Preeclampsia and Gestational Hypertensive Disorders Nursing Care Plans and Management

Preeclampsia kills mothers and babies when it is caught late. The whole job on this patient is to catch the rise before it turns into a seizure, a stroke, a HELLP picture, or a placental abruption. Watch the pressure, the protein, the reflexes, and the fetus, and remember that delivery is the only cure.

What are hypertensive disorders of pregnancy?

Hypertensive disorders of pregnancy (also called pregnancy-associated hypertensive disorders or pregnancy-induced hypertension) are among the most common pregnancy complications and a major cause of maternal and fetal morbidity and mortality. They include gestational hypertension, preeclampsia, eclampsia, chronic hypertension, and chronic hypertension with superimposed preeclampsia. Untreated preeclampsia can progress to HELLP syndrome (hemolysis, elevated liver enzymes, low platelet count). Preeclampsia alone complicates 2-8% of pregnancies worldwide.

The American College of Obstetricians and Gynecologists (ACOG) defines five categories.

Gestational Hypertensive Disorders

1. Gestational hypertension. Systolic blood pressure of 140 mm Hg or more, and/or diastolic blood pressure of 90 mm Hg or more, on two readings at least 4 hours apart after 20 weeks of gestation in a woman with previously normal blood pressure. It does not persist longer than 12 weeks postpartum and usually resolves about a week after delivery.
2. Preeclampsia. A pregnancy-specific condition: new-onset hypertension that most often appears after 20 weeks of gestation, with blood pressure above 140 mm Hg systolic and above 90 mm Hg diastolic. It is usually accompanied by new-onset proteinuria, though other features (thrombocytopenia, impaired liver function, pulmonary edema, visual disturbance) may appear without proteinuria.
3. Eclampsia. Seizure activity or coma in a woman with preeclampsia and no preexisting cause for seizures. Seizures cause severe maternal hypoxia, injury, and aspiration pneumonia, and carry a high maternal mortality rate, especially in low-resource settings.

Chronic Hypertensive Disorders

4. Chronic hypertension. Hypertension diagnosed or present before pregnancy or before 20 weeks of gestation. It is more common with late childbearing and obesity. Hypertension diagnosed for the first time during pregnancy that does not resolve postpartum is also classified as chronic.
5. Chronic hypertension with superimposed preeclampsia. Preeclampsia complicating preexisting chronic hypertension. About half of women with chronic hypertension develop it, and it raises maternal and fetal mortality.

Nursing Care Plans and Management

Care planning centers on early detection, thorough assessment, and prompt treatment. The other priority is keeping the mother safe and delivering a healthy newborn as close to full term as possible.

Nursing Problem Priorities

The following are the nursing priorities for patients with preeclampsia and gestational hypertensive disorders:

• Blood pressure management. Monitor and control elevated blood pressure to prevent complications.
• Fetal monitoring. Assess fetal wellbeing through nonstress tests, ultrasounds, or other methods and watch for distress.
• Maternal health evaluation. Track organ function, watch for severe-feature preeclampsia, and address preexisting conditions.
• Proteinuria monitoring. Test urine for protein to gauge severity and renal function.
• Medication management. Prescribe and monitor antihypertensives and other agents to control blood pressure.
• Fluid balance. Prevent both dehydration and overload, especially with edema or low urine output.
• Prevention of complications. Watch closely for eclampsia and HELLP syndrome and intervene early.
• Delivery planning. Work with obstetric specialists on timing and mode of delivery based on severity, gestational age, and maternal-fetal status.
• Maternal education and support. Teach the warning signs and the value of self-monitoring and prompt reporting.
• Postpartum care. Monitor for lingering effects, manage blood pressure, and support recovery.

Nursing Assessment

Assess for the following subjective and objective data:

• See nursing assessment cues under Nursing Interventions and Actions.

Nursing Diagnosis

After assessment, a nursing diagnosis names the specific problems this patient faces, based on clinical judgment and the patient's condition. Diagnostic labels organize care but matter less at the bedside than the nurse's judgment in prioritizing each patient's needs.

Nursing Goals

Goals and expected outcomes may include:

• The patient remains normotensive throughout the rest of the pregnancy.
• The patient reports no or fewer episodes of dyspnea.
• The patient alters activity level as the condition warrants.
• The patient adheres to the therapeutic regimen and participates in monitoring.
• The patient verbalizes understanding of close monitoring of weight, BP, urine protein, and edema.
• The patient is free of signs of generalized, pulmonary, and cerebral edema (epigastric pain, headaches, confusion, dyspnea, nausea, vomiting).
• The patient exhibits hemoglobin, hematocrit, and protein levels within normal limits.
• The patient exhibits physiologic edema with no pitting.
• The patient demonstrates normal central nervous system (CNS) reactivity on a nonstress test (NST).
• The patient is free of late decelerations.
• The patient has no drop in FHR on the contraction stress test/oxytocin challenge test (CST/OCT).
• The patient is full-term, appropriate for gestational age (AGA).
• The patient participates in treatment or environmental changes that protect herself and the fetus.
• The patient is free of signs of cerebral ischemia (visual disturbances, headache, changes in mentation).
• The patient displays normal clotting factors and liver enzymes.
• The patient maintains a regimen that controls or eliminates seizure activity.
• The patient verbalizes understanding of individual dietary needs.
• The patient develops a dietary plan within her own financial resources.
• The patient maintains or regains weight as the situation indicates.
• The patient is free of edema.
• The patient identifies signs and symptoms requiring medical evaluation.
• The patient maintains BP within individually acceptable parameters.
• The patient performs the necessary procedures correctly.
• The patient verbalizes understanding of the disease process and treatment plan.
• The patient initiates lifestyle and behavior changes as indicated.

Nursing Interventions and Actions

1. Managing Hypertension and Maintaining Effective Cardiac Output

In a hypertensive pregnancy, fluid shifts from the intravascular to the interstitial space. Circulating volume and total vascular volume fall, systemic vascular resistance rises, and heart rate and stroke volume drop. The result is reduced cardiac output.

Assess blood pressure and pulse every 1 hour or as indicated. Accurate measurement is essential for early detection. Hypertension is systolic above 140 mm Hg or diastolic above 90 mm Hg. Pressure rises with increased systemic vascular resistance, and low cardiac output shows up as diminished peripheral pulses. Rising pressure signals progression. Use a consistent, standardized technique every time.

Assess mean arterial pressure (MAP) at 11-13 and 20-24 weeks gestation. A MAP of 90 mm Hg is predictive of preeclampsia. MAP is the average arterial pressure across one cardiac cycle and reflects cardiac output and systemic vascular resistance. Prediction is best when measured during both windows rather than either alone, and MAP is elevated from the first trimester in pregnancies that go on to develop preeclampsia. Women with early-onset preeclampsia run higher MAP at 20 weeks.

Assess for crackles, wheezes, and dyspnea; note respiratory rate and effort, and note snoring. Pulmonary edema follows the shift of fluid from intravascular to interstitial spaces and a drop in plasma colloid osmotic pressure, flooding the lungs. New pregnancy-onset snoring can itself be a risk factor for gestational hypertension and preeclampsia.

Auscultate the apical pulse and assess heart rate and rhythm. Tachycardia appears as the body compensates for the drop in circulating volume reaching the periphery.

Assess neurological status. Low cardiac output reduces cerebral perfusion and alters the sensorium. Neurologic complications of preeclampsia include cerebral edema, hemorrhage, irritability, headaches, hyperreflexia, and seizures.

Assess for visual disturbances. Vision changes come from arteriolar vasospasm and reduced retinal blood flow: dimming, blind or dark spots, blurring, double vision.

Assess for indications for earlier delivery. Worsening preeclampsia that may progress to eclampsia calls for emergency delivery. If the fetal blood supply is cut off, fetal distress and death follow. Watch for uncontrolled severe-range blood pressure, refractory headaches, upper abdominal pain, visual disturbances, and stroke.

Measure urine output per protocol and maintain strict intake and output. In preeclampsia the kidneys retain water and sodium in response to low cardiac output. Intrarenal vasospasm and a falling glomerular filtration rate cause oliguria in severe disease, and intravascular contraction worsens renal sodium and water retention.

Measure 24-hour urine for proteinuria. A 24-hour collection is the ideal measure, though current guidelines no longer count massive proteinuria as a severe feature. Reduced kidney perfusion damages glomerular endothelial cells and lets protein leak into the urine. When a 24-hour sample is impractical, preeclampsia may be diagnosed as hypertension with thrombocytopenia, renal insufficiency, impaired liver function, or pulmonary edema.

Provide frequent rest periods. Restrict activity rather than ordering complete bed rest. Restricted activity improves venous return, cardiac output, and renal-placental perfusion. Activity diverts blood from the placenta and lowers fetal oxygen supply. Complete bed rest has not been shown to improve outcomes and adds the risks of immobility (muscle atrophy, weight loss, cardiovascular deconditioning, psychological stress). Restricted activity is preferred.

Instruct the patient to elevate her legs when sitting or lying down. This reduces venous stasis and the risk of thrombus and embolus formation during bed rest.

Monitor BP and teach home monitoring. Check BP every 15 minutes during the critical phase and every 1 to 4 hours as the patient improves. For outpatients, teach the patient and a family member to take the BP two to four times per day in the same arm and position. Rising readings may signal worsening preeclampsia.

Record and graph vital signs, especially BP and pulse. The preeclamptic patient lacks the normal cardiovascular response to pregnancy (left ventricular hypertrophy, increased plasma volume, vascular relaxation). Hypertension follows increased sensitization to angiotensin II, which raises BP, promotes aldosterone release, drives sodium and water reabsorption, and constricts vessels.

Monitor invasive hemodynamic parameters such as cardiac output, as indicated. These give a precise picture of vascular changes and fluid volume. Prolonged vasoconstriction, hemoconcentration, and fluid shifts lower cardiac output.

Administer low-dose aspirin as indicated. Started before 16 weeks gestation, low-dose aspirin prevents preeclampsia, severe preeclampsia, preterm birth, and intrauterine growth restriction in high-risk pregnancies. Daily aspirin is recommended late in the first trimester for women with a history of early-onset preeclampsia and preterm birth before 34 weeks, or preeclampsia in more than one prior pregnancy.

Administer antihypertensives as ordered and watch for side effects. When pressure does not respond to conservative measures, short-term medication may be needed alongside fluid replacement and magnesium sulfate. Treat acute-onset severe hypertension that persists as soon as reasonably possible. Antihypertensives relax cardiovascular smooth muscle and improve blood supply to the brain, kidneys, uterus, and placenta. Intravenous hydralazine, intravenous labetalol, and oral nifedipine are the three agents commonly used in pregnancy. See the pharmacologic section below.

Prepare for delivery once a severe preeclamptic or eclamptic patient is stabilized, by cesarean when vaginal delivery is not feasible. When conservative treatment fails and induction is ruled out, surgical delivery is the only way to stop the hypertensive process. Delivery cures preeclampsia. In severe disease the fetus is often in greater danger inside the uterus, where oxygen and nutrition may be cut off or growth restricted.

2. Preventing Fluid Retention

Some fluid retention is normal in pregnancy. In preeclampsia, low placental perfusion drops the GFR and alters glomerular permeability, so protein leaks through the kidneys. Losing intravascular protein lowers intravascular osmolality, fluid shifts to the interstitium, and edema and extravascular fluid retention follow.

Assess lung sounds, respiratory rate, and effort. Dyspnea and crackles can mean pulmonary edema, which needs immediate treatment. Lost intravascular protein lets fluid seep out and flood the lungs. Orthopnea and paroxysmal nocturnal dyspnea can result from excessive venous return from the lower extremities.

Weigh the patient at each hospital visit and have her record weight at home between visits. Weigh on the same scale, in the same clothing, at the same time of day. Abrupt, notable gain (more than 3.5 lb (1.8 kg) per week in the second or third trimester) reflects fluid retention and may signal preeclampsia.

Assess vital signs, watching blood pressure and pulse closely. BP can rise in response to catecholamines, vasopressin, prostaglandins, and reduced prostacyclin. A faster pulse can follow low intravascular colloid-osmotic pressure from increased capillary permeability, which drives fluid retention and congests the lungs.

Assess for edema and degree of pitting. Pitting edema (mild, 1+ to 2+; severe, 3+ to 4+) of the face, hands, legs, sacral area, or abdominal wall, or edema that does not clear after 12 hours of bed rest, is significant. Assess distribution, pitting, and degree. Edema is greatest where hydrostatic pressure is highest and is often most evident in the feet and ankles of an ambulatory patient.

Assess for progressive or excessive edema and for possible eclampsia. Eclampsia warning signs include epigastric pain, cerebral symptoms, nausea, and vomiting. Right upper quadrant pain points to fibrin deposition in the liver (HELLP), dyspnea to pulmonary involvement, cerebral edema toward seizures, and nausea and vomiting to GI edema.

Note changes in hematocrit and hemoglobin. These show the degree of hemoconcentration from fluid shift. If hematocrit is less than three times the hemoglobin level, hemoconcentration exists. It occurs because plasma volume rises faster than erythrocyte production.

Monitor intake and output, noting urine color and specific gravity. Urine output is a sensitive marker of circulating volume. Reduced renal blood flow cuts urine production. Oliguria with a specific gravity of 1.040 indicates severe hypovolemia and kidney involvement. Magnesium sulfate can cause a transient rise in output.

Encourage increased protein intake. Good nutrition lowers the risk of prenatal hypovolemia and hypoperfusion; too little protein or calories raises the risk of edema and preeclampsia. Intake of 80 to 100 g of protein daily may be needed to replace losses as damaged glomeruli let protein spill into the urine.

Allow moderate sodium intake of up to 6 g/day; teach the patient to read labels and avoid high-sodium foods. Some sodium is necessary, since levels below 2 to 4 g/day worsen dehydration in some patients. High-sodium foods include processed meats, hot dogs, and potato chips. Excess sodium increases edema and hypertension risk.

Schedule prenatal visits every 1-2 weeks for mild preeclampsia and weekly if severe. Closer monitoring protects mother and fetus. Twice-weekly BP checks combined with fetal nonstress test, amniotic fluid index, and lab work may be indicated.

Educate the patient and family on home monitoring and day-care programs, as appropriate. Some mildly hypertensive patients without proteinuria can be managed as outpatients if surveillance and support are adequate and the patient and family actively participate.

Substitute fluids orally or parenterally via infusion pump, as indicated. Fluid replacement treats hypovolemia but must be cautious to avoid overload, especially when interstitial fluid returns to circulation as activity drops. With renal involvement, restrict intake: if output falls below 700 ml/24 hr, limit total intake to output plus insensible loss. An infusion pump gives accurate control.

Address questions about avoiding diuretics for edema. Diuretics worsen dehydration by cutting intravascular volume and placental perfusion, and they can cause thrombocytopenia, hyperbilirubinemia, or altered carbohydrate metabolism in the fetus or newborn. They are useful only for pulmonary edema.

Test a clean-catch, first-voided specimen for protein each visit, or daily or hourly if hospitalized. Report readings of 2+ or greater. This tracks severity and progression. A 2+ reading suggests glomerular edema or spasm. Urine contaminated by vaginal secretions can test falsely positive, and dilution can give a false-negative; preeclampsia can also exist without significant proteinuria.

Collaborate with a dietitian as indicated. A nutrition consult helps define individual needs. Dietary sodium and potassium intake meaningfully affect blood pressure.

When fluid deficit is severe and the patient is hospitalized:

Insert an indwelling catheter if kidney output is reduced or below 50 ml/hr. This allows accurate monitoring of output and renal perfusion. Low cardiac output impairs kidney perfusion, drives sodium and water retention, and cuts urine output.

Assist with line insertion and monitoring of central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP). These give a precise fluid-volume measurement. Plasma volume normally rises 30% to 50% in pregnancy, an increase that does not happen in preeclampsia.

Monitor serum uric acid, creatinine, and blood urea nitrogen (BUN). Uric acid clearance falls while serum uric acid rises. Elevated uric acid signals impaired kidney function, a worsening maternal picture, and poor fetal outcome, and is a biomarker of preeclampsia.

Administer platelets, fibrinogen, or fresh frozen plasma (FFP) as indicated. Patients with HELLP awaiting delivery may benefit from platelet transfusion when the count is below 50,000/µL with active bleeding or hemorrhage risk (and below 20,000/µL even without bleeding). In coagulopathy, correct clotting factors with fibrinogen and fresh frozen plasma.

3. Maintaining Adequate Tissue Perfusion

Hypertensive disorders cut maternal blood and nutrient flow through the placenta and reduce fetal oxygen. The fetus may show intrauterine growth restriction, and fetal death can occur.

Evaluate fetal growth with McDonald's measurement; track progressive fundal growth at each visit. Reduced placental function causes intrauterine growth restriction (IUGR). Lower blood and nutrient flow cuts fetal oxygen, and chronic uteroplacental insufficiency reduces the fetal contribution to amniotic fluid.

Assess fetal heart rate (FHR) manually or electronically, as indicated. This gauges fetal wellbeing. An elevated FHR can be a compensatory response to hypoxia, prematurity, or abruptio placentae.

Assess fetal response to biophysical profile (BPP) or contraction stress test (CST), as maternal status allows. BPP evaluates the fetus and its environment on five parameters of CNS function and amniotic fluid contribution. CST assesses placental function and reserve.

Assess amniotic fluid volume (AFV), as indicated. AFV assessment detects oligohydramnios, by ultrasound or amniotic fluid index. Failed spiral-artery remodeling raises placental resistance and causes hypoperfusion, leading to oligohydramnios, fetal hypoxia, and distress.

Advise bedrest and reduced activity. Activity restriction conserves blood for the mother's vital organs and the placenta. The patient should rest on her side to improve placental blood flow.

Teach the mother and family to track daily fetal movements and when to seek immediate care. Reduced placental flow impairs gas exchange and placental function. Poor perfusion can produce a malnourished, low-birth-weight, or premature infant, and raises the risk of abruptio placentae and fetal death. Reduced fetal activity means fetal compromise.

Teach the mother and family which factors affect fetal activity. Cigarette smoking, medications, drug use, serum glucose, environmental sound, time of day, and the fetal sleep-wake cycle can all change fetal movement. The patient should report decreased movement or none during a 3-hour span.

Report signs of abruptio placentae (vaginal bleeding, uterine tenderness, abdominal pain, decreased fetal activity). Prompt intervention improves the outcome. Abruption occurs when the vascular structures supporting the placenta are compromised, cutting fetal oxygen and nutrients.

Give the patient and family a contact number for questions and changes in fetal movement or maternal condition. This allows quick attention to concerns and misconceptions.

Note fetal response to medications such as magnesium sulfate (MgSO4), phenobarbital, and diazepam. Their depressant effects reduce fetal respiratory and cardiac function and activity, even when placental circulation is adequate.

Assist with assessing fetal maturity and wellbeing using the lecithin-sphingomyelin (L/S) ratio, prostaglandins, estriol levels, fetal breathing movements, and sequential sonography from 20 to 26 weeks gestation. When maternal or fetal status declines, the risks of preterm delivery are weighed against continuing the pregnancy, using studies of lung and kidney maturity, fetal growth, and placental function. IUGR is linked to reduced maternal volume and vascular changes.

Assist with assessing maternal plasma volume at 24 to 26 weeks gestation using Evans' blue dye when indicated. This identifies a fetus at risk for IUGR or demise from reduced plasma volume and placental perfusion.

Assist with Doppler ultrasound of the fetal umbilical artery. Umbilical artery Doppler measures flow as an indicator of placental perfusion. Absent or reversed end-diastolic flow shows abnormally high placental resistance and reduced fetal blood flow.

Assist with ultrasound assessment of placental size. Reduced placental function and size are associated with preeclampsia, where the maternal arteries fail to make the normal adaptations that allow adequate perfusion.

Administer a single course of corticosteroid (dexamethasone, betamethasone) IM at least 24 to 48 hr but no more than seven days before delivery when severe preeclampsia forces premature delivery between 26 and 34 weeks gestation. Corticosteroids induce fetal pulmonary maturity (surfactant production) and prevent respiratory distress syndrome in the preterm fetus. Best results come when the fetus is less than 34 weeks and delivery occurs within a week of administration.

4. Preventing Injury

Vasospasm and reduced organ perfusion drive preeclampsia and can cause cerebral vasospasm. Endothelial dysfunction in the uterus and cerebral vasculature produces neurologic disorders, including eclampsia. Progression to eclampsia means one or more generalized tonic-clonic seizures, which can cause cerebral hemorrhage, abruptio placentae, fetal compromise, or death of mother or fetus.

Assess for central nervous system (CNS) involvement. Cerebral edema and vasoconstriction show up as symptoms, behavior, or retinal changes. Elevated pressure disrupts cerebral autoregulation, causing hypoperfusion, endothelial damage, or edema. Watch for headache, irritability, visual disturbances, or fundoscopic changes.

Assess for altered level of consciousness. In progressive preeclampsia, cerebral vasoconstriction and vasospasm reduce oxygen consumption by 20% and cause cerebral ischemia.

Assess deep tendon reflexes (3+ to 4+) and ankle clonus. Deep tendon reflexes become hyperactive from CNS irritability, and ankle clonus usually accompanies hyperreflexia. To test clonus, support the leg with the knee flexed, sharply dorsiflex the foot, hold briefly, then release. A negative result is no rhythmic oscillation; a positive result is palpable and visible oscillation against the pressure.

Assess for signs of labor at every visit. Ask about contractions, vaginal bleeding, or leaking fluid. Prenatal care catches complications early.

Assess vital signs. Systolic blood pressure 140 mmHg or higher with diastolic above 90 mmHg meets criteria for new-onset hypertension. Shortness of breath may mean pulmonary edema, which is concerning for preeclampsia.

Assess for epigastric or RUQ pain. Ask about epigastric pain, RUQ pain, or heartburn. Liver ischemia from reduced organ perfusion causes epigastric pain, nausea, vomiting, and elevated liver enzymes.

Perform fundoscopic examination regularly. This evaluates retinal involvement. Blurring, scotoma, and photopsia are common in preeclampsia and eclampsia as retinal arteriolar spasm disrupts vision.

Palpate for uterine tenderness or rigidity, check for vaginal bleeding, and review the medical history. These can indicate abruptio placentae, especially when a preexisting problem such as diabetes mellitus or a renal or cardiac disorder causes vascular involvement.

Stress prompt reporting of CNS symptoms. Delay can lead to tonic-clonic convulsions or eclampsia. Common pre-convulsion symptoms are severe persistent headache, blurred vision, photophobia, epigastric pain, or heartburn.

Take measures to lessen the chance of seizures. A quiet, dimly lit room, limited visitors, coordinated care, and rest reduce the stimuli that can trigger an irritable cerebrum.

Review clotting time, prothrombin time (PT), partial thromboplastin time (PTT), and fibrinogen levels. These can show depletion of coagulation factors and fibrinolysis and suggest disseminated intravascular coagulation (DIC), a sign of worsening preeclampsia. As vessels constrict and clot to repair endothelial damage, the platelet supply is consumed.

Enforce seizure precautions per protocol. A seizure protocol reduces the risk of injury if a seizure occurs.

Have the patient keep strict bedrest if prodromal signs or aura appear, and explain why. Eclampsia is usually preceded by persistent headache, blurred vision, severe epigastric pain, altered mental status, and abdominal pain. The patient may feel restless during the aural phase. Understanding the reason improves cooperation.

If a seizure occurs, ensure a patent airway and protect the patient.

Stay with the patient during and after a seizure. Do not leave the bedside; call for help. This protects the patient and reduces the sense of isolation.

Keep padded side rails up with pillows or folded blankets and set the bed in the lowest position. Women with eclampsia can fracture bones falling from bed during seizures. This minimizes injury.

Do not restrain or restrict movement during the seizure. Cradle the head, place it on a soft surface, and guide the patient to the floor if out of bed. Gentle guidance reduces injury when voluntary muscle control is lost. Restraint can increase erratic movement and injury.

Note the time of onset and duration; document motor involvement and post-seizure behavior. This helps localize the cerebral area involved and helps the patient and family manage future activity.

Turn the head to the side; insert an airway or bite block per protocol only if the jaw is relaxed; suction the nasopharynx as indicated. This maintains the airway and reduces oral trauma, but it should never be forced when teeth are clenched, since dental and soft-tissue damage can result.

Check IV patency and restart the line immediately if it has infiltrated. Start a new line with a gauge 18 needle and give magnesium sulfate as ordered. See the magnesium sulfate interventions below.

Administer oxygen 10 L/min by non-rebreather face mask and monitor pulse oximetry. Supplemental oxygen treats postictal hypoxemia after convulsions.

Watch for labor or uterine contractions; assess uterine activity, cervical status, and fetal status. Convulsions increase uterine irritability, making it hypercontractile and hypertonic. Membranes may rupture or the cervix may dilate rapidly, and labor may follow.

Assess fetal wellbeing, noting fetal heart rate (FHR). During a seizure, fetal bradycardia and late decelerations can occur. If placental blood flow is cut off, fetal distress and death follow.

Monitor for signs of DIC: easy or spontaneous bruising, prolonged bleeding, epistaxis, GI bleeding. Abruptio placentae releases thromboplastin and predisposes to DIC. Platelets are consumed repairing endothelial damage until bleeding results.

Be ready to assist with birth once the patient is stable. After an eclamptic seizure and stabilization of mother and fetus, the team decides on timing and method of birth. Eclampsia alone is not an indication for immediate cesarean; route and timing depend on maternal and fetal condition, gestational age, presence of labor, and cervix score.

Administer magnesium sulfate (MgSO4) IM or IV by infusion pump. Magnesium sulfate is the drug of choice for treating eclamptic seizures and preventing recurrence. It is a CNS depressant that reduces acetylcholine release, blocks neuromuscular transmission, and prevents seizures. It transiently lowers BP and raises urine output. IV administration is easier to regulate and lowers toxicity risk, though some facilities use the IM route when continuous monitoring or proper infusion equipment is unavailable. Adding 1 ml of 2% lidocaine to the IM injection may reduce discomfort. Phenytoin infusion may treat eclampsia without the respiratory depression and tocolytic effect that can stall labor.

Monitor BP before, during, and after magnesium sulfate, and note serum magnesium with respiratory rate, patellar/deep tendon reflexes (DTRs), and urine output. Therapeutic MgSO4 is a serum level of 4.0 to 7.5 mEq/L or 6 to 8 mg/dL. Toxic reactions develop above 10 to 12 mg/dL, with loss of DTRs first, respiratory paralysis between 15 and 17 mg/dL, and heart block at 30 to 35 mg/dL.

Keep calcium gluconate ready and give 10 ml (1 g/10 ml) over 3 minutes as indicated. It is the antidote for MgSO4 toxicity, which can present as diminished deep tendon reflexes, cardiopulmonary arrest, and respiratory depression.

Administer amobarbital (Amytal) or diazepam (Valium) as indicated. These depress cerebral activity and sedate when MgSO4 does not control convulsions. They are not first-line because they depress the gag reflex and sedate the fetus.

Review sequential platelet counts. Avoid amniocentesis if the platelet count is below 50,000/mm3. If thrombocytopenia is present during an operative procedure, use general anesthesia. Transfuse platelets, packed red blood cells, fresh frozen plasma, or whole blood as indicated, and rule out HELLP syndrome. Thrombocytopenia arises from platelet adherence to disrupted endothelium or reduced prostacyclin. Procedures requiring needle puncture (spinal or epidural) can cause excessive bleeding.

Monitor liver enzymes and bilirubin; note hemolysis and Burr cells on peripheral smear. Elevated AST and ALT and bilirubin, microangiopathic hemolytic anemia, and thrombocytopenia point to HELLP syndrome and the need for immediate cesarean delivery if the cervix is unfavorable for induction.

Hospitalize if CNS involvement is present. Early therapy limits complications.

Prepare for cesarean birth if preeclampsia is severe, placental function is compromised, and the cervix is not ripe or responsive to induction. When fetal oxygenation is severely reduced by vasoconstriction in the failing placenta, immediate delivery may be needed to save the fetus.

5. Promoting Adequate Nutrition

Reduced placental perfusion drives endothelial disruption, vasoconstriction, and water and sodium retention. Local vasospasm in the kidneys damages glomeruli, causing oliguria and proteinuria. Protein loss can cause malnutrition and muscle wasting, and lost protein lets water shift to the interstitium, producing generalized edema.

Assess nutritional status, dietary intake, hair and nails, height, and pregravid weight. This sets a baseline for dietary needs and teaching. Malnutrition may contribute to preeclampsia, especially with a low-protein diet, insufficient calories, or being overweight or underweight by 20% or more before conception.

Weigh the patient daily, preferably in the morning before breakfast. Use the same scale, the same clothing, and the same time of day. Changes over 0.5 kg (1.1 lb) may reflect fluid shifts.

Teach normal weight gain in pregnancy, adjusted to the patient's needs. An underweight patient (BMI below 18.5) should gain 28 to 40 pounds and may need more calories. An overweight patient (BMI 25.0 to 29.9) should gain 15 to 25 pounds and avoid dieting, which risks fetal ketosis.

Teach the patient and family about protein and its role in preeclampsia. Regular intake of 80 to 100 g/day (1.5 g/kg) of protein replaces protein lost in urine and maintains normal serum oncotic pressure. The DASH (Dietary Approaches to Stop Hypertension) and OmniHeart trials both confirmed the benefit of greater plant-protein consumption.

Advise frequent rest and limited activity to conserve protein. A lower metabolic rate from rest and reduced activity cuts protein needs, which fetal demands also draw on. Rest plus a good dietary plan conserves protein.

Encourage more protein-containing foods and a balanced diet with adequate fluids. Protein is plentiful in lean meat, vegetables, eggs, and fish. Poor nutrition in pregnancy is linked to excess gestational weight gain and preeclampsia.

Monitor labs such as BUN, sodium, and potassium. These indicate nutritional needs, restrictions, and the effectiveness of therapy.

Collaborate with a dietitian as indicated. A dietitian helps build individual plans around specific needs. Nutrition counseling in pregnancy is a chance to encourage adequate daily iron, folic acid, and other pregnancy-specific foods.

6. Initiating Patient Education and Health Teachings

The patient may not understand how preeclampsia develops or how it is prevented and managed. The patient and family need a clear picture of the disease and the interventions it calls for.

Assess the patient's or family's knowledge of the disease and teach the pathophysiology and its implications for mother and fetus. This sets a baseline and targets teaching. Pregnancy-induced hypertension stems from reduced placental perfusion that triggers systemic vascular endothelial dysfunction, as the uterine spiral arteries fail to vasodilate, cutting fetal blood and nutrient supply and raising maternal blood pressure.

Assess knowledge of the rationale for interventions, procedures, and tests. Understanding improves cooperation and reduces fear. Ongoing research may add options, such as low-dose (60 mg/day) aspirin to reduce platelet thromboxane and limit the severity and incidence of preeclampsia.

Teach the signs of worsening disease and when to call the provider. Prompt treatment may prevent a worsening preeclamptic state and further complications. The patient should report headaches, new-onset visual changes, new-onset epigastric or RUQ pain, decreased fetal movement, and severe dyspnea, all signs of severe preeclampsia that may progress to eclampsia.

Keep the patient informed of her health status, test results, and fetal wellbeing. Fear grows when information is missing. A patient who understands the consequences of inaction and is motivated typically participates in treatment.

Teach home weight monitoring and reporting gains over 2 lbs (0.9 kg)/wk or 0.5 lb (0.23 kg)/day. A gain of 3.5 lbs (1.59 kg) or more per month in the second trimester or 1 lb (0.45 kg) or more per week in the third trimester suggests preeclampsia.

Teach family members home blood pressure monitoring. This supports the regimen and allows quick intervention. Take the BP two to four times per day in the same arm and position.

Review stress management and diet restriction. This reinforces the patient's role in treatment. Assess stress levels and recommend practical strategies, since mental stress in pregnancy raises the risk of gestational hypertension.

Ensure adequate protein for the patient with possible or mild preeclampsia. Glomerular damage causes heavy urinary protein loss, and protein is essential for intravascular and extravascular fluid regulation.

Reinforce a diet low in sodium, saturated fat, and cholesterol. Excess saturated fat, cholesterol, sodium, and calories are nutritional risks in preeclampsia. A diet low in fat and high in polyunsaturated fat lowers BP.

Review self-testing of urine for protein and the reasons for it. A result of 2+ or greater is significant and must be reported. Specimens contaminated by vaginal discharge or red blood cells can test falsely positive.

Reinforce adherence and keeping followup appointments. Nonadherence is a common reason antihypertensive therapy fails, and ongoing participation is critical to success.

Explain prescribed medications: rationale, dosage, expected and adverse effects. Clear information improves commitment to the plan.

7. Administer Medications and Provide Pharmacologic Support

Medication management is central to controlling these disorders and preventing complications. Monitor the patient's response closely, including blood pressure, renal function, and side effects.

1. Hydralazine (Apresoline, Neopresol). Given intravenously, hydralazine lowers blood pressure by relaxing smooth muscle, reducing peripheral vascular resistance. Check BP every minute for 5 mins, then every 5 mins for 30 mins.

2. Labetalol Hydrochloride (Normodyne, Trandate). Given intravenously, labetalol is an alpha- and beta-blocker that lowers peripheral vascular resistance without a significant change in cardiac output or causing tachycardia. Contraindicated in asthma and congestive heart failure. Monitor blood pressure closely after administration.

3. Methyldopa (Aldomet). Interferes with chemical neurotransmission to reduce peripheral vascular resistance. Can cause CNS sedation, sleepiness, and postural hypotension.

4. Nifedipine (Adalat). A calcium channel blocker that dilates arterioles and lowers systemic vascular resistance by relaxing arterial smooth muscle. Can potentiate the CNS effects of magnesium sulfate. Monitor blood pressure closely after administration.

5. Sodium Nitroprusside (Nitropress). Reserved for rare cases where other antihypertensives have failed to control blood pressure.

Evaluation

• The patient exhibits a normal blood pressure of 120/70 mmHg.
• No protein is detected in the urine.
• Edema is minimized or confined to the lower extremities.