HYPERTENSIVE DISORDERS IN PREGNANCY
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
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.).
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 |
|
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.
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.
Chronic renal
disease Chronic hypertension Family history of
PIH Twin gestation Primigravidity Maternal age
<19 years; >40 years Diabetes Rh incompatibility Obesity |
Data
from
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 |
|
|
|
|
|
|
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 (
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.].
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
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.
|
|
|
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.].
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
|
|
PIH |
HELLP |
Hemoglobin/hematocrit |
12 to 16 gm/dl/37% to 47% |
May ↑ |
↓ |
Platelets |
150,000 to 400,000/mm3 |
Unchanged |
<100,000/mm3 |
PT/PTT |
12 to 14 sec/60 to 70 sec |
Unchanged |
Unchanged |
Fibrinogen |
150 to 400 mg/dl |
300 to 600 mg/dl |
Present |
Fibrin split products (FSP) |
Absent |
Absent |
↓ |
Blood urea nitrogen (BUN) |
10 to 20 mg/dl |
<10 mg/dl |
↑ |
Creatinine |
0.5 to 1.1 mg/dl |
<1 mg/dl |
↑ |
Lactate dehydrogenase
(LDH) |
45 to 90 U/L |
Unchanged |
↑ |
Aspartate aminotransferase (AST) |
4 to 20 U/L |
Unchanged |
↑ |
Alanine aminotransferase (ALT) |
3 to 21 U/L |
Unchanged |
↑ |
Creatinine clearance |
80 to 125 ml/min |
130 to 180 ml/min |
↓ |
Burr cells/schistocytes |
Absent |
Absent |
Present |
Uric acid |
2 to 6.6 mg/dl |
4.5 to 6 mg/dl |
>10 mg/dl |
Bilirubin (total) |
0.1 to 1 mg/dl |
Unchanged or ↑ |
↑ |
The hematocrit, hemoglobin, and platelet levels are monitored
closely for changes indicating a worsening of patient
status. Because hepatic involvement is a possible complication, serum glucose levels are monitored if liver function tests
indicate elevated liver enzymes. Once the platelet count drops below
100,000/mm3, coagulation profiles
are needed to identify developing DIC.
Proteinuria is
determined from dipstick testing of a clean-catch or catheterized urine
specimen. A reading of 2+
on two or more occasions at least 6 hours apart should be followed by a 24-hour urine collection (Gilbert & Harmon, 1998). A 24-hour
collection for protein and creatinine clearance is more reflective of true renal status. Proteinuria
is usually a late sign in the course
of preeclampsia. Protein readings are designated as follows:
0
negative
Trace trace
1 + 30
mg/dl (equivalent to 0.3 g/L)
2+ 100 mg/dl
3+ 300 mg/dl
4+
1000 mg (1 g)/dl
Urine output is assessed for volume
of at least 30 ml/hr or 120 ml/4 hr. Renal laboratory
assessments include monitoring trends in
serum creatinine and BUN levels. As renal function becomes compromised, renal excretion
of creatinine and other waste products, including magnesium sulfate, decreases. As renal excretion decreases,
serum levels for creatinine,
BUN, uric acid, and magnesium rise.
Nursing
diagnoses for the woman with hypertensive disorders in pregnancy may include the following:
• Anxiety
related to
- preeclampsia and its effect on woman and infant
• Deficient
knowledge related to
-management
(diet, medications, activity restrictions)
• Ineffective
individual/family coping related to
-woman's restricted
activity and concern over a complicated pregnancy
-woman's
inability to work outside the home
-transfer of
woman to tertiary care center for more intensive management
• Powerlessness
related to
-inability to
prevent or control condition and outcomes
• Ineffective
tissue perfusion related to
-hypertension
-cyclic
vasospasms
-cerebral edema
-hemorrhage
• Risk for
injury to fetus related to
-uteroplacental
insufficiency
-preterm birth
-abruptio placentae
• Risk for
injury to mother related to
-CNS irritability secondary to cerebral edema, vasospasm, decreased renal perfusion
-magnesium sulfate and antihypertensive therapies
-abruptio placentae
Expected Outcomes of Care
Expected outcomes
for care of women with hypertensive disorders of pregnancy include that the
woman will do the following:
•
Recognize and immediately report signs and symptoms indicative of
worsening condition
•
Adhere to the medical regimen to minimize risk to herself and her fetus
•
Identify and use available support systems
•
Verbalize her fears and concerns to cope with the condition and situation
•
Develop no signs of eclampsia and its
complications
•
Give birth to a healthy infant
•
Develop no sequelae to her condition or its management
Plan of Care and Interventions
Preeclampsia
Nursing
actions are derived from medical management, health care provider directives,
and nursing diagnoses. The most effective therapy
is prevention. Early prenatal care, identification of pregnant women at risk
for preeclampsia, and
recognition and reporting of physical warning signs are essential components in the optimization of
maternal and perinatal outcomes. The role of
the nurse's skills in assessing the woman
for factors and symptoms of preeclampsia cannot be
overestimated.
The goals of therapy are to ensure maternal
safety and to deliver a healthy newborn as close to term as possible. At or near term, the plan of care for a woman
with preeclampsia is most likely to be induction of labor, preceded, if necessary, by cervical ripening. When preeclampsia is diagnosed in a woman who is less than 37 weeks of gestation, however, immediate
delivery may not be in the best
interest of the fetus. In this situation, the initial intervention is usually a thorough
evaluation of both the maternal
and fetal condition. This evaluation may be done in the high risk clinic or the physician's office, or the woman may be hospitalized.
Emotional and psychologic support is essential in assisting the woman and her family to cope. Their
perception of the disease process, the reasons
for it, and the care received will affect
their compliance with and participation in therapy. The family needs to use
coping mechanisms and support systems to help them through this crisis. A plan of care specifically designed for the
woman with preeclampsia
must be superimposed on the nursing care
all women need during labor and the birth process.
Mild preeclampsia and
home care
If the woman
has mild preeclampsia (e.g., blood pressure is stable, urine protein is less than 500 mg in
a 24-hour collection, and no
subjective complaints), she may be
managed expectantly, usually at home. The maternal-fetal condition must be assessed two to three times
per week. Many
agencies are available to provide this assessment
in the home. Arrangements for this service may be made, depending on the woman's insurance coverage. If home nursing care is not an option, the woman may
be asked to perform self-assessment
daily, including weight, urine dipstick protein determinations, blood
pressure measurement, and fetal movement counting (Lowdermilk
& Grohar, 1998). She will be instructed to report the
development of any subjective symptoms immediately to her health care provider (see Self-Care box) and to return to
the physician's office or high risk
clinic for assessment as scheduled.
The only reason
for expectant management of preeclampsia
is to allow additional time for fetal growth and maturation. The fetal condition is closely monitored.
An evaluation of fetal growth by
ultrasound should be obtained
every 3 weeks. Fetal movement is counted daily. Other
fetal assessment tests include a nonstress test (NST)
or BPP once or twice a week as needed.
Fetal jeopardy as evidenced by
inappropriate growth or abnormal test results necessitates immediate
delivery (Sibai, 2002).
Activity restriction. Bed rest in the lateral recumbent position is a standard therapy for preeclampsia and maximizes uteroplacental
blood flow during pregnancy. It has been shown to be beneficial in decreasing
blood pressure and promoting diuresis. However, recommendations for bed rest for all high risk pregnant women are
becoming more controversial.
Maloni (1994) documented adverse physiologic outcomes related to complete bed
rest, including cardiovascular
deconditioning; diuresis
with accompanying fluid, electrolyte, and
weight loss; muscle atrophy; and psychologic stress.
These changes begin on the first day of bed rest
and continue for the duration of therapy.
Sibai (2002) recommends rest at home and no activity limits for patients hospitalized with mild preeclampsia.
Women with mild preeclampsia
feel reasonably well; boredom from activity
restriction is therefore common. Diversionary activities, visits from
friends, telephone conversations, and creation
of a comfortable and convenient environment are just a few ways of
coping with this boredom (see Self-Care
box). Gentle exercise (e.g., range of motion,
stretching, Kegel exercises, pelvic tilts) is important in maintaining muscle tone, blood flow, regularity
of bowel function, and a sense of well-being (Maloni,
1998). Relaxation techniques can help
reduce the stress associated with the high risk condition and prepare
the woman for labor and birth.
Diet. Diet
and fluid recommendations are much the same as for healthy pregnant women. The efficacies of
a high-protein diet, avoidance of foods high in sodium, and forgoing additional
salt at the table have
not been proven. Therefore Sibai (2002) recommends a regular diet with no salt restriction. Because pregnant women with hypertension have a lower plasma volume
than do normotensive women, sodium
restriction is not necessary.
Women need salt for maintenance of blood volume and placental perfusion. The exception may be the woman with chronic hypertension that was
successfully controlled with a
low-salt diet before the pregnancy. Adequate
fluid intake helps maintain optimum fluid volume and aids in renal perfusion and filtration. The
nurse uses assessment data
regarding the woman's diet to counsel
her as needed in areas of deficiency (see Self-Care box).
Successful home
care requires the woman to be well educated
about preeclampsia and motivated to follow the plan of care. She must also be reliable about
keeping appointments. The effects of illness, language, age, culture, beliefs, and support systems must be considered.
The woman's support
systems must be mobilized and involved
in planning and implementing her care (see Plan of
Care).
Patient Instructions for Self-Care 1.
Assessing and Reporting Clinical Signs of Preeclampsia Report
immediately any increase in your blood pressure, protein in urine, weight
gain greater than 1 lb/wk, or edema. Take your
blood pressure on the same arm in a sitting position each time for consistent
and accurate readings. Support arm on a table in a horizontal position at
heart level. Use the same
scale, wearing the same clothes, at the same time each day, after voiding,
before breakfast, for reliable daily weights. Dipstick test
your clean-catch urine sample to assess proteinuria;
report frequency or burning on urination. Report to your
health care provider if proteinuria is +2 or more
or if you have a decrease in urine output. Assess your
baby's activity daily. Decreased activity (three or fewer movements per hour)
may indicate fetal compromise and should be reported. It is
important to keep your scheduled prenatal appointments so that any changes in
you or your baby's condition can be detected. Keep a daily
log or diary of your assessments for your home health care nurse, or bring it
with you to your next prenatal visit. 2.
Coping with Bed Rest In bed, lie on
your side. This allows more blood to get to your uterus (womb) and baby. The
bed or sofa should be near a window and a bathroom. Increase your
fluid intake to 8 glasses/day and add roughage (bran, fruits, leafy vegetables) to your diet to decrease constipation.
Keep a bowl of fruit and a large container full of water close by. Include
diversionary activities, such as puzzles, reading, and crafts, to reduce
boredom. Place a box or table within reach to store magazines, books,
telephone, etc. Do gentle
exercises, such as circling your hands and feet or gently tensing and
relaxing arm and leg muscles. This improves muscle tone, circulation, and
sense of well-being. Encourage
family participation in your care. Have
significant others assist you with care of the house, children, etc. Use relaxation
to help cope with stress. Relax your body one muscle at a time, or imagine
some pleasant scene, word, or image. Soothing music can also help you relax. 3.
Nutrition Eat a
nutritious, balanced diet (60 to 70 g protein, 1200 mg calcium, and adequate
zinc, magnesium, and vitamins). Consult with registered dietitian on the diet
best suited for you as an individual. There is no
sodium restriction; however, consider limiting excessively salty foods
(luncheon meats, pretzels, potato chips, pickles, sauerkraut). Eat foods with
roughage (whole grains, raw fruits, and vegetables). Drink six to
eight 8-oz glasses of water per day. Avoid alcohol
and limit caffeine intake. |
Severe preeclampsia
and HELLP syndrome
If the woman's condition worsens or
she already has severe preeclampsia
or HELLP syndrome and is critically ill, she should receive appropriate management (usually in a tertiary
care center), ranging from immediate birth to conservative management of the pregnancy (Leicht
& Harvey, 1999). Important
components of management include the administration
of magnesium sulfate as prophylaxis against
seizures and an antihypertensive agent if diastolic blood pressure is higher than 100 to 110 mm Hg.
Antepartum
care focuses on stabilization and preparation for birth. The woman may be admitted to an antepartum or a labor and birth unit, depending on the hospital. If the woman's condition is severe, she
may be placed in an obstetric critical care
unit or a medical intensive care unit (if an obstetric critical care unit is
not available) for any necessary hemodynamic monitoring. Maternal and fetal surveillance,
patient education regarding the disease process, and supportive measures
directed toward the woman and her family are
initiated. Assessments include
review of the cardiovascular system, pulmonary system, renal system, hematologic system, and CNS. Fetal assessments for well-being (e.g., NST, BPP, Doppler velocimetry) are important because of the potential for hypoxia
related to uteroplacental insufficiency. Baseline laboratory assessments include metabolic studies
for liver enzyme (AST, ALT, LDH) determination, complete blood count
with platelets, coagulation profile to assess for DIC, and electrolyte studies to establish renal functioning.
Weight is measured on admission and
every day thereafter. An indwelling urinary catheter facilitates monitoring of
renal function and effectiveness of therapy. If appropriate, vaginal examination may be done to check for cervical changes.
Abdominal palpation establishes uterine tonicity and fetal size, activity, and
position. Electronic monitoring to
determine fetal status is initiated at least once a day. The nurse's skill
in implementing the techniques described here can be reassuring to the woman and her family. The woman's room must be close to staff and
emergency drugs, supplies, and
equipment. Noise and external stimuli must be
minimized. Seizure precautions are taken (
·
Environment - Quiet - Nonstimulating - Lighting subdued ·
Seizure precautions - Suction equipment
tested and ready to use - Oxygen
administration equipment tested and ready to use ·
Call button within easy reach ·
Emergency medication tray immediately accessible - Hydralazine and magnesium sulfate in or adjacent to woman's room - Calcium gluconate immediately available ·
Emergency birth pack accessible |
Bed rest is
commonly ordered. The nurse's ingenuity may be called on to help the woman cope physically and
psychologically with the side effects of immobility
and an environment limited in stimuli and
support. Thromboembolic events, a risk factor during
normal pregnancy, pose an even
greater risk with preeclampsia (see Plan of Care).
Intrapartum nursing care of the woman with severe preeclampsia
or HELLP syndrome involves continuous monitoring
of maternal and fetal status as labor progresses. The assessment and prevention of tissue hypoxia and
hemorrhage, both of which can lead to
permanent compromise of vital organs, continue throughout the intrapartum and postpartum
periods (Leicht & Harvey, 1999).
Magnesium sulfate. One
of the important goals of care
for the woman with severe preeclampsia is prevention or control of convulsions. Magnesium sulfate
(MgSO4) is the drug of choice in the prevention and treatment of convulsions caused by preeclampsia
or eclampsia (ACOG, 1996). Benefits of magnesium sulfate therapy include
an increase in uterine blood flow to protect the fetus and an increase in prostacyclins to prevent uterine vasoconstriction (Gilbert & Harmon, 1998).
Magnesium sulfate is administered as
a secondary infusion to the main intravenous
(IV) line (e.g., piggybacked) by volumetric infusion pump. An initial loading
dose of 4 to 6 g of magnesium sulfate per protocol or physician's order
is infused over 20 to 30 minutes. This dose is followed by a maintenance dose of magnesium sulfate that is diluted in an IV solution per physician's order
(e.g., 40 g of magnesium sulfate in
1000 ml of lactated Ringer's solution) and administered by infusion pump at 1
to 3 g/hr (Gilbert & Harmon, 1998; Mandeville & Troiano, 1999). This dose
should maintain a therapeutic serum magnesium level of 4 to 8 g/dl.
Serum magnesium levels are obtained after
the patient has received magnesium sulfate for 4 to 6 hours. The infusion rate is adjusted to maintain the therapeutic level (Sisson & Sauer, 1996) (
Magnesium Sulfate Administration PATIENT AND FAMILY TEACHING Explain
technique, rationale, and reactions to expect • Route and rate • Purpose of "piggyback" Reasons
for use • Tailor information to patient's
readiness to learn • Explain it is to prevent disease progression • Explain it is to prevent seizures Reactions
to expect from medication •
Initially patient will feel flushed, hot, sedated,
nauseated, especially
during the bolus • Sedation will continue Monitoring to anticipate • Maternal: blood pressure, pulse, DTRs,
level of consciousness, urine output (indwelling
catheter), presence of headache, visual disturbances, epigastric
pain • Fetal: FHR and activity ADMINISTRATION • Verify physician order • Position woman in side-lying
position • Prepare solution and administer with an infusion
control device (pump) • Piggyback a solution of 40 g
magnesium sulfate in 1000 ml lactated Ringer's solution with an infusion control device at the ordered rate: loading dose—initial
bolus of 4 to 6 g over 15 to 30 min; maintenance dose—1 to 3 g/hr MATERNAL
AND FETAL ASSESSMENTS •
Monitor blood pressure, pulse, respiratory rate,
FHR, and contractions
every 15 to 30 min, depending on patient condition • Monitor intake and output, proteinuria, DTRs, presence of headache, visual disturbances, level of
consciousness and epigastric
pain at least hourly • Restrict hourly fluid intake
to a total of 100 to 125 ml/hr; urinary output should be at least 30 ml/hr REPORTABLE
CONDITIONS • Blood pressure: systolic
>160 mm Hg, diastolic >110 mm Hg, or both • Respiratory rate: <12
breaths/min • Urinary output <30 ml/hr • Presence of headache, visual
disturbances, or epigastric pain • Increasing severity or loss of DTRs;
increasing edema, proteinuria • Any abnormal laboratory values
(magnesium levels, platelet
count, creatinine clearance, levels of uric acid, AST, ALT, prothrombin
time, partial thromboplastin
time, fibrinogen, fibrin split
products) • Any other significant change in maternal or fetal
status EMERGENCY
MEASURES • Keep emergency drug tray at
bedside with calcium gluconate and intubation
equipment • Keep side rails up • Keep lights dimmed and
maintain a quiet environment DOCUMENTATION • All of the above |
Intramuscular (IM) magnesium sulfate
is seldom used because absorption rate cannot
be controlled, injections are painful,
and tissue necrosis may occur. However, the IM route may be used with
some women who are being transported to a
tertiary care center. The IM dose is 4 to 5 g given in each buttock, a total of 10 g (with 1% procaine possibly being added to the solution to reduce
injection pain), and can be repeated
at 4-hour intervals. Z-track technique
should be used for the deep IM injection, followed by gentle massage at the site.
Magnesium
sulfate interferes with the release of acetylcholine at the synapses, decreasing neuromuscular irritability, depressing cardiac conduction, and
decreasing CNS irritability. Because magnesium
circulates free and unbound to protein and
is excreted in the urine, accurate recordings
of maternal urine output must be obtained. Diuresis is an excellent prognostic
sign; however, if renal function declines, all of the magnesium sulfate will
not be excreted and can cause magnesium
toxicity.
Serum magnesium
levels are obtained on the basis of the woman's response and if any signs of toxicity are present. Early
symptoms of toxicity include nausea, a feeling of warmth, flushing, muscle weakness, decreased
reflexes, and slurred speech.
NURSE ALERT Loss
of patellar reflexes, respiratory depression, oliguria, and
decreased level of consciousness are signs of magnesium toxicity. Actions are
needed to prevent respiratory or cardiac arrest. If magnesium toxicity is
suspected, the infusion should be discontinued immediately. Calcium gluconate, the antidote for magnesium sulfate, may also be ordered
(10 ml of a 10% solution, or 1 g) and given by slow IV push (usually by the physician) over at least 3
minutes (Sibai, 2002) to avoid undesirable reactions such as arrhythmias, bradycardia,
and ventricular fibrillation.
NURSE
ALERT Because magnesium sulfate is also a tocolytic agent, its use may increase the duration of
labor. A preeclamptic woman receiving magnesium sulfate may need augmentation with oxytocin during labor. The amount of oxytocin
needed to stimulate labor
may be more than that needed for a woman who is not on magnesium sulfate.
Control
of blood pressure. For the severely hypertensive preeclamptic woman, antihypertensive medications may be ordered to lower the diastolic blood
pressure. Initiation of antihypertensive therapy reduces maternal morbidity and
mortality rates associated with left ventricular failure and cerebral hemorrhage. Because a degree of maternal hypertension is necessary to maintain uteroplacental perfusion, antihypertensive therapy must not
decrease the arterial
pressure too much or too rapidly. The target range for the diastolic pressure is therefore 90 to
100 mm Hg (Leicht & Harvey, 1999).
IV hydralazine remains the antihypertensive agent of choice for the treatment of hypertension in severe preeclampsia.
IV labetalol hydrochloride and oral methyldopa and nifedipine are also
used (Cunningham et al., 2001; Sisson
& Sauer, 1996). The choice of agent used depends on patient response
and physician preference. Table 5 compares
antihypertensive agents used to treat hypertension in pregnancy.
Table 5 Pharmacologic
Control of Hypertension in Pregnancy
ACTION |
TARGET TISSUE |
EFFECTS |
NURSING ACTIONS |
|
MATERNAL |
FETAL |
|||
HYDRALAZINE (APRESOLINE, NEOPRESOL) |
||||
Arteriolar vasodilator |
Peripheral arterioles: to decrease muscle tone, decrease peripheral
resistance; hypothalamus and medullary vasomotor
center for minor decrease in sympathetic tone |
Headache, flushing, palpitation, tachycardia, some decrease in uteroplacental blood flow, increase in heart rate and cardiac
output, increase in oxygen consumption, nausea and vomiting |
Tachycardia; late decelerations and bradycardia
if maternal diastolic pressure <90 mm Hg |
Assess for effects of medications, alert mother (family) to expected
effects of medications, assess blood pressure frequently because precipitous
drop can lead to shock and perhaps abruption placentae;
assess urinary output; maintain bed rest in a lateral position with side
rails up; use with caution in presence of maternal tachycardia |
LABETALOL HYDROCHLORIDE (NORMODYNE) |
||||
|
|
Peripheral arterioles (see hydralazine) |
|
|
β-blocking agent causing vasodilation
without significant change in cardiac output |
|
Minimal: flushing, tremulousness; minimal
change in pulse rate |
Minimal, if any |
See hydralazine;
less likely to cause excessive
hypotension and tachycardia; less rebound hypertension than hydralazine |
METHYLDOPA (ALDOMET) |
||||
Maintenance therapy if needed: 250-500 mg orally every 8 hr (a2-receptor agonist) |
Postganglionic nerve endings: interferes with chemical neurotransmission to reduce
peripheral vascular resistance, causes CNS sedation |
Sleepiness, postural hypotension,
constipation; rare: drug-induced fever in
1% of women and positive
Coombs' test result in 20% |
After 4 mo maternal therapy, positive Coombs' test result in infant |
See hydralazine |
NIFEDIPINE (PROCARDIA) |
||||
Calcium channel blocker |
Arterioles: to reduce systemic vascular resistance by relaxation
of arterial smooth muscle |
Headache, flushing; possible potentiation
of effects on CNS if administered concurrently with magnesium sulfate, may
interfere with labor |
Minimal |
See hydralazine;
use caution if patient also getting magnesium sulfate |
Eclampsia
The convulsions that occur in eclampsia are frightening to observe. Increased
hypertension and tonic contraction of all
body muscles (seen as arms flexed, hands clenched, legs inverted) precede the tonic-clonic
convulsions (Fig. 5). During this stage, muscles alternately relax and
contract. Respirations are halted and then
begin again with long, deep, stertorous
inhalations. Hypotension follows, and coma ensues. Nystagmus and muscular twitching
persist for a time. Disorientation and amnesia cloud the immediate recovery. Oliguria and anuria are notable. Seizures may recur within minutes of the first convulsion, or the woman may never have another. Eclamptic
seizures can result in tissue damage
to the woman during the convulsion, especially if she is in a bed with unpadded side rails. During
the convulsion the pregnant woman and fetus are not receiving oxygen, so eclamptic
seizures produce a marked metabolic insult
to both the woman and the fetus.
Fig. 5 Eclampsia (convulsions or seizures)
Immediate care. The
immediate care during a convulsion
is to ensure a patent airway (see Emergency box). When convulsions occur, the woman is turned onto her side to prevent aspiration of vomitus and supine hypotension
syndrome. After the convulsion ceases, food and fluid are suctioned from the
glottis or trachea, and oxygen is administered
by face mask. Magnesium sulfate (e.g., 2 g IV push over 3 minutes) or other anticonvulsant is given as ordered (Leicht & Harvey, 1999). If an IV infusion is not in place, one is begun with a large-bore needle.
Time, duration, and description of
convulsions are recorded, and any
urinary or fecal incontinence is noted. The fetus is monitored for adverse effects. Transient fetal bradycardia
and decreased FHR variability are common.
Aspiration is a leading cause of
maternal morbidity and mortality after eclamptic
seizure. After initial stabilization and
airway management, the nurse should anticipate orders for a chest radiograph and possibly arterial blood gases to rule out the possibility of aspiration.
A rapid
assessment of uterine activity, cervical status, and fetal status is performed after a convulsion.
During the convulsion, membranes may have ruptured; the cervix may have dilated because the uterus becomes hypercontractile and hypertonic; birth may be imminent. If not, once a woman's seizure activity and blood pressure are controlled, a decision should be made regarding whether birth
should take place. The more serious the condition of the
woman, the greater the need to proceed to
birth. The route of birth—induction of labor versus cesarean
birth—depends on maternal and fetal
condition. If fetal lungs are not mature and the birth can be delayed
for 48 hours, steroids such as betamethasone may be
given to the woman.
The woman may
have been incontinent of urine and stool during the convulsion; she will need assistance with hygiene and a change of gown. Oral care with a soft toothbrush may be of comfort.
Immediately
after a seizure, the woman may be confused and can be combative, necessitating
the temporary use of restraints. It may take several hours for the woman to regain her usual level of mental functioning. The health care
provider explains procedures briefly and quietly. The woman is never left alone. The family is also kept informed of management, rationale for treatment, and
the woman's progress.
Laboratory
tests are ordered to assess for HELLP syndrome and to have blood typed and crossmatched
for administration of
packed red blood cells as needed. Blood must be available for emergency transfusion because abruptio placentae,
with accompanying hemorrhage and shock,
often occurs in women with
eclampsia. Other tests include determination of electrolyte
levels, liver function battery,
and complete hemogram and clotting profile, including platelet count and fibrin split product levels (to assess for
DIC).
EMERGENCY Eclampsia TONIC-CLONIC
CONVULSION SIGNS Stage of invasion: 2 to 3 sec,
eyes are fixed, twitching of facial muscles occurs Stage of
contraction: 15 to 20 sec, eyes protrude and are bloodshot, all body muscles are in tonic contraction Stage of convulsion: muscles
relax and contract alternately (clonic), respirations are halted and then begin again with long, deep, stertorous
inhalation, coma ensues INTERVENTION Keep airway
patent: turn head to one side, place pillow under one shoulder or back if possible Call for assistance Protect with side rails up Observe and record convulsion activity AFTER
CONVULSION OR
SEIZURE Do not leave
unattended until fully alert Observe for postconvulsion coma, incontinence Use suction
as needed Administer oxygen via face mask
at 10 L/min Start IV
fluids and monitor for potential fluid overload Give
magnesium sulfate or other anticonvulsant drug as ordered Insert
indwelling urinary catheter Monitor
blood pressure Monitor
fetal and uterine status Expedite
laboratory work as ordered to monitor kidney function, liver function,
coagulation system, and drug levels Provide
hygiene and a quiet environment Support and
keep woman and family informed Be prepared for delivery
when woman is in stable condition |
Postpartum nursing care
After birth the symptoms of preeclampsia or eclampsia resolve quickly, usually within 48 hours. The hematopoi-etic and hepatic complications of HELLP syndrome may persist longer. These patients often show an
abrupt decrease in platelet count, with a concomitant increase in LDH and AST
levels, after a trend toward normalization of values has begun. Generally the laboratory abnormalities seen
with HELLP syndrome resolve in 72 to 96 hours.
The nursing
care of the woman with hypertensive disease
differs from that required in the usual postpartum period in a number of respects. The following variations in the nursing process are described.
Careful assessment of the woman with
a hypertensive disorder continues throughout
the postpartum period. Blood pressure
is measured at least every 4 hours for 48
hours or more frequently as the woman's condition warrants. Even if no
convulsions occurred before the birth, they
may occur within this period. Magnesium sulfate infusion may be
continued 12 to 24 hours after the birth. Assessments
for effects and side effects continue until the medication is discontinued.
NURSE
ALERT! The woman is at
risk for a boggy uterus and
a large lochial flow as a result of the magnesium
sulfate therapy. Uterine tone and lochial flow must
be monitored closely.
The preeclamptic woman is unable to tolerate excessive postpartum blood loss because of hemoconcentration. Oxytocin or
prostaglandin products are used to control bleeding.
Ergot products (e.g., Ergotrate, Methergine)
are contraindicated because they can
increase blood pressure.
The woman is
asked to report symptoms such as headaches and blurred vision. The nurse
assesses affect, level of consciousness, blood pressure, pulse, and
respiratory status before
an analgesic is given for headache. Magnesium sulfate potentiates the action of narcotics, CNS depressants, and calcium-channel blockers; these drugs must be
administered with caution.
The woman may need to continue an antihypertensive
medication regimen if her diastolic blood pressure
exceeds 100 mm Hg at discharge.
The woman's and family's responses
to labor, birth, and the neonate are
monitored. Interactions and involvement in the care of the neonate are encouraged to the extent that the woman and her family desire. In addition,
the woman and her family need
opportunities to discuss their emotional
response to complications. The nurse provides information concerning the prognosis. Preeclampsia
and eclampsia do not necessarily recur in
subsequent pregnancies (recurrence rate is
approximately 30%), but prenatal care
is essential.
Prevention
Early prenatal
care for identification of women at risk and early detection of development of preeclampsia is the best prevention because there is no
known etiology for preeclampsia. There have been numerous clinical trials studying various methods for prevention. These interventions included the use of calcium, magnesium,
zinc, fish oil dietary
supplementation, and possibly exercise (see Research box). Antihypertensive agents, diuretics, and low-salt diets have also been studied (Mattar & Sibai, 1999; Sibai, 1998). None of these interventions demonstrated a benefit in reducing the incidence or severity of preeclampsia in healthy pregnant women. Nurses should be aware of what strategies are being studied and
use the most reliable evidence about
the results so that they can counsel pregnant women about interventions that
are likely to be beneficial. One resource is the Cochrane Pregnancy and Childbirth Database (Enkin
et al., 1995).
RESEARCH Exercise and Blood Pressure in Pregnancies with
Risk of Hypertension Regular
exercise during pregnancy may reduce nausea and fatigue and may improve ease of labor and birth outcomes. Moderate exercise is encouraged in low
risk pregnancies, but it is still customary to limit exercise when there is a risk of hypertensive
disorder of pregnancy. The rationale
behind this restriction has been
that vascular function is disrupted by inflammation, which decreases perfusion to the placenta and to maternal
kidneys, and that exercise would increase the
blood pressure and the inflammation. However, there is evidence that
exercise by at risk pregnant women may enhance vasodilation
and perfusion and tend to decrease the likelihood of preeclampsia. To
prospectively study whether moderate exercise during pregnancy lowers blood pressure, a research team recruited 16
pregnant women before 14 weeks of
gestation. All the women had a history of mild hypertension, gestational
hypertension, or family history of hypertension and were thus at risk for pregnancy-induced
hypertension. Researchers randomly assigned
half of the women to a group that engaged in supervised 45-minute
treadmill sessions, three times a week,
from gestational weeks 18 to 28; the
other half were placed in a control group. Results showed that both groups had similar body fat and similar daily total energy expenditures.
Systolic and diastolic blood pressures decreased in the treatment group and increased in the control group, although none of the changes achieved
significance. The trend was strongest for diastolic pressures. One subject in each group developed gestational
hypertension, and both delivered at term. Other outcomes were not noted. IMPLICATIONS FOR PRACTICE Regular,
moderate exercise appears to be acceptable, possibly even desirable, in
pregnancies of women at risk
for pregnancy-induced hypertension. Exercise appears to have more influence on lowering blood pressure than either body fat composition or overall daily physical
activity. Until research provides more evidence
about exercise in these high risk women, nurses should ask all women at risk for pregnancy-induced
hypertension about their exercise habits, encourage
them to discuss an acceptable level of exercise with the physician or
nurse-midwife, and monitor them closely for signs of hypertension at each prenatal visit. Source: Yeo, S., et al.
(2000). Effect of exercise in
pregnant women with a risk of gestational
hypertensive disorders. J Reprod Med, 45(4),
293-298. |
Evaluation
Evaluation of the effectiveness of
care of the woman with preeclampsia is based on the expected outcomes.
PLAN OF CARE
Mild Preeclampsia:
Home Care
NURSING DIAGNOSIS Risk
for injury related to signs of preeclampsia
Expected Outcomes Patient will demonstrate ability to assess self and
fetus for signs of worsening preeclampsia; no adverse
sequelae will occur as result of preeclamptic
condition.
Nursing Interventions/Rationales
Review warning
signs/symptoms of preeclampsia to ensure adequate knowledge base exists for decision
making.
Assess home
environment, including woman's ability to assume self-care responsibilities, support
systems, language, age, culture, beliefs, and effects of illness, to determine if home care is viable option.
Teach woman how
to do a self-assessment for clinical signs of preeclampsia
(take and record blood pressure, measure urine protein, maintain daily weight
log, assess edema formation, assess fetal activity) to provide immediate evidence of a worsening condition.
Teach woman to
report any increases in blood pressure, +2 proteinuria,
weight gain greater than 1 lb per week, presence of edema, and decreased fetal
activity to her health care provider immediately to prevent worsening of preeclamptic
condition.
Teach woman
about use of rest and relaxation as palliative treatment options to decrease blood pressure and promote diuresis.
NURSING DIAGNOSIS Fear/anxiety related to preeclampsia and its effect on the fetus
Expected Outcome Patient's feelings and symptoms of fear/anxiety will
decrease/ease.
Nursing Interventions/Rationales
Provide a calm, soothing atmosphere and teach family to provide
emotional support to facilitate coping.
Encourage
verbalization of fears to decrease intensity of emotional response.
Involve woman
and family in the management of her preeclamptic
condition to promote a greater sense of control.
Help woman
identify and use appropriate coping strategies and support systems to reduce
fear/anxiety.
Explore use of
desensitization strategies such as progressive muscle relaxation, visual
imagery, or thought stopping to reduce fear-related emotions and related
physical symptoms.
NURSING DIAGNOSIS Deficient diversional
activity related to imposed bed rest.
Expected Outcome Patient will verbalize diminished feelings of
boredom.
Nursing Interventions/Rationales
Assist woman to
explore creatively personally meaningful activities that can be pursued from
the bed to ensure activities that have meaning, purpose, and value to the
individual.
Maintain
emphasis on personal choices of woman to promote control and minimize
imposition of routines by others.
Evaluate what
support and system resources are available in the environment to assist in
providing diversional activities.
Explore ways for
woman to remain an active participant in home management and decision making to
promote control.
Engage support
of family and friends in carrying out chosen activities and making necessary
environmental alterations to ensure success.
Teach woman
about stress management and relaxation techniques to help manage tension of
confinement
PLAN OF CARE
Severe Preeclampsia:
Hospital Care
NURSING DIAGNOSIS Risk for injury to woman and fetus related to CNS
irritability
Expected
Outcome Patient will show diminished signs of CNS
irritability (e.g., DTRs 2+, absence of clonus) and have no convulsions.
Nursing
Interventions/Rationales
Establish
baseline data (e.g., DTRs, clonus)
to use as basis for evaluating
effectiveness of treatment.
Administer IV
MgS04 per physician's orders to
decrease hy-perreflexia and minimize risk of
convulsions.
Monitor maternal
vital signs, FHR, urine output, DTRs, IV flow rate,
and serum levels of MgSO4 to
assess for and prevent MgSO4 toxicity (e.g., depressed respirations, oliguria, sudden drop in blood pressure, hyporeflexia, fetal distress).
Have calcium gluconate at bedside if needed as antidote for MgSO4 toxicity.
Maintain a
quiet, darkened environment to
avoid stimuli that may precipitate seizure activity.
NURSING
DIAGNOSIS Ineffective tissue perfusion related to preeclampsia
secondary to arteriolar vasospasm
Expected Outcome Patient
will exhibit signs of increased vasodilation (i.e., diuresis, decreased edema, weight loss).
Nursing
Interventions/Rationales
Establish
baseline data (i.e., weight, degree of edema) to use as basis for evaluating
effectiveness of treatment.
Administer
intravenous magnesium sulfate per physician order, which serves to relax vasospasms
and increase renal perfusion.
Place woman on
bed rest in a side-lying position to
maximize uteroplacental blood flow, reduce blood
pressure, and promote diuresis.
Monitor intake
and output, edema, and weight to
assess for evidence of vasodilation and increased
tissue perfusion.
NURSING
DIAGNOSES Risk for
excess fluid volume to increased sodium
retention secondary to administration of MgSO4
impaired gas exchange related to
pulmonary edema secondary to increased vascular resistance
decreased cardiac output related to use of
antihypertensive drugs
injury to fetus related to uteroplacental insufficiency secondary to use antihypertensive
medications
Expected Outcomes Patient
will exhibit signs of normal fluid volume (i.e., balanced intake and output,
normal serum creatinine levels, normal breath
sounds); adequate oxygenation (i.e., normal respirations, fully oriented to
person, time, and place); normal range of cardiac output (i.e., normal pulse
rate and rhythm); and fetal well-being (i.e., adequate fetal movement, normal
FHR).
Nursing
Interventions/Rationales
Monitor woman
for signs of fluid volume excess (increased edema, decreased urine output,
elevated serum creatinine level, weight gain, dyspnea, crackles) to detect potential complications.
Monitor woman
for signs of impaired gas exchange (i.e., increased respirations, dyspnea, altered blood gases, hypox-emia) to detect potential complications.
Monitor woman for signs of decreased cardiac output (i.e., altered pulse
rate and rhythm) to
detect potential complications.
Monitor fetus for signs of difficulty (i.e., decreased fetal activity,
decreased FHR) to
prevent complications.
Record findings
and report signs of increasing problems to physician to enable timely interventions