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Hypertension In Pregnancy

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Author:    Patricia Hartley (RNC, MSN)

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 –
  • Teenagers and primigravidas are at risk for the development of this condition
  • 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:

  •  AST
  •  ALT
  •  BUN
  • Creatinine
  • SGOT

Signs of impaired liver function:

  • Elevated liver enzymes
  • Signs of malaise
  • Anorexia
  • Nausea and vomiting
  • Jaundice
  • Epigastric pain.
  • Enlarged liver
  • Evidence of low platelets.

Delivery of the infant is essential because liver function rapidly deteriorates in this condition. Hemorrhage may occur within the mother’s 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 Ringer’s 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 woman’s chances of developing this dangerous condition. In a study conducted by the National Institute of Child Health and Human Development’s (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:
    •  Disorder progress
    •  Consequences
    •  Potential outcomes
    • Assessment and treatment procedures
    •  Coping measures for complete bed rest
    •  Stress reduction measures
    •  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 woman’s 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 patient’s 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.

REFERENCES

Berkowitz, D., Constan, D., Mayoshiko, T. (2000). Handbook of Drugs in Pregnancy, Toronto, Churchhill-Livingstone.

Burke, M. (1999). Hypertensive Crisis and the Perinatal Period. Journal of Perinatal and Neonatal Nursing, Rockville, Md. Aspen Publishers. 3(2) 33-47.

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.

National Institutes of Health Bulletin (October 24, 2000). NHLBI Publishes Update on High Blood Pressure in Pregnancy.

Olds, London, Ladewig. (2000). Obstetric Nursing, Addison-Wesley Publishing Company.

Queenan, J. & Hobbins, J.C. (1999). Protocols for High Risk Pregnancies 3rd Ed., Oradell, New Jersey, Medical Economics Books.