HYPERTENSION IN PREGNANCY
PRE-ECLAMPSIA
Patricia Hartley, RNC, MSN is the Education/Employee Health
Coordinator at Lake
City Medical
Center. She received her
Masters Degree in Perinatal Nursing from Indiana University/Purdue University
at Indianapolis.
She has 4 years experience in Staff and Patient Education; 28 years clinical
experience that include almost 20 years of Neonatal Intensive Care. She is
certified in High Risk Neonatal Nursing and Fetal Monitoring.
PURPOSE/GOALS
This
course is intended to update the healthcare professional on the identification
and treatment of Hypertension in pregnancy.
OBJECTIVES:
Upon completion of this module the learner will:
1. identify the ACOG classifications
for hypertensive states of pregnancy,
2. describe the characteristics of
pre-eclampsia,
3. describe the incidence of
pre-eclampsia,
4. list potential causes of
pre-eclampsia, and
5. identify essential aspects of
treatment.
INTRODUCTION
Hypertensive
disorders are the most common medical complication of pregnancy affecting 5 to
10 percent of all pregnancies.
Approximately 30 percent of hypertensive disorders in pregnancy are due to
chronic hypertension and 70 percent are due to gestational
hypertension/pre-eclampsia. The spectrum of the disease ranges from mildly elevated
blood pressure with minimal clinical significance to severe hypertension and
multi-organ dysfunction. Hypertensive disorders remain a major cause of
maternal and perinatal morbidity and mortality. Pre-eclampsia, known also by
such names as acute hypertension of pregnancy, toxemia, and pregnancy-induced
hypertension, is a progressive disease that becomes clinically apparent in the
last trimester of pregnancy. It begins as mild and proceeds to severe
pre-eclampsia. PIH (pregnancy-induced hypertension) is characterizes by
hypertension, proteinuria, and edema.
PIH
is classified as mild or severe pre-eclampsia based on severity of symptoms. It
is classified as eclampsia once convulsions occur, or as HELLP (H: hemolysis,
EL: elevated liver enzymes, and LP: low platelet count) Syndrome when
pre-eclampsia and eclampsia have increased in severity. The cause is unknown
but the pathophysiology is caused by arterial vasospasm, which causes decreased
organ perfusion, resulting in the symptoms of the disorder. It is cured by
termination of the pregnancy. It is the leading cause of maternal death and is
particularly troubling because it can strike without warning.
The
objective is identification of high-risk patients and early symptoms of the
milder form of the disease, followed by preventive measures, to avoid the
severe forms of pre-eclampsia and its complications. The most common severe
complications are:
Maternal
cerebrovascular accident or cerebral edema
Placental
abruption with or without hyofibrinogenemia or disseminated intravascular
coagulation (DIC)
Fetal death
CLASSIFICATION OF PREGNANCY
RELATED HYPERTENSION
The
definition of hypertension relating to pregnancy can be confusing and often
misleading. The term toxemia of pregnancy was used for a number of years,
meaning anything from pre-eclampsia and eclampsia to essential hypertension.
Currently the term pregnancy-induced hypertension may be misused to describe
various conditions involving pregnancy and hypertension. The American College
of Obstetricians and Gynecologists (ACOG) has classified the hypertension
states of pregnancy as follows:
Gestational
edema:
Gestational edema is the occurrence of a general and
excessive accumulation of fluid in the tissues of greater than 1+ pitting edema
after 12 hours of rest in bed, or of a weight gain of 5 pounds or more in one
week due to the influence of pregnancy.
Gestational
proteinuria:
Gestational proteinuria is the presence of proteinuria
during or under the influence of pregnancy in the absence of hypertension,
edema, renal infection or known intrinsic renal vascular cause.
Pregnancy-induced
hypertension or Gestational hypertension:
Pregnancy-induced hypertension or Gestational
hypertension is the development of hypertension during pregnancy or within the
first 24 hours postpartum in a previously normotensive woman.
Pre-eclampsia:
Pre-eclampsia is the development of hypertension with
proteinuria, edema or both due to pregnancy or the influence of a recent
pregnancy. It begins as mild and can progress to severe. It occurs after
the 20th week of gestation but may develop before this time in the
presence of trophoblastic disease (hydatidiform mole molar pregnancy).
Pre-eclampsia is predominately a disorder of primigravida (first pregnancy)
Eclampsia:
Eclampsia is the occurrence of one or more convulsions not
attributable to other cerebral disorders in a patient with pre-eclampsia.
Superimposed
pre-eclampsia or eclampsia:
Superimposed pre-eclampsia or eclampsia is the development
of pre-eclampsia or eclampsia in a patient with chronic hypertensive, vascular
or renal disease. When the hypertension antedates the pregnancy as established
by previous blood pressure readings, a rise in the systolic pressure of 30 mm
Hg, a rise in diastolic pressure of 15 mm Hg and the development of
proteinuria, edema, or both are required during pregnancy to establish the
diagnosis.
Chronic
hypertensive disease:
Chronic hypertensive disease is the presence of persistent
hypertension of whatever cause before pregnancy or prior to the 20th
week of gestation or persistent hypertension beyond the 42nd day of
the postpartum period.
HELLP:
HELLP is a group of symptoms that occur in pregnant women,
who have hemolytic anemia, elevated liver enzymes, and low platelet counts. It
is a particularly severe form of pre-eclampsia.
CHARACTERISTICS
Pre-eclampsia
is characterized by hypertension and excessive weight gain caused by fluid
retention resulting in edema and proteinuria. Pre-eclampsia is seen most often
in the last 10 weeks of pregnancy, during labor, or in the first 12 to 24 hours
after delivery. Predisposing factors include:
Diabetes
Hypertensive or
renal disease
Hydatidiform
mole
Multiple pregnancy
Hydramnios.
Maternal age
o
Teenagers and
primigravidas are at risk for the development of this condition
o
The incidence of
pre-eclampsia also increases with advancing maternal age.
Eclampsia
is manifested by convulsions and coma. If prompt and intensive Antepartal care
is given to pregnant women eclampsia may be prevented.
Pre-eclampsia may be subdivided into mild or severe. The
distinction between the two is based on the severity of hypertension and
proteinuria as well as involvement of other organs. Close surveillance of
patients with pre-eclampsia is warranted as either type may progress to
fulminant disease. All women with suspected or diagnosed pre-eclampsia should
be instructed to report any symptoms. Women with mild pre-eclampsia may exhibit
an almost asymptomatic pregnancy. They may have little or nor peripheral edema
evident following bed rest. Their blood pressure may be 140/90 or more or about
30 mm Hg above their baseline systolic pressures and 15 mm Hg above their
baseline diastolic pressures. This is an important consideration, because a
young woman who may normally have a blood pressure of 90/60 would be
hypertensive at 120/80, which is a marked increase above her baseline norm.
Therefore, it is an essential part of the nursing assessment to obtain a
baseline blood pressure in early pregnancy. Urine testing may show a +1 or +2
albumin in a clean mid-stream specimen and 24 hour urine collection may contain
1 gram of protein.
Severe pre-eclampsia may develop suddenly. Edema becomes generalized and
readily apparent in face, hands, sacral area, lower extremities and the
abdominal wall. It is characterized by an excessive weight gain of more than
0-9 Kg (2 lbs.) over a couple of days to a week. Blood pressure is 160/100 or
higher, a dipstick albumin measure is +3 to +4, and a 24 hour urine protein is
> 5 grams. Other characteristic symptoms are frontal headaches, blurred
vision, nausea, vomiting, irritability, hyper-reflexia, cerebral disturbances,
oliguria (< 400 ml of urine in 24 hours), and finally epigastric pain. The
epigastric pain is often the sign of impending convulsion (eclampsia) and is
thought to be caused by increased vascular engorgement of the liver.
HELLP syndrome is a rare but severe complication of
pregnancy-induced hypertension. The diagnosis may be deceptive because blood
pressure measurements may only be marginally elevated. Hepatic damage may
result secondary to vasospasm, ischemia, and necrosis. The patient may
experience hemorrhagic necrosis along the edge of the liver, resulting in a
subcapsular hematoma. Rupture may occur if the hematoma is extensive. This is a
surgical emergency and must be dealt with immediately. Fortunately, it is an
extremely rare occurrence. More commonly, laboratory tests document a rise in
the SGOT, often without significant symptomatology in the patient. The
patient may present with signs of hemolysis which are:
- Bleeding
- Bruising
- Petechiae
Abnormal lab values that are elevated:
o AST
o ALT
o BUN
o Creatinine
o
SGOT
Signs
of impaired liver function:
o
Elevated liver
enzymes
o
Signs of malaise
o
Anorexia
o
Nausea and
vomiting
o
Jaundice
o
Epigastric pain.
o
Enlarged liver
o
Evidence of low
platelets.
Delivery
of the infant is essential because liver function rapidly deteriorates in this
condition. Hemorrhage may occur within the mothers liver. Permanent liver
damage may occur if delivery is delayed. A patient diagnosed with HELLP
Syndrome is automatically classified as having severe pre-eclampsia.
Differential diagnosis is difficult as HELLP may be confused with other medical
conditions especially in the face of normo-tension.
Blood
pressure determination requires consistency in measurement. A cuff too small or
too large may result in blood pressure readings that are inaccurately high or
low. Blood pressure in the arteries is affected by position. When sitting, the
pressure in the brachial artery is highest; and when lying on the right or left
side, it is lowest. Blood pressure taken while the woman is flat on her back
may be inaccurate especially toward the end of pregnancy. An elevated systolic
but normal diastolic pressure may indicate anxiety. In order to determine
hypertension in the mother, her baseline blood pressure must be known or blood
pressure elevations on two occasions 6 hours or more apart indicates
hypertension. Look for the systolic to rise 30 mmHg or more above the baseline;
the diastolic to rise 15 mmHg or more above the baseline; or any blood pressure
above 140/90 mmHg.
OTHER EFFECTS OF
PRE-ECLAMPSIA
Renal
Renal
function increases in normal pregnancy. Plasma blood volume normally increases
by 40% to 50% by the 30th week of gestation. The glomerular
filtration and renal plasma flow increase by 30% to 50% through the first
trimester. Serum BUN levels are decreased secondary to the increase in plasma
volume. Uric acid and creatinine clearance are increased due to the increased
glomerular filtration rate.
Subsequently,
the serum BUN, uric acid, and creatinine levels are decreased in pregnancy.
Capillary endotheliosis, a glomerular lesion, may develop, associated with
proteinuria. It causes partial obstruction and ischemia of the lumen. The
mechanism for the development of the lesion is not well understood; however, it
has been hypothesized that vasospasm in conjunction with increased
hypercoaguability in pregnancy precipitates the formation of fibrin-fibrinogen
immunoglobulins.
Plasma
volume, renal plasma flow, and the glomerular filtration rate decrease in
pre-eclampsia and may be dramatically decreased in chronic hypertension. This
is especially true if the underlying cause of chronic hypertension is renal
disease. Serum BUN, uric acid, and creatinine levels rise. Urine creatinine
clearance may be decreased. Urine output may fall to oliguric levels, possibly
reflective of severe regional vasospasm or volume depletion. Hematuria may be
present from red cell destruction, resulting in urine resembling cranberry
juice. Renal changes normally reverse in the postpartum period unless severe
renal cortical damage has occurred.
Uteroplacental
Vasospasm
and decreased blood flow are the changes that develop with problems of
uteroplacental perfusion. This may in turn lead to IUFD (intrauterine fetal
death), IUGR (intrauterine growth retardation), and oligohydramnios. The spiral
artery, which is the main connection from maternal circulation to the placental
intervillous space, is contracted in women with PIH. Lesions may develop that
impede uteroplacental circulation. The degree of involvement of these vessel
wall changes relates to the degree of hypertension. The result is a decrease in
placental perfusion.
Pulmonary
Pregnancy
normally causes a hormonally mediated decrease in colloid osmotic pressure
(COP). COP, reduced to a simplistic level, is the gradient by which fluid is
kept in the capillary space or moves into the interstitial space. Colloids are
protein molecules. The majority of plasma protein molecules are albumin,
followed by globulin and fibrinogen. Colloids do not cross uninjured
semipermeable membranes and therefore will travel from lower colloidal numbers
to higher colloidal numbers. COP plays a major role in keeping fluid inside the
capillary, thereby preventing the loss of fluid to the interstitial fluid.
`Clinically,
patients with pre-eclampsia are frequently noted to develop pulmonary edema.
Decreased COP values have been associated with the development of pulmonary
edema. It is believed that the lower COP is due to the damage to the
capillaries, allowing for the movement of serum proteins (colloids) across the
now permeable capillary wall and into either the interstitial spaces or the
urine.
Fluid
balance shifts accordingly, with plasma fluid volume moving from the
intravascular space to the interstitial space. It is important not to
give the patient high volumes of crystalloid solutions (e.g. Lactated Ringers
solution), which cause this movement. Even volumes of 125 to 150 ml/h can cause
this event. It has been shown that 1L of saline causes a 12% reduction of COP.
This change may persist for two to five days after fluid resuscitation.
Central
Nervous System
Central
nervous system changes range from mild to those associated with the high
maternal and fetal mortality as previously mentioned. The patient may have
scotomata, blurry or double vision, headache, hyperreflexia, clonus, altered
consciousness, convulsions, cerebral edema, or cerebral hemorrhage. Eclamptic
convulsions are perhaps the most disturbing CNS manifestation of pre-eclampsia
and remain the major cause of maternal mortality.
Cerebral
vascular resistance is increased, although cerebral blood flow remains the
same. The exact mechanism of cerebral edema is unclear. It may be caused by a
loss of cerebral autoregulation secondary to the hypertension, or it may be
associated with an eclamptic convulsion. It is recommended that crystalloid
infusion be closely monitored to decrease the occurrence of cerebral edema.
Radiologic studies may show evidence of cerebral edema and hemorrhagic lesions,
particularly in the posterior hemispheres, which may explain the visual
disturbances.
Hematologic
Hemoconcentration
in the pregnant patient with pre-eclampsia is a common occurrence. Hemoglobin
and hematocrit levels are usually above the normal pregnant values. There may
be a dramatic drop in hemoglobin and hematocrit when the patient mobilizes
extravascular fluid. The decrease may also be the result of red cell
destruction with HELLP.
Thrombocytopenia
has also been identified as a complication of pre-eclampsia. This may impact
clinical decision making in the care of the patient. Surgical risks are
increased in the patient who may not be able to coagulate rapidly. Anesthesia
may be limited to local for vaginal delivery or general for cesarean section.
Patients
may also exhibit signs of disseminating intravascular coagulation (DIC). These
symptoms include oozing of blood from puncture or surgical sites, decreased
fibrinogen levels, increased levels of fibrin-degradation products, and
prolonged thrombin time.
INCIDENCE
Pre-eclampsia occurs in about 7 percent of all pregnancies.
About 5 percent of first-time mothers and 1 to 2 percent of mothers having
subsequent pregnancies develop pre-eclampsia. Rates are increased if they had
pre-eclampsia in a previous pregnancy and if they had a diastolic blood
pressure reading from 100 to 110 mmHg early in pregnancy. Because of improved
Antepartal care, pre-eclampsia has declined considerably and eclampsia rarely
occurs.
ETIOLOGY
The
cause of pre-eclampsia and eclampsia is still unknown. The syndrome is characterized by vasoconstriction,
hemoconcentration and possible ischemic changes in the placenta, kidney, liver
and brain. The many factors that are believed to play a role include:
- Functioning pregnancy
- Environmental factors such as: climate and
socioeconomic status
- Diet
- Activity
- Health status.
- Uteroplacental ischemia
- Pre-pregnancy nutritional status.
Having high blood pressure for at least four years before
getting pregnant increases a womans chances of developing this dangerous
condition. In a study conducted by the National Institute of Child Health and
Human Developments (NICHD) Network of Maternal-Fetal Medicine Units it was
determined that protein in the urine very early in pregnancy increases the risk
of such adverse outcomes as giving birth prematurely, having a child who is
small for gestational age, or having an infant who would need to be admitted to
a newborn intensive care unit.
Women that
have protein in their urine prior to pregnancy, pre-eclampsia is defined as
having either an elevated level of SGOT (a liver enzyme) or worsening
hypertension together with worsening proteinuria, persistent severe headaches,
or stomach pain. It is no longer advised to restrict weight gain by restricting
calories in pregnancy. Salt restrictions have been lifted although women with
evident pitting edema may not be allowed to increase their salt intake.
OUTCOMES
Prenatal mortality associated with pre-eclampsia is
approximately 10% and that associated with eclampsia is 30%. When pre-eclampsia
is superimposed on hypertensive vascular disease the perinatal mortality rate
increases. Women who developed pre-eclampsia were more likely to develop
abruptio placenta. Abruptio Placentia is a detachment of the placenta from the
uterine wall, a potentially serious complication of pregnancy.
Infants born to women who went on to develop pre-eclampsia
are at increased risk of hemorrhaging while in the womb and to die shortly
before, during or after birth. At the time of delivery, the neonate may be
over-sedated because of medications administered to the mother. He may also
have hyper magnesia due to treatment of the mother with large doses of
magnesium sulfate.
MANAGEMENT
The management of the severely pre-eclamptic patient is
aimed at the prevention of convulsions by decreasing the blood pressure,
establishing adequate renal function, and continuing the pregnancy until the
fetus is mature.
The main cause of intrauterine death or SGA (small for gestational age) infants
is uteroplacental insufficiency, which causes decreased blood supply. All
patients with severe pre-eclampsia should be admitted and initially observed in
a labor and delivery unit. Routine management includes the following:
Bed
rest in the left lateral decubitus position increases renal and uterine blood
flow, which in turn may encourage diuresis and return of B/P to normal limits.
Fetal
well-being should be assessed daily by NST (non-stress test) and weekly
amniotic fluid index determinations.
Vital
signs are recorded regularly as is strict intake and output measurements.
Reflexes
should be monitored as well as signs of clonus (CNS hyperactivity).
Laboratory
assessments should include hemocrit, platelet count, serum creatinine,
aspratate aminotranferase (AST) and 24-hour urine for total protein. These
tests should be done daily or every other day.
An
ultrasound for fetal growth and amniotic fluid index should be performed every
two to three weeks.
Seizure precautions should be in place.
High Protein diet (1 gm/kg/day), a salt limitation is not
necessary.
Patient and family education should include:
o
Disorder progress
o
Consequences
o
Potential outcomes
o
Assessment and treatment procedures
o
Coping measures for
complete bed rest
o
Stress reduction
measures
o
Preparation for birth
Research is being conducted to determine if low-dose aspirin
would reduce the incidence of hypertension in women at risk for the condition.
Current medications include Magnesium Sulfate, sedatives like Valium or
Phenobarbital, and an antihypertensive like Apresoline.
The only cure for pre-eclampsia is termination of the
pregnancy. If the cervix is favorable for labor, induction should be
considered. A cesarean section should be done if induction fails, if the
womans condition worsens, or if fetal distress is noted.
Following delivery the symptoms diminish rapidly. The first
sign of recovery in the post-partum period is diuresis. Edema and proteinuria
usually disappear by the fifth post partum day. Complete recovery of
hypertension and signs of organ dysfunction associated with pre-eclampsia
typically disappear within six weeks of delivery. However, women with
early-onset pre-eclampsia or pre-eclampsia in more than one pregnancy are more
likely to develop hypertension later in life.
MAGNESIUM SULFATE
Magnesium
sulfate is the agent of choice in the United States for prevention and
control of maternal eclamptic seizures. Magnesium Sulfate is not an
antihypertensive agent. It works by reducing acetylcholine release in the
central nervous system thereby interfering with and decreasing the number of
impulses through the ganglia. It also decreases the excitability of muscle
fibers to direct stimulation and relaxes smooth muscle.
Magnesium sulfate does cause an initial transient decrease
in MAP (mean arterial pressure) for patients with severe pre-eclampsia;
however, this response is short lived and not carried on with continuous infusion.
In the treatment and control of seizure activity in
pregnancy-induced hypertension and pre-eclampsia, MgS04 competes with the
calcium necessary for conduction of nerve impulses by blocking the release of
acetylcholine at the synapses, thus decreasing neuromuscular irritability. The
tocolytic effect of interfering with uterine smooth muscle contractions is not
well understood. It is thought that MgSO4 interferes with the transport of
calcium so that less calcium is available for muscle contractions.
Magnesium sulfate is administered as
a bolus of 4 to 6 grams in 150 ml of dextrose 5% over 20 to 30 minutes followed
by a continuous infusion of 1 to 3 grams per hour dependant on the status of
the patients patellar reflexes, renal output, and serum magnesium. MgSO4 may
be administered for a prolonged period of time.
Nursing management not only includes the administration of
medication and monitoring for effectiveness, but also assessment for side
effects and interventions when potentially life-threatening outcomes occur.
Therapeutic levels are generally considered to be between 4 to 7 mEq/liter. The patient should be monitored
for signs and symptoms of magnesium toxicity. Rising blood levels may be
detected by performing hourly reflex and clonus checks. To elicit a deep
tendon reflex the patient must be relaxed. Support the extremity to be tested.
Reflexes are graded on a 0 to 4+ scale.
4 + = Very brisk (called hyperactive) frequently indicate a
disease state of central nervous system hyperirritability.
3 + = Brisker than average
2 + = Average; normal
1 + = Somewhat diminished; low normal
0 = flat; no response
Clonus is another way to monitor for CNS hyperactivity. The
presence of clonus indicates that the central nervous system is highly
irritated although in some patients it can simply be the result of anxiety.
Clonus is often associated with moderate to severe pre-eclampsia. It is
measured and recorded by the number of beats present. Test for clonus should be
performed if reflexes are > 3 +. Support the knee in a partially
flexed position. With your other hand, sharply dorsiflex the foot (that is bend
it back toward the knee) and maintain it. If clonus is present you will see and
feel the foot moving back and forth in small rhythmic movements.
Labor
& Delivery Room Nurses must be aware that when patients are receiving
epidural anesthesia that the patellar reflexes are not reliable for magnesium
monitoring. Upper extremity reflexes are used in this situation.
Magnesium
Sulfate is not a benign treatment. Patients receiving Magnesium Sulfate are at
increased risk for postpartum hemorrhage due to uterine atony. This should be
anticipated and steps should be taken to ensure availability of cross-matched
blood if the need arises. Neonates are at increased risk of respiratory
depression as the magnesium crosses the placenta.
Parenteral MgSO4 is excreted through the kidneys; therefore
urinary output must be monitored hourly. Excretion may be slowed if there is
poor perfusion to the kidneys.
Toxicity symptoms also include respiratory depression and
cardiac arrest. Cardiac arrest can occur with serum levels > 12
mEq/liter. If a patient develops signs of toxicity, the infusion should be
stopped immediately. The patient should then be evaluated by exam and pulse
oximetry; oxygen should be administered and serum magnesium should be obtained.
If toxicity is diagnosed, the patient should be treated with 10 ml of 10%
calcium gluconate infusion over 3 minutes. Calcium competitively inhibits
magnesium at the neuromuscular junction and decreases the toxic effects. The
impact of calcium is transient and the patient should be closely monitored for
continued magnesium toxicity. The antidote for Magnesium Sulfate is Calcium
Gluconate.
Side effects of magnesium sulfate include nausea, vomiting,
headache, visual blurring, and sensations of heat and burning.
CONCLUSION
The care of the patient with pre-eclampsia or any other
hypertensive disorder of pregnancy is a high-risk situation requiring close
medical supervision and expert nursing skill. Both are important in decreasing
the morbidity and mortality rates for the hypertensive patient in the perinatal
period. Hypertensive disorders are the most common medical complication of
pregnancy. A clear understanding of the pathophysiology will aid healthcare
providers in promoting optimal outcome for the mother and her infant.
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in Pregnancy, Toronto,
Churchhill-Livingstone.
Burke,
M. (1999). Hypertensive Crisis and the Perinatal Period. Journal of Perinatal and Neonatal Nursing, Rockville, Md.
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Foley,
M. & Strong, T. (2004). Garite, Thomas J., Obstetric Intensive Care Manual (2nd ed.). McGraw-Hill, New
York.
Knupple
R. & Drucker J. (1999). Hypertension
in Pregnancy: A High Risk Team Approach. Philadelphia, W. B. Saunders.
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Institutes of Health Bulletin (October
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Update on High Blood Pressure in Pregnancy.
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