly present Commonly present Usual distribution* Fetal effects Normal fetal heart rate patten Nonreassuring fetal heart rate pattern Nonreassuring fetal heart rate pattern, death can occur Normal fetal heart rate pattern

Vital signs may be normal, even with heavy blood loss, because a pregnant woman can lose up to 40% of blood volume without showing signs of shock. Clinical presentation and decreasing urinary output may be better indicators of acute blood loss than vital signs alone (Gilbert & Harmon, 1998). The fetal heart rate is reassuring unless there is a major detachment of the placenta. Abdominal examination usually reveals a soft, relaxed, nontender uterus with normal tone. If the fetus is lying longitudinally, the fundal height is usually greater than expected for gestational age because the low placenta hinders descent of the presenting fetal part. Leopold's maneuvers may reveal a fetus in an oblique or breech position or lying transverse because of the abnormal site of placental implantation.

Maternal and fetal outcome. The maternal morbidity rate is approximately 5% and the mortality rate is less than 1% with placenta previa (Clark, 1999). Complications associated with placenta previa include premature ROM, preterm birth, surgery-related trauma to structures adjacent to the uterus, anesthesia complications, blood transfusion reactions, overinfusion of fluids, abnormal placental attachments to the uterine wall (e.g., placenta accreta), postpartum hemorrhage, thrombophlebitis, anemia, and infection  (Crane et al., 2000).

The greatest risk of fetal death is caused by preterm birth. Other fetal risks include hypoxia in utero and congenital anomalies. Infants who are small for gestational age or have IUGR have been associated with placenta previa; this association may be related to poor placental exchange  or hypovolemia resulting from maternal blood loss and maternal anemia (Clark, 1999).

CARE MANAGEMENT

Assessment and Nursing Diagnoses

A woman with third-trimester vaginal bleeding requires immediate evaluation. Necessary history data include gravidity, parity, and a description of the bleeding (how long, precipitating event, estimation of amount). Other assessment data to be collected are the woman's general status, estimated gestational age, current amount of bleeding, vital signs, and fetal status (see Box 6). Laboratory studies include a complete blood count, determination of blood type and Rh status, a coagulation profile, and a possible type and crossmatch.

Placenta previa can be diagnosed using transabdominal ultrasound, which is accurate 93% to 97% of the time. Transvaginal ultrasound examination may also be used. If the ultrasound reveals a normally implanted placenta, a speculum examination may be performed to rule out local causes of bleeding (e.g., cervicitis, polyps, or carcinoma of the cervix), and a coagulation profile is obtained to rule out other causes of bleeding. If expectant management is to be implemented, a vaginal speculum examination is postponed until fetal viability has been reached (preferably after 34 weeks of gestation). If a pelvic examination is needed before that time, anticipate the possibility that an immediate cesarean birth may be required. The woman is taken to a delivery room or an operating room set up for cesarean birth because profound hemorrhage can occur during the examination. This type of vaginal examination, known as the double-setup procedure, is not done often.

Potential nursing diagnoses for the woman experiencing placenta previa include the following:

Deficient fluid volume related to

-excessive blood loss secondary to placenta previa

Risk for excess fluid volume related to

-fluid resuscitation

Ineffective peripheral tissue perfusion related to

-hypovolemia and shunting of blood to central circulation

Risk for injury (fetal) related to

-decreased placental perfusion secondary to placenta previa

Anxiety/fear related to

-maternal condition and pregnancy outcome

Interrupted family processes related to

-woman's condition and hospitalization

Anticipatory grieving related to

-actual/perceived threat to self, pregnancy, or infant

Risk for infection related to

-anemia, hemorrhage, placenta previa, and transfusions

Risk for injury (mother) related to

-invasive monitoring procedures and treatment

Expected Outcomes of Care

Expected outcomes for the woman experiencing placenta previa may include that the woman will do the following:

• Verbalize understanding of her condition and its management

• Identify and use available support systems

• Demonstrate compliance with prescribed activity limitations

• Develop no complications related to bleeding

• Give birth to a healthy infant at or near term

Plan of Care and Interventions

Active management

Once placenta previa has been diagnosed, a management plan is developed based on gestational age, amount of bleeding, and fetal condition. If the woman is at term (greater than or equal to 37 weeks of gestation) and in labor or bleeding persistently, immediate delivery by cesarean is almost always indicated. In women with partial or marginal previa who have minimal bleeding, vaginal birth may be attempted. Vaginal birth may also be indicated for previable gestations or births involving intrauterine fetal demise (Benedetti, 2002).

If cesarean birth is undertaken, the nurse continuously assesses maternal and fetal status while preparing the woman for surgery. Maternal vital signs are assessed frequently for decreasing blood pressure, rising pulse rate, changes in level of consciousness, and oliguria. Fetal assessment is maintained by continuous electronic fetal monitoring to assess for signs of hypoxia.

Blood loss may not cease with the birth of the infant. The large vascular channels in the lower uterine segment may continue to bleed because of that segment's diminished muscle content. The natural mechanism to control bleeding so characteristic of the upper part of the uterus—the interlacing muscle bundles, the "living ligature" contracting around open vessels-is absent in the lower part of the uterus. Postpartum hemorrhage may therefore occur even if the fundus is contracted firmly.

Emotional support for the woman and her family is extremely important. The actively bleeding patient is concerned not only for her own well-being but for the wellbeing of her fetus. All procedures should be explained, and a support person should be present. The woman should be encouraged to express her concerns and feelings. If the woman and her support person or family desire spiritual support, the nurse can notify the hospital chaplain service or provide information about other supportive resources.

Expectant management

If the woman is less than 36 weeks of gestation and not in labor, and the bleeding is mild or has stopped, expectant management is generally the treatment of choice to give the fetus time to mature in utero. Expectant management consists of rest and close observation. The woman is usually placed on bed rest, although she may be allowed bathroom privileges and limited activity (up in a wheelchair for an hour or so daily). Bleeding is assessed by checking the amount of bleeding on perineal pads, bed pads, and linens. Weighing pads, although not frequently used, is one way to more accurately assess blood loss: 1 g represents 1 ml of blood.

Ultrasonographic examinations may be done every 2 to 3 weeks. Fetal surveillance may include NSTs or BPPs once or twice weekly. Antepartum steroids (betamethasone) may be ordered to promote fetal lung maturity if the woman is less than 34 weeks of gestation. No vaginal or rectal examinations are performed, and the woman is placed on pelvic rest (nothing in the vagina). Once she reaches 37 weeks of gestation and fetal lung maturity is documented, cesarean birth can be scheduled.

The woman with placenta previa should always be considered a potential emergency because massive blood loss with resulting hypovolemic shock can occur quickly if bleeding resumes. The possibility that she may require an emergency cesarean for birth always exists. Placenta previa in a preterm gestation may be an indication for transfer to a tertiary perinatal center because many community hospitals are not equipped to perform emergency cesarean births 24 hours per day, 7 days per week.

Home care

Criteria for home care management vary with primary perinatal provider and home care agency. To be considered for home care referral, the woman must be in stable condition with no evidence of active bleeding and must have resources to be able to return to the hospital immediately if active bleeding resumes (Lowdermilk & Grohar, 1998). She must have close supervision by family or friends in the home. The woman should be taught how to assess fetal and uterine activity and bleeding and told to avoid intercourse, douching, and enemas. She should limit her activities according to the advice of her physician and be informed to keep all appointments for fetal testing, laboratory assessments, and prenatal care. Visits by a perinatal home care nurse may be arranged.

If hospitalization or home care with activity restriction is prolonged, the woman may have concerns about her work- or family-related responsibilities or may become bored with inactivity. She should be encouraged to participate in her own care and decisions about care as much as possible. Provision of diversionary activities or encouragement to participate in activities she enjoys and can do during bed rest is needed (see suggestions for activities in the Self-Care box on p. 613). Participation in a support group made up of other women on bed rest while hospitalized may be a helpful coping mechanism (Maloni & Kutil, 2000).

Evaluation

The expected outcomes of care are used to evaluate the care for the woman with placenta previa (see Plan of Care).

PLAN OF CARE Placenta Previa

NURSING DIAGNOSIS Decreased cardiac output related to bleeding secondary to placenta previa

Expected Outcomes Patient will exhibit signs of increased blood volume and restoration of cardiac output (i.e., normal pulse and blood pressure, normal heart and breath sounds, normal skin color, tone and turgor, normal capillary refill).

Nursing Interventions/Rationales

Palpate uterus for tenderness and tone; assess bleeding rate, amount, color, degree of bleeding, CBC values, and coagulation profile to determine severity of situation. (Do not perform vaginal examination, because it may stimulate further bleeding.)

Establish baseline data for cardiac output (vital signs; heart and breath sounds; skin color, tone, turgor; capillary refill; level of consciousness; urinary output; pulse oximetry) to use as basis for evaluating effectiveness of treatment.

Initiate intravenous therapy or blood transfusions and medications per physician order to restore blood volume and prevent organ compromise to mother and fetus.

Place woman on bed rest to decrease oxygen demands.

Monitor vital signs, intake and output, hemodynamic status, and laboratory values to evaluate treatment response.

Provide emotional support to woman and her family (i.e., explain procedures and their rationale; explain what is happening and what to expect; keep support person present) to allay fears and provide the family with some sense of control.

After stabilization, teach woman home management, including bed rest, watching for spotting/bleeding, close followup with her health care provider and preparation for immediate return to hospital if needed to prevent or stem further complications.

NURSING DIAGNOSIS Risk for injury to the fetus related to decreased uterine/placental perfusion secondary to bleeding

Expected Outcome Patient will exhibit ongoing signs of fetal well-being (i.e., adequate fetal movement, normal FHR, reactive NST, normal BPP).

Nursing Interventions/Rationales

Monitor fetus daily for signs of tachycardia, decreased movement, loss of reactivity on NST to identify and treat changes in fetal status early.

Obtain BPP per physician order to assess for signs of chronic asphyxia.

Maintain maternal side-lying position to prevent compression of aorta and vena cava.

NURSING DIAGNOSIS Risk for infection related to anemia and bleeding secondary to placenta previa

Expected Outcome Patient will show no signs of intrauterine infection.

Nursing I nterventions/ Rationales

Monitor vital signs for elevated temperature, pulse, and blood pressure; monitor laboratory results for elevated WBC count, differential shift; check for uterine tenderness and malodorous vaginal discharge to detect early signs of infection resulting from exposure of placenta! tissue.

Provide/teach perineal hygiene to decrease the risk of ascending infection.

Premature separation of placenta

Premature separation of the placenta, also termed abruptio placentae (Fig. 13) occurs in the area of the decidua basalis after the twentieth week of pregnancy and before the birth of the baby.

Fig. 13 Abruptio placentae. Premature separation of normally implanted placenta.

Incidence and etiology. Premature separation of the placenta is a serious event that accounts for significant maternal and fetal morbidity and mortality rates. One percent of all pregnancies are complicated by abruptio placentae, but it accounts for approximately 15% of all perinatal deaths. More than 50% of these deaths are the result of preterm birth; many others are the result of intrauterine hypoxia.

Maternal hypertension is probably the most consistently identified risk factor for abruption (Benedetti, 2002). Cocaine use is also a risk factor, probably in part because cocaine use is associated with the development of hypertension (Andres & Day, 2000). Blunt external abdominal trauma, most often the result of motor vehicle accidents or maternal battering, is an increasingly significant cause of placental abruption (Benedetti, 2002). Maternal smoking and poor nutrition may be associated with an increased risk. Abruption is more likely to occur in twin gestations (Ananth et al., 2001). There is a significant risk for recurrence of placental abruption in subsequent pregnancies.

Classification. The most common classification of placental abruption is according to type and severity. This classification system is summarized in Table 8.

Clinical manifestations. The separation may be partial or complete, or only the margin of the placenta may be involved. Bleeding from the placental site may dissect (separate) the membranes from the decidua basalis and flow out through the vagina, it may remain concealed (retroplacental hemorrhage), or it may do both (see Fig. 13). Clinical symptoms vary with degree of separation (see Table 8).

Classic symptoms of abruptio placentae include vaginal bleeding, abdominal pain, and uterine tenderness and contractions. Although abdominal pain and uterine tenderness are characteristic for this complication, either finding may be absent in the presence of a silent abruption (Konje & Walley, 1995). Bleeding may result in maternal hypovolemia (shock, oliguria, anuria) and coagulopathy. Mild to severe uterine hypertonicity is present. Pain is mild to severe and localized over one region of the uterus or diffuse over the uterus with a boardlike abdomen.

Extensive myometrial bleeding damages the uterine muscle. If blood accumulates between the separated placenta and the uterine wall, it may produce a Couvelaire uterus. The uterus appears reddish or purplish, it is ecchymotic, and contractility is lost. Shock may occur and is out of proportion to blood loss. Laboratory findings include a positive result of Apt test (blood in amniotic fluid); a drop in hemoglobin and hematocrit levels (which may appear later); and a drop in coagulation factor levels. Clotting defects (such as DIC) develop in 10% to 30% of patients. A Kleihauer-Betke stain may be ordered to determine the presence of fetal-to-maternal bleeding (transplacental hemorrhage).

Maternal and fetal outcomes. Maternal mortality rates approach 1% for abruptio placentae; this condition remains a leading cause of maternal death. The mother's prognosis depends on the extent of placental detachment, overall blood loss, degree of DIC, and time between placental detachment and birth. Renal failure and pituitary necrosis may result from ischemia. In rare cases, women who are Rh negative can become sensitized if fetal-to-maternal hemorrhage occurs and the fetal blood type is Rh positive.

Perinatal mortality rates range from 15% to 30%. Death occurs as a result of fetal hypoxia, preterm birth, and status as small for gestational age. Risk for neurologic defects is increased (Cunningham et al., 2001).

CARE MANAGEMENT

Abruptio placentae should be highly suspected in the woman with a sudden onset of intense, usually localized, uterine pain, with or without vaginal bleeding. Initial assessment is much the same as for placenta previa. Physical examination usually reveals abdominal pain, uterine tenderness, and contractions. Vaginal bleeding is present in approximately 80% of cases (Benedetti, 2002). Approximately 60% of live fetuses exhibit nonreassuring signs on the electronic fetal heart monitor, such as loss of variability and late decelerations; uterine hyperstimulation and increased resting tone may also be noted on the monitor tracing (Benedetti, 2002). Many women demonstrate coagulopathy, as evidenced by abnormal clotting studies (fibrinogen, platelet count, PT, PTT, fibrin split products). Sonographic examination is used to rule out placenta previa; however, it is not always diagnostic for abruption (Cunningham et al., 2001).

Nursing diagnoses and expected outcomes of care are similar to those described for placenta previa.

Treatment depends on the severity of blood loss and fetal maturity and status. Women with abruptio placentae are not usually managed out of the hospital because the placenta can separate further at any time and immediate intervention or delivery may be necessary. If the abruption is mild and the fetus is less than 36 weeks of gestation and not in distress, expectant management may be implemented. The woman is hospitalized and observed closely for signs of bleeding and labor. The fetal status is also monitored with intermittent FHR monitoring and NSTs or BPPs until fetal maturity is determined or until the woman's condition deteriorates and immediate birth is indicated. Use of corticosteroids to accelerate fetal lung maturity is appropriately included in the plan of care for expectant management (ACOG, 1994; Hunter & Weiner, 1996). Women who are Rh negative may be given Rho(D) immune globulin if fetal-to-maternal hemorrhage occurs and the fetal blood is Rh positive. Vaginal birth is expected; cesarean birth may be necessary for cases of fetal distress or other obstetric indications.

Delivery is the treatment of choice if the fetus is at term gestation or if the bleeding is moderate to severe and mother or fetus is in jeopardy. At least one large-bore (16- gauge) IV line should be started. Maternal vital signs are monitored frequently to observe for signs of declining hemodynamic status, such as increasing pulse rate and decreasing blood pressure. Serial laboratory studies include hematocrit or hemoglobin determinations and clotting studies. Continuous electronic fetal monitoring is mandatory. An indwelling Foley catheter is inserted for continuous assessment of urine output, an excellent indirect measure of maternal organ perfusion (Benedetti, 2002).

Blood and fluid volume replacement will most likely be ordered, with a goal of maintaining the urine output at 30 ml/hr or greater and the hematocrit at 30% or greater. If this goal is not reached despite vigorous attempts at replacement, hemodynamic monitoring may be necessary (Benedetti, 2002). Fresh frozen plasma or cryoprecipitate may be given to maintain the fibrinogen level at a minimum of 100 to 150 mg/dl.

Vaginal birth is possible and is especially desirable in cases of fetal demise; however, cesarean birth is common because of fetal or maternal distress.

Nursing care of patients experiencing moderate-tosevere abruption is demanding because it requires close monitoring of the maternal and fetal condition. All procedures should be explained to the woman and her family. Emotional support is also extremely important because the woman and her family may be experiencing grief over fetal loss in addition to the mother's critical illness.

Cord insertion and placental variations

Velamentous insertion of the cord is a rare placental anomaly associated with placenta previa and multiple gestation. The cord vessels begin to branch at the membranes and then course onto the placenta (Fig. 14, A). ROM or traction on the cord may tear one or more of the fetal vessels. As a result the fetus may quickly bleed to death. Battledore (marginal) (Fig. 14, B) insertion of the cord increases the risk of fetal hemorrhage, especially after marginal separation of the placenta.

Fig. 14 Cord insertion and placental variations. A, Velamentous insertion of cord. B, Battledore placenta. C, Placenta succenturiate.

Rarely, the placenta may be divided into two or more separate lobes, resulting in placenta succenturiate (Fig. 14, C). Each lobe has a distinct circulation; the vessels collect at the periphery, and the main trunks unite eventually to form the vessels of the cord. Blood vessels joining the lobes may be supported only by the fetal membranes and are therefore in danger of tearing during labor, birth, or expulsion of the placenta. During recovery of the placenta, one or more of the separate lobes may remain attached to the decidua basalis, preventing uterine contraction and increasing the risk of postpartum hemorrhage.

Clotting disorders in pregnancy

Normal clotting. Normally, there is a delicate balance (homeostasis) between the opposing hemostatic and fibrinolytic systems. The hemostatic system is involved in the lifesaving process. This system stops the flow of blood from injured vessels, in part through the formation of insoluble fibrin, which acts as a hemostatic platelet plug. The phases of the coagulation process involve an interaction of the coagulation factors in which each factor sequentially activates the factor next in line, the "cascade effect" sequence. The fibrinolytic system is the process through which the fibrin is split into fibrinolytic degradation products and circulation is restored.

Clotting problems. A history of abnormal bleeding, inheritance of unusual bleeding tendencies, and a report of significant aberrations of laboratory findings indicate a bleeding or clotting problem. For the obstetric patient, bleeding disorders are suspected if the woman has PIH, HELLP syndrome, retained dead fetus syndrome, amniotic fluid embolism, sepsis, or hemorrhage. Determination of hemostasis is made by testing the usual mechanisms for the control of bleeding, the function of platelets and the necessary clotting factors. Most clotting disorders are more of a concern in the immediate postpartum period. Recognition in the antepartal period may decrease hemorrhagic problems (see Chapter 25).

Disseminated intravascular coagulation. Disseminated intravascular coagulation (DIC) is a pathologic form of clotting that is diffuse and consumes large amounts of clotting factors, causing widespread external bleeding, internal bleeding, or both. It is important to understand that DIC is always a secondary diagnosis. In the obstetric population, HELLP syndrome and gram-negative sepsis are examples of conditions that can trigger DIC because of widespread damage to vascular integrity. Medical management is discussed in Chapter 25.

The nurse caring for the woman at risk for DIC must be aware of risk factors. Careful and thorough assessment is required, with particular attention to signs of bleeding (petechiae, oozing from injection sites, and hematuria). Because renal failure is one consequence of DIC, urinary output is carefully monitored, using an indwelling Foley catheter. Vital signs are assessed frequently.

The pregnant woman is maintained in a side-lying tilt to maximize blood flow to the uterus. Oxygen may be administered through a tight-fitting, rebreathing mask at 10 to 12 L/min, or per hospital protocol or physician order. Blood and blood products must be administered safely.

The educational and emotional needs of the woman and her family must be recognized and supported. They need information about her condition and explanations of procedures and will most likely be very anxious about the health of mother and baby.

HYPEREMESIS GRAVIDARUM

Nausea and vomiting complicate approximately 70% of all pregnancies and are usually confined to the first trimester (Gordon, 2002). Although these manifestations are distressing, they are typically benign, with no significant metabolic alterations or risks to the mother or fetus.

When vomiting during pregnancy becomes excessive enough to cause weight loss of at least 5% of prepregnancy weight and is accompanied by dehydration, electrolyte imbalance, ketosis, and acetonuria, the disorder is termed hyperemesis gravidarum. The estimated incidence varies from 0.5 to 10 per 1000 births (Snell et al., 1998). Hyperemesis gravidarum usually begins during the first 10 weeks of pregnancy. Women with hyperemesis tend to be younger than 20 years of age, obese, and nonsmokers. They are also more likely to have multifetal or molar pregnancies (Riely, 1999). The effects of hyperemesis gravi darum on perinatal outcome vary with the severity of the disorder. Women who lose weight are more likely to have low-birth-weight infants.

ETIOLOGY

The etiology of hyperemesis gravidarum remains obscure. Several theories have been proposed as to the cause, although none of them adequately explains the disorder. Hyperemesis gravidarum may be related to high levels of estrogen or human chorionic gonadotropin (hCG) and may be associated with transient hyperthyroidism during pregnancy. It may be accompanied by liver dysfunction

with elevation in transaminase and bilirubin levels. Esophageal reflux, reduced gastric motility, and decreased secretion of free hydrochloric acid may contribute to the disorder. Other possible causes include vitamin B deficiencies and increased sensitivity to circulating sex steroid hormones (Hill & Fleming, 1999; Riely, 1999; Snell et al, 1998).

Psychologic factors may also play a part in the development of hyperemesis gravidarum, at least in some women. Ambivalence toward the pregnancy and difficult relationships with mothers or partners have been identified as causative factors. High stress levels are probably also associated with this condition (Hill & Fleming, 1999; Snell et al., 1998). Conflicting feelings regarding prospective motherhood, body changes, and lifestyle alterations may contribute to episodes of vomiting, particularly if these feelings are excessive or unresolved.

CLINICAL MANIFESTATIONS

The woman with hyperemesis usually has significant weight loss and dehydration. She may have a decreased blood pressure, increased pulse rate, and poor skin turgor (Snell et al., 1998). She is almost always unable to keep down even clear liquids taken by mouth. Laboratory tests may reveal electrolyte imbalances.

CARE MANAGEMENT

Whenever a pregnant woman has nausea and vomiting, the first priority is a thorough assessment to determine the severity of the problem. In most cases, the woman should be told to come immediately to the health care provider's office or to the emergency department, because the severity of the illness is often difficult to determine by phone conversation.

The history includes information about the frequency, severity, and duration of episodes of nausea and vomiting. Other symptoms such as diarrhea, indigestion, and abdominal pain or distention are also identified. The woman is asked to report any precipitating factors relating to the onset of her symptoms. Any pharmacologic or nonpharmacologic treatment measures should be recorded. Prepregnancy weight and documented weight gain or loss during pregnancy are important to note.

The woman's weight and vital signs are measured and a complete physical examination is performed, with attention to signs of fluid and electrolyte imbalance and nutritional status. The most important initial laboratory test to be obtained is a dipstick determination of ketonuria. Other laboratory tests that may be ordered are a urinalysis, a complete blood cell count, electrolytes, liver enzymes, and bilirubin levels. These tests help rule out the presence of underlying diseases such as pyelonephritis, pancreatitis, cholecystitis, and hepatitis (Cruikshank et al., 2002). Because of the recognized association between hyperemesis gravidarum and hyperthyroidism, thyroid levels may also be measured.

Psychosocial assessment includes asking the woman about anxiety, fears, and concerns related to her own health and the effects on pregnancy outcome. Family members should be assessed both for anxiety and in regard to their role in providing support for the woman.

Initial Care

Initially, the woman who is unable to keep down clear liquids by mouth will require IV therapy for correction of fluid and electrolyte imbalances. She should be kept on nothing-by-mouth (NPO) status until dehydration has been resolved and for at least 48 hours after vomiting has stopped to prevent rapid recurrence of the problem (Cruikshank et al., 2002). In the past, women requiring IV therapy were admitted to the hospital. Today, however, they may be, and often are, successfully managed at home. Antiemetic medications may be used if nausea and vomiting are uncontrolled; commonly used drugs include pyridoxine, droperidol, promethazine, chlorpromazine, prochlorperazine, and metoclopramide. Corticosteroids have  also been used successfully to treat refractory hyperemesis gravidarum. In addition to medical management, some women can also benefit from psychotherapy or stress reduction techniques (Hill & Fleming, 1999; Snell et al., 1998). Once the vomiting has stopped, feedings are started in small amounts at frequent intervals, and the diet is slowly advanced as tolerated.

Nursing care of the woman with hyperemesis gravidarum involves implementing the medical plan of care, whether this care be given in the hospital or home setting. Interventions may include initiating and monitoring IV therapy, administering drugs and nutritional supplements, and monitoring the woman's response to interventions. The nurse observes the woman for any signs of complications such as metabolic acidosis, jaundice, or hemorrhage and alerts the physician should these occur.

Accurate measurement of intake and output, including the amount of emesis, is an important aspect of care. Oral hygiene while the woman is receiving nothing by mouth, and after episodes of vomiting, helps allay associated discomforts. Assistance with positioning and providing a quiet, restful environment, free from odors, may increase the woman's comfort. When the woman begins responding to therapy, limited amounts of oral fluids and bland foods such as crackers or toast are begun. The diet is progressed slowly as tolerated by the woman until she is able to consume a nutritionally sound diet. Because sleep disturbances may accompany hyperemesis gravidarum, promoting adequate rest is important. The nurse can assist in coordinating treatment measures and periods of visitation to provide opportunity for rest periods.

Follow-up Care

Most women are able to take nourishment by mouth after several days of treatment. Education at this time is important to prevent rapid recurrence of nausea and vomiting. Women should be encouraged to eat small, frequent meals and low-fat protein foods, to avoid greasy and highly seasoned foods, and to increase their dietary intake of potassium and magnesium. Herbal teas such as chamomile or raspberry leaf may decrease nausea (Beal, 1998). Taking fluids between meals, rather than with them, sometimes helps decrease nausea. Many pregnant women find exposure to cooking odors nauseating. If other family members can take over cooking chores, even temporarily, the woman's nausea and vomiting may decrease. The woman is counseled to contact her health care provider immediately if the nausea and vomiting recurs, especially if accompanied by abdominal pain, dehydration, or significant weight loss (e.g., more than 2.5 kg [5 pounds] in 1 week) (Lowdermilk & Grohar, 1998).

A few women will continue to experience intractable nausea and vomiting throughout pregnancy. Rarely, it may be necessary to maintain a woman on enteral, parenteral, or total parenteral nutrition to ensure adequate nutrition for the mother and fetus (Hill & Fleming, 1999; Snell et al., 1998). Many home health agencies are able to provide these services, and arrangements for service may be made depending on the woman's insurance coverage. Regardless of the site of care, the nurse must remain calm, compassionate, and sympathetic, recognizing that the manifestations of hyperemesis can be physically and emotionally debilitating. Irritability, tearfulness, and mood changes are often consistent with this disorder. Fetal well-being is a primary concern of the woman. The nurse can provide an environment conducive to discussion of those concerns and assist the woman in identifying and mobilizing sources of support. The family should be included in the plan of care whenever possible. Their participation may help alleviate some of the emotional stress associated with this disorder.

PREGNANCY INDUCED HYPERTENSION

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).