Hypertensive Disorders in Pregnancy

References:

1. Maternal & Child Health Nursing: Care of the childbearing & childrearing family, 8th Edition, ISBN 978-1-4963-4813-5, by JoAnne Silbert-Flagg and Adele Pillitteri (Ch. 21)
2. Dr. RPS Maternal and Newborn Care: A Comprehensive Guide and Source Book for Teaching and Learning, 2nd Edition, ISBN 978-971-98-2265-3, by Rosalinda Parado Salustiano (pp. 117-195)
3. The Topranker’s Guide: A Comprehensive Study Guide for the Nurse Licensure Exam (pp. 283–284)
4. Comprehensive Nursing Licensure Review Book: Local and International Test Prep, Volume 1, 3rd Edition, ISBN 978-971-51-3383-8, by Josie Quiambao-Udan (Unit 6)

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Gestational hypertension is a condition in which vasospasm occurs in both small and large arteries during pregnancy, causing increased blood pressure. Preeclampsia is a pregnancy-related disease process evidenced by increased blood pressure and proteinuria.

A disorder characterized by proteinuria, edema, and hypertension appearing after the 20th to 24th week of pregnancy and disappearing 6 weeks after delivery. This occurs in 5% to 10% of all pregnancies and is one of the major causes of maternal and neonatal mortality. Its actual cause is unknown, although women with antiphospholipid syndrome (APS) or the presence of antiphospholipid antibodies in maternal blood are much more likely to develop preeclampsia. The condition tends to occur most frequent in:

1. Women of color
2. Primiparity with extremes of age (<20, >40)
3. Grand multiparity (≥5)
4. Multiple pregnancy
5. Low socioeconomic status; nutritional deficiency (low protein and low calorie diet)
6. Coexisting conditions: diabetes mellitus, multiple pregnancies, polyhydramnios, chronic hypertension, renal disease

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Pathophysiology

The symptoms of preeclampsia affect almost all organs. Vascular spasm may be caused by the release of a prostaglandin vasoconstrictor (thromboxane, also increases platelet aggregation) due to endothelial injury from increased cardiac output during pregnancy. Prostaglandin vasodilators (prostacyclin) is also inhibited/reduced because of endothelial injury. This reduces the body’s responsiveness to blood pressure changes, which allows blood pressure to increase dramatically. Beginning about the 20th week of pregnancy, almost all body systems begin to be affected.

1. The cardiac system can easily become overwhelmed because the heart is forced to pump against rising peripheral resistance. This causes a reduced blood supply to organs, most markedly the kidney, pancreas, liver, brain, and placenta.
   • Arterial vasospasm will force a larger portion of maternal blood to be kept in venous circulation.
   • Thrombocytopenia can occur due to platelet aggregation.
   • Hematocrit levels can help assess the extent of plasma loss due to edema. A hematocrit level above 40% suggests significant fluid loss into interstitial spaces.
2. Placental insufficiency reduces fetal nutrient and oxygen supply. This can retard fetal growth leading to a small-for-gestational-age fetus. Gestational hypertension is also a strong risk factor for placental abruption.
3. Pancreatic ischemia can result in epigastric pain and an elevated amylase-creatinine ratio.
4. Arterial spasm of the retina can result in vision changes and even blindness from retinal hemorrhage.
5. Renal vasospasm increases blood flow resistance. Degenerative changes develop in the kidney glomeruli because of back pressure. The kidneys also release angiotensin in response to decreased perfusion, resulting in further vasospasm and hypertension.
   1. This increases glomerular membrane permeability, allowing serum protein albumin and globulin to escape into the urine (i.e., proteinuria).
   2. The degenerative changes also result in decreased glomerular filtration, so there is lowered urine output and clearance of creatinine.
   3. If tubular reabsorption increases, sodium retention begins. This directly leads to edema formation in conjunction with decreasing osmotic pressure from proteinuria.
6. Extreme edema can lead to maternal cerebral and pulmonary edema and seizures (eclampsia). Cerebral hypoxia and CNS irritability can manifest as visual disturbances (double vision, blurring, dimness of vision), hyperreflexia or hyperirritability (e.g., ankle clonus), convulsions, and coma in severe cases.

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Signs and Symptoms

Symptoms result from generalized vasospasm and arteriolar vasoconstriction increasing peripheral resistance, decreased tissue perfusion, and hypertension. The decreased tissue perfusion affects the kidneys, brain, and uterus in particular.

• Rapid weight gain (over 2 lbs/week in the second trimester, over 1 lb/week in the third trimester)
• Swelling of the face or fingers. Some edema of the ankles is normal, particularly after standing for long periods of time. Reports such as tightening of rings, difficulty in opening the eyes from edema of the eyelids, or impaired speech from swelling of the tongue are indicative of edema that is becoming more extensive.
• Ocular changes—flashes of light or dots before the eyes, dimness or blurring of vision—or a severe continuous headache may point to cerebral edema or acute hypertension.
• Decreased urine output, reflective of decreased tissue perfusion.
• Right upper quadrant pain unrelated to fetal position. This may indicate liver damage.
• Blood pressure increased above 140/90 mm Hg, based on two readings six hours apart while the woman stays in bed rest (the position in which blood pressure is lowest). A criterion of 140/90 mm Hg is useful for women with no baseline of blood pressure. A criterion of a systolic rise of 30 mm Hg or diastolic rise of 15 mm Hg can be used for women with preexisting hypertension. It may also be useful for women who have a historically low blood pressure (e.g., a normal value of 98/61 would already be hypertensive if her blood pressure rises to 128/76 mm Hg in pregnancy).

Signs	Gestational Hypertension	Mild Preeclampsia	Severe Preeclampsia
Hypertension	140/90 mm Hg or an increase from pre-pregnancy baseline by 30 mm Hg systolic or 15 mm Hg diastolic	140/90 mm Hg or an increase from pre-pregnancy baseline by 30 mm Hg systolic or 15 mm Hg diastolic	160/110 mm Hg
Proteinuria	No proteinuria	1+ to 2+ on a random sample 1 g on a 24-hour sample	3+ to 4+ on a random sample ≥5 g on a 24-hour sample
Edema	No edema	Mild edema in upper extremities or face Weekly weight gain of >2 lbs in the second trimester or >1 lb in the third trimester	Extensive peripheral edema Excessive weight gain of 5 lbs. per week or more. Epigastric pain—edema of the liver capsule or abdomen, ischemia of the pancreas and liver Cerebral edema: headache, vision changes, hyperreflexia (e.g., hyperactive DTRs, ankle clonus), dizziness, vomiting, disorientation.
Oliguria		Absent; 500 mL or more in 24 hours	Present; 500 mL or less in 24 hours, altered renal function tests—elevated creatinine (>1.2 mg/dL)
IUGR		Absent	Present
Others			Pulmonary (pulmonary edema) or cardiac involvement, hepatic dysfunction, thrombocytopenia

1. Gestational Hypertension: elevated blood pressure unaccompanied by the characteristic manifestations of proteinuria and edema. Perinatal mortality is not increased with simple gestational hypertension, so careful observation but no drug therapy is necessary.
2. Mild Preeclampsia: Preeclampsia without severe features; any status above gestational hypertension but below a point of seizures (eclampsia). Proteinuria of 1+ on a urine dip or 300 mg in a 24-hour urine protein collection or 0.3 or higher on a protein-creatinine ratio.
3. Severe Preeclampsia: a woman has passed preeclampsia with severe features when her blood pressure rises to 160/110 mm Hg on at least two occasions six hours apart at bed rest, or her diastolic pressure is 30 mm Hg above her prepregnancy level. Proteinuria becomes marked, up to 3+–4+ on a random urine sample or ≥5 g in a 24-hour sample. Edema is most readily palpated over bony surfaces. This edema will reduce a woman’s urine output to approximately 400 to 600 mL per 24 hours.
   • Some women report severe epigastric pain and nausea or vomiting, possible because abdominal edema or ischemia to the pancreas and liver has occurred.
   • If pulmonary edema has developed, a woman may report feeling short of breath.
   • If cerebral edema has occurred, reports of visual disturbances such as blurred vision or seeing spots before the eyes may be reported. Cerebral edema also produces symptoms of severe headache and marked hyperreflexia and perhaps ankle clonus (i.e., a pulsed motion of the foot after flexion).

Ankle Clonus

To elicit ankle clonus, dorsiflex the woman’s foot three times in rapid succession. As you take your hand away, observe the foot. If no further motion is present, no ankle clonus is present. If the foot continues to move involuntarily, clonus is present. Although usually just rated as present or absent, it can be rated as (a) mild, resulting in two movements; (b) moderate, resulting in three to five movements, and (c) severe, over six movements.

4. Eclampsia is the most severe classification of pregnancy-related hypertensive disorders. A woman has passed into this stage when cerebral edema is so acute a grand mal (tonic-clonic) seizure or coma has occurred. Maternal mortality can be as high as 20% from cerebral hemorrhage, circulatory collapse, or renal failure. Fetal prognosis becomes poor because of hypoxia, possibly caused by the seizure, with consequent fetal acidosis. If premature separation of the placenta from extreme vasospasm occurs, the fetal prognosis becomes even graver. If a fetus must be born before term, all the risks of immaturity will be faced.
   • Severe headaches and epigastric pain may be indicators of an impending convulsion. The first nursing action if the patient complains of a severe headache or epigastric pain is to check blood pressure. The first objective sign of a convulsion is rolling of the eyeballs.

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Nursing Intervention

Nursing Diagnoses and Related Interventions

The nursing diagnoses used with gestational hypertensive disorders are numerous because the disease process has such wide-ranging effects. Some possible nursing diagnoses include:

• Ineffective tissue perfusion related to vasoconstriction of blood vessels
• Deficient fluid volume related to fluid loss to SQ tissue
• Risk for fetal injury related to reduced placental perfusion secondary to vasospasm
• Social isolation related to prescribed bed rest

Interventions for Mild Preeclampsia

Patients with preeclampsia without severe features prior to full term can be managed at home with frequent follow-up care and fetal testing.

1. Monitor antiplatelet therapy (e.g. low-dose aspirin) to counteract increased platelet aggregation.
2. Promote bed rest to improve sodium excretion and diuresis of edema fluid. Be certain women know how to rest in a way that avoids supine hypotensive syndrome.
3. Promote good nutrition. Sodium is not restricted, as low sodium may activate the renin-angiotensin-aldosterone system and increase blood pressure further.
4. Promote emotional support. Make sure the woman is aware of the gravity of the disorder and does not disregard it as unimportant just because edema is distant from the growing fetus and the only medication prescribed is low-dose aspirin.

Interventions for Severe Preeclampsia

A woman with severe preeclampsia is admitted to a healthcare facility for care. If the pregnancy is greater than 37 weeks, labor can be induced or a cesarean birth performed to end the pregnancy at that point. Otherwise, measures to alleviate symptoms will be instituted to allow the fetus to come to term. If ineffective, a preterm delivery may be the best course of action.

1. Support bed rest (bathroom privileges are given). Loud noises can be sufficient to trigger a seizure that initiates eclampsia. Place the patient in a private room. Limit visitors. Raise side rails in case of seizure. Dim the lights. Explain all procedures and plans to prevent inducing stress, which is another potential trigger.
2. Monitor maternal well-being. Take blood pressure frequently, at least every 4 hours, or with a continuous monitoring device.
   • Blood studies to assess renal and liver function, monitor for DIC, monitor plasma estriol levels (a test for placenta function), and monitor electrolyte levels are done. Blood-typing and cross-matching is done due to the high risk for placental abruption and resulting hemorrhage.
   • Hematocrit and daily weighing reflects fluid retention and edema. An indwelling urinary catheter may be put in place to accurately measure intake and output.
3. Monitor fetal well-being. Single Doppler auscultation at approximately 4-hour intervals is sufficient at this stage of management. A nonstress test or biophysical profile can be done daily to assess uteroplacental sufficiency. If fetal bradycardia occurs, oxygen administration to the mother may be necessary to maintain adequate fetal oxygenation.
4. Support a nutritious intake. A diet moderate to high in protein and moderate in sodium is required to compensate for proteins lost in urine. An intravenous fluid line is usually initiated and maintained to serve as an emergency route for drug administration as well as to administer fluid to reduce hemoconcentration and hypovolemia.
5. Administer medications to prevent eclampsia. Hypotensive drugs—Hydralazine (Apresoline), Labetalol (Normodyne), Nifedipine—may be prescribed to reduce hypertension. These do not interfere with placental circulation; they lower blood pressure by peripheral dilatation. Ensure diastolic pressure does not drop below 80 to 90 mm Hg or inadequate placental perfusion could occur.
   • The drug of choice remains as magnesium sulfate. It reduces edema by shifting fluid into the intestine (which is why it also acts as a cathartic) and a central nervous system depressant action, which lessens the possibility of seizures. It is given as a bolus followed by a maintenance to achieve immediate reduction of blood pressure. It requires continuous administration due to its short period of effectivity. A solution of 10 mL of a 10% calcium gluconate solution (1 g) should be kept ready nearby for immediate intravenous administration should a woman develop signs and symptoms of magnesium toxicity, as calcium is the specific antidote for magnesium toxicity.
   • Diazepam (Valium) is given to halt seizures.

Interventions for Eclampsia

Immediately before a seizure, a woman’s blood pressure rises suddenly from additional vasospasm. The increased cerebral pressure causes her temperature to rise sharply to 39.4°C to 40°C. Vision changes and a severe headache appear, and reflexes become hyperactive. The woman feels a premonition or aura that “something is happening.” Severe epigastric pain and nausea vomiting appear from vascular congestion of the liver or pancreas. Urinary output may decrease abruptly to less than 30 mL/hr.

Tonic-clonic seizures occur in sages. After the preliminary signal or aura that something is happening, the tonic phase appears—all the muscles of the woman’s body contract. Her back arches, her arms and legs stiffen, and her jaw closes so abruptly she may bite her tongue. Respirations halt from contraction of the thoracic muscles. This lasts for approximately 20 seconds before the second stage, the clonic phase, begins. The woman’s bladder and bowel muscles contract and relax; incontinence of urine and feces may occur. Breathing may remain ineffective. The clonic phase lasts for up to one minute. Following this, the woman enters an hour-long postictal stage, during which she remains unconscious.

1. The priority care for a woman with a tonic–clonic seizure is to maintain a patent airway. To prevent aspiration, turn her onto her side to allow secretions to drain from her mouth.
2. Magnesium sulfate or diazepam (Valium) may be administered intravenously as emergency measures.
3. Assess oxygen saturation via a pulse oximeter. Administer oxygen by face mask as needed to protect fetal oxygenation.
4. Fetal monitoring: apply an external fetal heart monitor if one is not already in place to assess the FHR. The seizure may announce the beginning of labor, so assess as well for uterine contractions. Check for vaginal bleeding to detect placental separation, although evidence placental separation has occurred will probably appear first on the fetal heart record; vaginal bleeding will strengthen the presumption.
5. Be certain to assess for uterine contractions as the mother will be unable to report the sensation of contractions. The painful stimulus may also trigger another seizure. Keep the woman on her side and on NPO status. Check for vaginal bleeding every 15 minutes.

Decisions about birth may begin when the child has reached a point of viability and the woman’s condition stabilizes, usually 12 to 24 hours after the seizure. Fetal lung maturity appears to advance rapidly likely due to the stress brought on by preeclampsia; fetal lung maturity as indicated by the lecithin/sphingomyelin ratio may already be adequate even before 37 weeks.

1. The preferred method for birth is a vaginal delivery with minimal anesthesia. Cesarean birth is less favorable for the fetus. The mother is also a poor candidate for surgery due to her blood pressure. Anesthesia combined with her low vascular blood volume will result in hypotension with regional anesthesia, such as an epidural block.
2. If labor does not begin, induction of labor with an amniotomy or intravenous oxytocin may be instituted. If these are still ineffective and the fetus is in imminent danger, cesarean birth becomes the birth method of choice.

General Interventions

1. Prevention: Health Teaching
   • Well-balanced dieting with high protein (increase blood osmolarity, prevent fluid shifting)
     • Supplemental iron: 30 to 60 mg per day in the second and third trimester, continued 2 to 3 months postpartum
     • Increased caloric intake by 10% in pregnancy (total 2,300 – 2,500 kcal/day)
     • Sodium is not restricted as it may decrease circulating volume, cause fluid and electrolyte imbalance, and eliminate vital nutrients.
   • Adequate rest and sleep in the left lateral (Sims’) position.
   • Regular prenatal care with careful monitoring for danger signs: (a) visual disturbances, (b) severe, persistent headache and dizziness, (c) digital and periorbital edema, (d) irritability, and epigastric pain.
2. Treatment and Nursing Care
   • Maintain bedrest in the left lateral recumbent position: increase tissue perfusion, induce diuresis, reduce supine hypotensive syndrome
   • Provide a high-protein diet with moderate sodium: replace protein losses (from proteinuria), retain fluid in the intravascular compartment, and reduce edema.
   • Frequent monitoring: the room should be easily accessible from the nurse’s station:
     • Vital signs
     • Intake and output: oliguria is a grave sign; diuresis is good.
     • Daily weight/edema: degree and distribution of fluid retention; periorbital edema is a dangerous sign found in severe preeclampsia.
     • Reflexes: particularly of deep tendon reflexes in magnesium sulfate toxicity.
     • Onset and progress of labor, and signs of placental abruption.
3. Administering drugs as ordered:
   • Magnesium sulfate is used as an anticonvulsant.
     • Prior to administration, check the respiratory rate. MgSO₄ can reduce respiratory rate by impeding the respiratory center and the smooth muscles of respiration.
     • Check the knee-jerk reflex to determine toxicity before administering next doses. It should at least be 1+.
     • Check blood pressure.
     • Keep 10% calcium gluconate, the antidote for MgSO₄, ready.
     • Procaine hydrochloride may be mixed with MgSO₄ to reduce irritation and pain; this requires a doctor’s order. The same is true for lidocaine/lignocaine (Xylocaine). In 2023 BEmONC standards, the standard procedure is to add 1 mL of 2% lignocaine in the same syringe with 5 grams of 50% MgSO₄ for deep IM in each buttock (dose is divided to reduce irritation). Use the Z-track technique and do not massage the site.
     • After administration, monitor BP, RR, DTRs, I&O, and FHT.
   • Hydralazine (Apresoline; 5 mg IV over 1 to 2 minutes) is used as an antihypertensive. Give with meals and monitor blood pressure. This is done for patients with ≥160 mm Hg/≥110 mm Hg. Other antihypertensives include:
     • Nifedipine immediate-release only: 5–10 mg p.o. q30min until desired blood pressure is achieved, max. of 30 mg
     • Labetalol oral: 200 mg p.o. q1° until desired blood pressure is achieved, max. of 1,200 mg in 24 hours
     • Labetalol IV: 10 mg IV, double dose every 10 minutes to 80 mg until goal is achieved, max. of 300 mg, then switched to oral. Not used in congestive heart failure, asthma, or hypovolemic shock.
   • Diazepam (Valium) as an anxiolytic, promoting rest and is used as an adjunct in seizure disorder. Blood pressure is monitored while lying and standing (orthostatic hypotension), assess degree of anxiety, give with food or milk for GI symptoms, and give sugarless gum and frequent sips of water for dry mouth.
4. Prevent convulsions: reduce environmental stimuli (dim, quiet room, restrict visitors), and utilize a room close to the nurse’s station. Magnesium sulfate may be administered as ordered. Emergency items (airway, cath. set, IV fluids, emergency drugs) are prepared. Monitor closely for signs of impending convulsion:
   • Severe (frontal) headache
   • Severe epigastric pain
   • Sharp cry
   • Fixed, unresponsive eyes
   • Facial twitchings
   • Hyperreflexia
5. Provide care during convulsions: first priority— maintain a patent airway by positioning the patient on a lateral position, gentle suctioning, and provide oxygen as ordered; second priority— promote safety and prevent injury by setting bedrails, and not using restraints.
   • Record and monitor the type of convulsion: duration, progress, resultant coma, or bowel or bladder evacuation.
   • Continue strict monitoring for 48 hours after delivery because convulsions may still occur in the postpartum period.

Postpartum Period

Preeclampsia persists from 10 to 14 days after birth, although it usually disappears within 48 hours after birth. Therefore, monitoring blood pressure in the postpartum period and at healthcare visits and being alert for preeclampsia, which can occur as late as 2 weeks postbirth, are essential to detect this residual hypertension.