Preeclampsia(redirected from preeclampsia-eclampsia syndrome)
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Essentially, the pathology responsible for the elevation of blood pressure is spasm of the blood vessels. Normally, the blood vessels of a pregnant woman have a diminished response to the effects of such pressor substances as angiotensin and norepinephrine. In pregnancy-induced hypertension, resistance to vasospasm is somehow comprised and so blood pressure increases. It is not known whether the change in responsiveness to pressors is a cause or a result of vasospasm and elevated blood pressure.
Blood pressure can also be evaluated by determining the mean arterial pressure on two occasions at least 6 hours apart. A pregnant patient is considered hypertensive when her mean arterial pressure rises 15 mm Hg from her baseline or is over 100 mm Hg.
Pathologic changes in the glomeruli of the kidney produce proteinuria, oliguria, and edema. Increased permeability of the glomerular membrane allows passage of serum proteins into the urine (proteinuria), diminished glomerular filtration lowers urine output, and increased reabsorption of sodium causes fluid retention and edema and weight gain.
Mild preeclampsia is said to be present when the patient has elevated blood pressure, proteinuria of 1+ or 2+ on a reagent test strip or 500 mg/24 hours or more, swelling in the upper part of her body rather than the usual ankle edema associated with pregnancy, and a weight gain of more than 1 kg (2 pounds) a week in the second trimester and 0.5 kg (1 pound) a week in the third trimester.
Mild preeclampsia is managed by bed rest to facilitate sodium excretion, which takes place more rapidly when the body is at rest. While resting in bed the patient is positioned on her left side to avoid pressure of the uterus against the vena cava and supine hypotension syndrome. Rest is often all that is needed to relieve the symptoms of mild preeclampsia. Some physicians also prescribe a high-protein diet to compensate for the protein lost in the urine and, perhaps, mild restriction of sodium intake. However, restriction of sodium can activate the angiotensin system and cause an undesirable elevation in blood pressure.
Diuretics are not used for control of edema because they can only aggravate the condition by increasing glomerular vessel permeability and stimulating angiotension activity.
While magnesium sulfate is being administered, whether intravenously or intramuscularly, the patient must be monitored at frequent intervals to assess deep tendon reflexes and respiratory rate, which are indicators of its depressant effect. Urine output is measured every 4 hours or more often. If a patient excretes less than 100 ml of urine in four hours, she is likely to have a high level of serum magnesium because this mineral is excreted almost exclusively in the urine. In readiness for magnesium overdosage should it occur, a 10 per cent solution of calcium gluconate, the specific antidote for magnesium toxicity, should be on hand.
Other drugs that may be prescribed include hypotensive drugs to reduce blood pressure and sedatives such as phenobarbital to manage central nervous system irritability. Because of the high fetal and maternal morbidity and mortality associated with pre-eclampsia and eclampsia, the pregnancy is terminated as soon as feasible.
Maternal mortality from eclampsia is distressingly high. The cause of death can be cerebral hemorrhage, circulatory collapse, or renal failure. Mothers who survive eclampsia and the birth of their babies can continue to have hypertension for 10 to 14 days after delivery. Follow-up care is needed to evaluate residual or preexisting hypertension and renal disease and to initiate long-term management as indicated.
Infant mortality also is high when the mother is eclamptic. The status of the fetus is closely monitored before delivery to assure that hypoxia and life-threatening acidosis do not develop. When it is necessary to deliver the infant before term, problems of low birth weight and prematurity must be managed.
preeclampsiaObstetrics A hypertensive disorder occurring in the 3rd trimester in ± 5% of pregnancies Clinical HTN, proteinuria, dependent edema, vasospasm, coagulation defects Treatment Low-dose aspirin ↓ preeclampsia in nulliparas, especially with systolic HTN; aspirin ↑ risk of abruptio placentae, but does not ↓ perinatal mortality. See Eclampsia.
|Mean LOS:||4.8 days|
|Description:||SURGICAL: Cesarean Section With CC or Major CC|
|Mean LOS:||2.4 days|
|Description:||MEDICAL: Vaginal Delivery Without Complicating Diagnoses|
Preeclampsia is a pregnancy-specific syndrome of reduced organ perfusion secondary to vasospasm and endothelial activation that affects approximately 7% of all pregnant women. It is characterized by hypertension (blood pressure [BP] > 140/90) and proteinuria (300 mg in 24 hours or 1+ dipstick) after 20 weeks’ gestation. Although it is often present, edema is no longer included as a diagnostic criterion for preeclampsia because it is an expected occurrence in pregnancy and has not been shown to be discriminatory.
If untreated (or sometimes even with aggressive treatment), the symptoms get progressively worse. Symptoms relate to decreased perfusion to the major organs: kidneys (proteinuria, oliguria), liver (epigastric pain, elevated enzymes), brain (headache, blurred vision, hyperreflexia, clonus, seizures) and the placenta (fetal distress, intrauterine growth restriction). Two different complications of preeclampsia are (1) eclampsia (seizure occurs) and (2) HELLP syndrome (hemolysis, elevated liver enzyme levels, low platelet count). Eclampsia and HELLP may or may not occur together. Another complication can be disseminated intravascular coagulation, which is often fatal. Not only is preeclampsia life-threatening for the mother, but it can also cause intrauterine growth retardation, decreased fetal movement, chronic hypoxia, or even death in the fetus caused by decreased placental perfusion. If seizures occur, the patient has a risk for placental abruption, neurological deficits, aspiration pneumonia, pulmonary edema, cardiopulmonary arrest, acute renal failure, and death. Fetal bradycardia is typical during the seizure, usually with slow recovery to the baseline heart rate upon the seizure ending.
In addition to preeclampsia, there are four other categories of hypertension disorders in pregnancy: (1) gestational hypertension—BP of 140/90 after 20 weeks' gestation in a normotensive woman, no proteinuria, and postpartum return to normal BP; (2) preeclampsia—which includes eclampsia or the development of seizures along with preeclampsia and HELLP syndrome; (3) superimposed preeclampsia on chronic hypertension—new onset of proteinuria in a hypertensive woman; and (4) chronic hypertension—BP greater than 140/90 before pregnancy occurred or hypertension diagnosed before the 20th week that persists past the 12th week postpartum. Patients with proteinuria without hypertension initially have a higher incidence of progressing to preeclampsia than women with gestational hypertension.
The cause of preeclampsia is unknown; it is often called the “disease of theories” because many causes have been proposed, yet none has been well established. Immune maladaptation to paternal antigens associated with the fetus and placenta may lead to a situation similar to acute graft rejection. Experts believe that decreased levels of prostaglandins and a decreased resistance to angiotensin II lead to a generalized arterial vasospasm that then causes endothelial damage. The brain, liver, kidney, and blood are particularly susceptible to multiple dysfunctions. Several risk factors have been identified that may predispose a woman to developing preeclampsia: maternal age; obesity; nulliparity; familial history; multiple gestation; patient history of diabetes mellitus, chronic hypertension, renal disease, urinary tract infection, trophoblastic disease, peridontal disease, and malnutrition. Calcium deficiency is also linked to hypertensive disorders in pregnancy. Bariatric surgery for obese women may decrease their chances of becoming preeclamptic.
There is a genetic component in the development of both preeclampsia and pregnancy-induced hypertension (PIH). Several genes, such as the gene that codes for the angiotensin II type 1 receptor, have been associated, and mutations in the STOX1 gene has been found to cause preeclampsia in some Dutch families. Other candidate loci await confirmation.
Gender, ethnic/racial, and life span considerations
Preeclampsia tends to occur most frequently in pregnant adolescents, in women over age 35, and in African American women. It is also more common in primigravidas.
Global health considerations
The global incidence of preeclampsia ranges from 2% to 15% of all pregnancies, with developing regions in Africa having the highest incidence.
Obtain a thorough medical and obstetric history early in the pregnancy to determine if the patient has any of the risk factors. If she had a previous delivery, obtain information on any problems that occurred. Assess the patient’s level of consciousness and orientation because her mental status may deteriorate as preeclampsia progresses. Ask the patient if she has noticed an increase in edema, especially in her face; nondependent edema is more significant than dependent edema. The significant other may report that the patient’s face is “fuller.” Ask the patient if her hands and feet swell overnight and if her rings feel tight; she may even report that she is unable to take off her rings. Question her about any nausea, headaches, visual disturbances (blurred, double, spots), or right upper quadrant pain. Ask the patient and significant others if she has had seizures.
Common symptoms include hypertension, proteinuria, pitting edema, headache, and oliguria. Although most pregnant women experience some edema, it has a more abrupt onset in preeclampsia. Weigh the patient daily in the same clothes and at the same time to help estimate fluid retention; often, the patient gains several pounds in 1 week. BP should be taken on the right arm while the patient is supine and also in the left lateral position. Compare BP readings to determine increasing trends.
A funduscopic inspection of the retina may reveal vascular constriction and narrowing of the small arteries. Auscultate the patient’s lungs bilaterally to assess for pulmonary edema. Assess the deep tendon reflexes and assign a rating from 1 to 4; with PIH, reflexes are brisker than normal. Check for clonus bilaterally by dorsiflexing the foot briskly and checking if the foot comes back and “taps” your hand. Count the beats of clonus present; presence of clonus is indicative of central nervous system involvement. Perform a sterile vaginal examination to determine if the patient is in labor or to determine the “ripeness” of her cervix for labor. Also note if the amniotic sac is intact or ruptured and if there is any bloody “show,” which signals the onset of labor. If the amniotic sac is ruptured, note the color, amount, and presence of odor of the fluid. Assess the uterus for the presence of contractions, noting the frequency, duration, and intensity. Place the patient on the fetal monitor immediately to determine the status of the fetus. Provide ongoing assessments of the baseline fetal heart rate and of the presence or absence of variability, accelerations, and decelerations in the heart rate. Often, a nonstress test (NST) is done on admission to assess the fetus’s well-being.
Remember that the patient’s condition can deteriorate rapidly. Vigilantly monitor for signs and symptoms of progressive disease and impending eclampsia and HELLP. Assess the blood pressure, pulse, respirations, and urine output hourly. Check deep tendon reflexes and for clonus hourly or as ordered. Report upward trends. Be alert for such signs and symptoms of impending eclampsia as accelerating hypertension, headache, epigastric pain, nausea, visual disturbances, and altered sensorium, and also increased bleeding tendencies.
Many women expect pregnancy to be a happy and normal process; the hospitalization is unexpected. Assess the patient’s ability to cope with the disorder and her social supports. In addition to concern about the pregnancy, she may have other children who need care while she is hospitalized. Assess the resources of the patient and significant others to manage job, child-care, financial, and social responsibilities.
General Comments: The minimum diagnostic criteria for preeclampsia is BP > 140/90 mm Hg after 20 weeks' gestation and proteinuria > 300 mg in 24 hours or > 1+ dipstick. Other evidence to support the diagnosis of preeclampsia is elevated serum creatinine, lactate dehydrogenase (LDH), alanine aminotransferase (ALT), or aspartate transaminase (AST); low platelets; persistent headache or visual disturbance; persistent epigastric pain; and increasing BP and proteinuria. Serial laboratory tests are done to assist with diagnosis and monitoring of the disease. Increasing and decreasing trends indicate improvement or worsening of the disease state and help diagnose multiorgan involvement.
|Test||Normal Result||Abnormality With Condition||Explanation|
|Dip/24-hr urine for protein and creatinine||Dip–negative 80–125 mL/min||2+ or higher > 3g/L for 24 hr elevated||Increase in protein and creatinine in the urine indicates renal disease|
|Uric acid||2–6.6 mg/dL||Elevated||Indicates renal disease|
|Blood urea nitrogen (BUN)||10–20 mg/dL||Elevated||Indicates renal disease|
|Liver enzymes || ||Elevated||Increases indicate liver involvement|
|Platelets||150,000–400,000/mm3||Decreased||Decrease caused by endothelial damage and activation of thrombin|
Other Tests: Tests include complete blood count and coagulation studies. Starting at the 26th week of gestation, fetal testing assesses well-being and includes modified biophysical profiles (BPP), and with decreased amniotic fluid or lack of fetal reactivity, a full BPP (ultrasonography to measure fetal breathing, fetal movement, fetal tone, and amniotic fluid volume); contraction stress or Doppler velocimetry; for women in labor, continuous fetal monitoring and possible scalp pH. If the fetus is premature, an amniocentesis may be done to obtain amniotic fluid for fetal lung maturity tests. If cerebral edema or intracranial bleeding is suspected, computed tomography scanning and magnetic resonance imaging are used.
Primary nursing diagnosis
DiagnosisAltered tissue perfusion (cardiopulmonary, cerebral, peripheral, renal) related to arterial vasospasm and obstruction to flow
OutcomesVital signs status; Urinary elimination; Fluid balance; Neurological status; Coagulation status; Tissue perfusion: Abdominal organs; Fetal status: Intrapartum
InterventionsFluid monitoring; Fluid/electrolyte management; Seizure precautions; Medication administration; Vital signs monitoring; Fluid management; Bedside laboratory testing; Electronic fetal monitoring
Planning and implementation
Tight BP control in both mild chronic essential and gestational nonproteinuric hypertension in pregnancy leads to better perinatal outcomes and less severe hypertension. Often, preeclampsia occurs before the fetus is term. The goals of treatment are to prevent seizures, intracranial hemorrhage, and serious organ damage in the mother and to deliver a healthy term infant. The only cure for preeclampsia is delivery of the infant; however, if the infant is preterm, care is balanced between preventing maternal complications and allowing the fetus more time in utero. If the symptoms in preeclampsia are mild, often the patient is treated at home on bedrest, with careful instructions and education on the danger signs and frequent prenatal visits to monitor progression of the disorder. Antihypertensives are usually not prescribed for mild preeclamptics; no differences in gestational age or birthweight have been noted, and growth-restricted infants were twice as frequent in mothers who took labetalol than in those treated with bedrest/hospitalization alone. Mild preeclampsia is really a misnomer because it can become severe very rapidly. Frequent tests of fetal well-being are done throughout the pregnancy, including an NST and BPP, to detect the effects of preeclampsia on the fetus.
If symptoms of preeclampsia worsen, hospitalization is mandatory. Maintain the patient on complete bedrest. If the urine output is below 30 mL/hr, suspect renal failure and notify the physician. Readings of 2+ to 4+ protein in the urine and urine-specific gravities of greater than 1.040 are associated with proteinuria and oliguria. Hemodynamic monitoring with a central venous pressure catheter or a pulmonary artery catheter may be initiated to regulate fluid balance. Magnesium sulfate is given via intravenous (IV) infusion to prevent seizures. Serum magnesium levels are done to determine if the level has reached the therapeutic level; serum levels also alert the caregiver of a move toward toxicity. If the magnesium sulfate infusion does not prevent seizure, the physician may order phenobarbital or benzodiazepines. Using either low doses of aspirin or dietary calcium supplementation is being explored as means to prevent preeclampsia.
If the patient is alert and is not nauseated, a high-protein, moderate-sodium diet is appropriate. Low-salt diets are not indicated. Glucocorticoids may be given to the mother intramuscularly at least 48 hours before delivery to assist in maturing fetal lungs to decrease the severity of respiratory difficulties in the preterm neonate. A cesarean section is indicated if the fetus is showing signs of distress or if preeclampsia is severe and the patient is not responding to aggressive treatment. All efforts are made to stabilize the patient’s condition before surgery.
|Medication or Drug Class||Dosage||Description||Rationale|
|Magnesium sulfate||6 g IV piggyback (PB) loading dose; 2 g/hr IV maintenance dose for 12 to 24 hr||Anticonvulsant||PIH can progress to eclampsia; drug of choice to prevent seizures|
|Calcium gluconate||1 g IV push (IVP) slowly over 3 min||Antidote for magnesium sulfate||Respiratory depression occurs with magnesium toxicity|
| ||Varies with drug ||Antihypertensive||Given if diastolic is > 110 mm Hg; IV medication is used if oral is ineffective|
Maintain the patient on bedrest in the left lateral position as much as possible. This position assists with venous return and organ perfusion. Maintain a quiet, dim environment for rest, close to the nurse’s station. Eliminate extraneous noises, lights, visitors, and interruptions that might precipitate a seizure. Plan assessments and care to ensure optimal rest. Pad the side rails and keep the bed in the low position with the call light in reach at all times. To be prepared for emergencies, keep a “toxemia kit,” which includes an artificial airway, calcium gluconate (antidote for magnesium sulfate), syringes, alcohol pads, and other medications, at the bedside. If the patient is receiving magnesium sulfate, monitor for signs of magnesium toxicity: hyporeflexia, decreased respirations, and oliguria. Expect the patient receiving magnesium sulfate to be lethargic.
If the patient is in labor, closely monitor fetal heart rate patterns and contractions. If the fetal heart rate shows signs of stress, turn the patient to her left side, increase the rate of the IV fluids, administer humidified oxygen per mask at 10 L/min, and notify the physician. Because abruptio placentae is a potential complication of preeclampsia, be alert for any of the following signs of placental detachment: profuse vaginal bleeding, increased abdominal pain, and a rigid abdomen. The fetus also shows signs of distress (late decelerations, bradycardia).
Provide emotional support to the patient and family. The onset and severity of preeclampsia, along with its potential outcomes for the infant, are worrisome. If delivery of a preterm infant is imminent, educate the family on the environment and care given in the neonatal intensive care unit (NICU). Tour the NICU with the father and explain what can be expected after the birth. This preparation helps alleviate some of the new parents’ fears after the delivery.
After delivery, complications of preeclampsia can still manifest over the next 48 hours. Continue ongoing monitoring; be alert for seizures and indications that the patient is going into HELLP syndrome.
Evidence-Based Practice and Health Policy
Robinson, C.J., Alanis, M.C., Wagner, C.L., Hollis, B.W., & Johnson, D.D. (2010). Plasma 25-hydroxyvitamin D levels in early-onset severe preeclampsia. American Journal of Obstetrics and Gynecology, 203(4), 366.e1–6. doi 10.1016/j.ajog.2010.06.036
- In a study in which 50 women with early-onset severe preeclampsia (EOSP) were compared to 100 gestation-matched healthy control women, a greater proportion of women with EOSP had deficient vitamin D levels (< 20 ng/mL) compared to women without EOSP (54% versus 27%; p = 0.005).
- Mean plasma vitamin D levels were 18 ng/mL among women with EOSP compared to 32 ng/mL in women without EOSP (p < 0.001), and each 10 ng/mL increase in maternal plasma vitamin D was associated with a 63% decreased odds of EOSP (95% CI, 0.22 to 0.62; p < 0.001).
- Women with EOSP were younger (mean age, 24 years versus 28 years; p = 0.001), had higher body mass indexes (mean, 34 versus 28; p < 0.001), and had a mean arterial pressure more than 1.5 times that of women without EOSP (mean, 125 mmHg versus 78 mmHg; p < 0.001).
- Compared to infants of women without EOSP, infants of women with EOSP were significantly more likely to experience intrauterine growth restriction (42% versus 10%; p < 0.001), delivery at a younger gestational age (mean, 29 weeks versus 39 weeks; p < 0.001), and lower birthweight (mean, 1,170 versus 3,260 grams; p < 0.001).
- Vital signs: BP (value and patient’s position); heart rate; daily weights; intake and output
- Edema: Location, presence or absence of pitting, numerical rating (1 to 4)
- Reflexes rated on a 1 to 4 scale and presence or absence of clonus
- Presence or absence of headache, visual disturbances, altered sensorium, epigastric discomfort, nausea
- Response to treatment: Anticonvulsants, antihypertensives, sedatives, bedrest
- Fetal assessment: Baseline heart rate; presence or absence of accelerations, decelerations, variability, fetal movement; response to movement
- Patient’s response to pain during labor and to pain relief measures (analgesics, epidural)
Discharge and home healthcare guidelines
home care if undelivered.If the patient is discharged undelivered, emphasize that follow-up appointments are important for timely diagnosis of progressive preeclampsia. Educate the patient on the importance of the left lateral position for bedrest. Tell the patient to notify the physician immediately for any of the following symptoms: headache; visual disturbance; right upper quadrant pain; change in level of consciousness or “feeling funny”; decreased urine output; increase in edema, especially facial; or any decrease in fetal movement. Tell the patient to weigh herself daily and notify the physician of a sudden weight gain. Be sure the patient understands the seriousness of the disorder and the potential complications to her and her infant.
home care if delivered.If the patient is discharged delivered, she needs to receive similar teaching because preeclampsia does not resolve immediately after delivery.
Patient discussion about Preeclampsia
Q. I pee when I laugh, what to do? Whenever I laugh really hard, I can't help peeing. Help! What to do? This is embarrassing.
Q. Hi, I´m bleeding when I pee,suggestions? I´m 42 years old,and I had a lot of pain days ago just like before when I had a kidney stone and now I´m bleeding when I pee but I don´t know if could be a different problem