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Not all hospitals have standardized protocols for caring for women with preeclampsia.1 Recent reports from the World Health Organization (WHO) estimate that preeclampsia is responsible for 70,000 maternal deaths annually in the world.2 Preeclampsia and elevated blood pressures are a serious problem that must be treated appropriately and quickly. It is important to review the different types of hypertension in pregnancy when caring for pregnant women with blood pressure issues. Chronic hypertension is diagnosed when a woman has systolic blood pressures (SBP) ≥ 140 or diastolic blood pressures (DBP) ≥ 90, and this occurs pre-pregnancy or <20 weeks gestation. Gestational hypertension is diagnosed with SBP ≥ 140 or DBP ≥ 90, and the patient is > 20 weeks, and there is an absence of proteinuria or systemic signs/symptoms.
Preeclampsia is defined as SBP ≥ 140 or DBP ≥ 90 and proteinuria with or without signs/symptoms OR presentation of signs/symptoms/lab abnormalities but no proteinuria. Preeclampsia with severe features is defined as systolic BP of 160 mm Hg or higher, or diastolic BP of 110 mm Hg or higher on 2 occasions at least 4 hours apart while the patient is on bed rest (unless antihypertensive therapy is initiated before this time), thrombocytopenia (platelet count less than 100,000/microliter), impaired liver function as indicated by abnormally elevated blood concentrations of liver enzymes (to twice normal concentration), severe persistent right upper quadrant or epigastric pain unresponsive to medication and not accounted for by alternative diagnoses, progressive renal insufficiency (serum creatinine concentration greater than 1.1 mg/dL or a doubling of the serum creatinine concentration in the absence of other renal disease), pulmonary edema, OR new-onset cerebral or visual disturbances. Eclampsia is diagnosed if the woman has seizures.
HELLP syndrome is considered to be a variant of preeclampsia. Sometimes the presence of HELLP syndrome is due to an underlying disease such as antiphospholipid syndrome. In women with preeclampsia or eclampsia, HELLP develops in 10% to 20% of pregnancies. HELLP is characterized by hemolysis (the breakdown of red blood cells), elevated liver enzymes, and low platelets.3
However, the cause of hypertension really is not important with severely elevated blood pressures. Acute onset, persistent (lasting 15 min or more), severe systolic (≥160 mm Hg) or severe diastolic hypertension (≥ 110 mm Hg) or both in pregnant or postpartum women with preeclampsia/eclampsia constitutes a hypertensive emergency, and it is inadvisable to wait 4 hours for treatment.4 “Controlling blood pressure is the optimal intervention to prevent deaths due to stroke in women with preeclampsia.5” Prompt treatment to lower BP can decrease maternal morbidity and mortality.
There are known risk factors for preeclampsia. Not all women with these risk factors will develop preeclampsia. And not all women with preeclampsia had these risk factors. The risk factors may be useful in the early identification and treatment of women (see table 1).2
Table 1: Summary of Principal Risk Factors for Preeclampsia
Mean RR (95% CI)
Relative Risk of Preeclampsia
Family History of Preeclampsia
Age >40 Years
Abbreviations: CI = confidence interval; RR = relative risk
Patients with preeclampsia require close monitoring. A thorough initial assessment of the woman with possible preeclampsia should include a complete history, a complete physical exam with close attention to preeclampsia symptoms including unremitting headaches, edema, visual changes, and epigastric pain, fetal activity, and vaginal bleeding. The RN should review baseline BPs throughout pregnancy, medications and/or drugs throughout pregnancy (illicit & OTC). The patient should have current vital signs, including O2 saturation. The RN should also review current and past fetal assessment: FHR monitoring results estimated fetal weight and recent biophysical profile. Labs that should be drawn are CBC, platelets, LDH, liver function tests, electrolytes, BUN and creatinine, and a urine sample sent for a protein/creatinine ratio.
The nursing assessments needed vary depending on the diagnosis. Women with preeclampsia without severe features need vital signs, including pulse ox, and lung sounds every 4 hours. Level of consciousness, edema, and assessment for headache, visual disturbances, epigastric pain should occur every 8 hours. Intake and output should be monitored hourly. Fetal monitoring should be done as ordered.
Women with preeclampsia with severe features OR women on magnesium sulfate need vital signs, including pulse ox every 30 minutes (should be done every 5 minutes during loading dose of magnesium sulfate). These women need lung sounds assessed every 2 hours. Level of consciousness, edema, and assessment for headache, visual disturbances, epigastric pain should occur every 8 hours. Strict (hourly) intake and output should be monitored, and intake should be ≤ 125 mL/hour. Fetal monitoring should be continuous as ordered.4 Once the woman is stable without severe features and not on magnesium sulfate, she may be monitored as a patient with preeclampsia without severe features.
Persistent, severe hypertension can occur antepartum, intrapartum, or postpartum. Two severe BP values (≥ 160/110) taken 15-60 minutes apart require treatment within 60 minutes of the 2nd elevated BP. The acceptable treatments for severe BP are intravenous (IV) labetalol, intravenous hydralazine, or oral nifedipine. One medication should be chosen and initiated (see table 2).1
Table 2: Antihypertensive Medications
Labetalol (20, 40, 80, 80 mg IV* over 2 minutes, escalating doses, repeat every 10 minutes or 200 mg orally if no IV access); avoid in asthma or heart failure, can cause neonatal bradycardia
Hydralazine (5-10 mg IV* over 2 minutes, repeat in 20 minutes until target blood pressure is reached)
Repeat blood pressure every 10 minutes during administration
* Maximum cumulative IV administered doses should not exceed 25 mg hydralazine; 220 mg labetalol in 24 hours.
Intravenous hydralazine may increase the risk of maternal hypotension. Intravenous labetalol may cause neonatal bradycardia and should be avoided in women with asthma, heart disease, or congestive heart failure. Nifedipine has been associated with an increase in maternal heart rate and less risk of overshoot hypotension. No significant changes in umbilical blood flow have been observed with the use of either labetalol or hydralazine, and outcomes are similar for both drugs. No significant changes in the uteroplacental blood flow or the fetal heart have been noted with the use of immediate-release oral nifedipine for the treatment of severe pregnancy-induced hypertension. However, immediate-release oral nifedipine should not be given sublingually because of risk of hypotension.1
Using an algorithm similar to what is shown in table 3 can improve treatment times and patient outcomes.1
Magnesium sulfate may also be administered as a central nervous system depressant, to decrease the risk of seizures. While magnesium may decrease BP, it is not used as an antihypertensive. Myasthenia gravis is a contraindication to giving Mag sulfate.
Magnesium is usually given as a 4 to 6gm loading dose followed by 2 gm/hr IV. This may be started antepartum or intrapartum and continue for 24 hours after delivery. The therapeutic range: 4.8-8.4. Serum levels are not indicated unless signs and symptoms of toxicity or renal insufficiency. Before starting mag sulfate, a BUN and creatinine should be drawn to assess renal function.4 Magnesium toxicity is dangerous and can cause severe complications, such as renal failure or death. The RN must perform proper assessments, which include checking for headache, visual changes, altered level of consciousness. Vital signs need to be monitored, as well as reflex status, and intake and output. Provider should be notified of any of the following signs of magnesium toxicity: depressed or absent reflexes, respirations less than 12 per minute, or urinary output of less than 30 mL per hour or less than 120 mL in four hours.4 Early signs of magnesium toxicity are warm/hot “all over”, flushing, increased thirst, diaphoresis, depressed reflexes, hypotension, or flaccidity. Late signs are CNS depression, increased drowsiness, lethargy, slurring of speech, respiratory paralysis, or circulatory collapse. The antidote for magnesium sulfate toxicity is 10% Calcium Gluconate 1-gram IV push over 3 minutes.
An eclamptic seizure would include the same antihypertensives, magnesium sulfate, and also anticonvulsants.
Preeclampsia and eclampsia are dangerous diseases that can cause complications to both the woman and the fetus. Women with preeclampsia are at increased risk for damage to the kidneys, liver, brain, and other organs and blood systems. Central nervous system disturbances are possible (seizure, unremitting headache, visual disturbance). A woman with preeclampsia is at an increased risk of pulmonary edema, thrombocytopenia, hemolysis, coagulopathy, and oliguria. These women are also at an increased risk of stroke.6
Preeclampsia may affect the placenta. This could lead to placental abruption, preterm delivery, intrauterine growth restriction, or stillbirth.6
Women with preeclampsia are still at risk for problems after discharge. Women who had preeclampsia are four times more likely to develop hypertension and are twice as likely to develop later ischemic heart disease, a blood clot in a vein, and stroke than women who did not have preeclampsia. Mothers who had preeclampsia can also experience permanent damage to their organs, such as their kidneys and liver. These women can experience fluid in the lungs and remain at increased risk for developing eclampsia and seizures.6 Studies show that many women do not know their risks when being discharged.7 Education is a vital part of preeclampsia.
These women need to know their risks and signs and symptoms to look for, such as headache, visual changes, shortness of breath, or altered level of consciousness. Women need to understand that they must call their provider or go to the emergency department with any of these symptoms. Women treated with medications for elevated BPs should have a visit to their provider 3 days after discharge for a blood pressure check. These women also need to know the long-term consequences of preeclampsia and the importance of seeing their family physician. Women with preeclampsia should see their physician or a visiting nurse within 3-5 days after delivery and again in 7-10 days after delivery.4 Some hospitals are beginning to use telemedicine to follow up with these patients. Some of these women may see nephrologists in the outpatient setting. It is important that emergency departments are also aware of the signs and symptoms of postpartum preeclampsia.
24-year-old G2, P0-0-1-0 @ 39 wks. Prenatal course unremarkable, blood pressure normal throughout the prenatal period.? Presented to the office with a complaint of regular uterine contractions, BP: 142/95. Urinalysis negative for protein. The patient was admitted for spontaneous labor and gestational hypertension. On admission to labor and delivery: BP 133/74, urinalysis negative, platelet count: 187,000/unit, AST 14, ALT 18. BP remained modestly elevated throughout labor and postpartum stay. The patient had primary late-term c/section for failure to progress. The postpartum course was unremarkable. No documented complaints of headache, blurred vision or epigastric pain. On day 3 post-op, the patient complained of “acute, crushing headache,” pain rated 8/10. Discharge orders are already written. The patient received hydrocodone 15 mg/acetaminophen 650 mg and discharged 30 minutes later. Post-op day #4: Patient reported worsening headache to family. Post-op day #5: Progressively worsening headache and new-onset visual changes.
The family called 911. The initial seizure occurred shortly thereafter, and multiple seizures witnessed by family. The patient was intubated in the field and transported to the hospital, where she was started on Magnesium sulfate, Ativan, Keppra, and labetalol. The patient was extubated shortly after admission, and BP’s remained elevated with max 148/98; SBP mostly 130’s; DBP mostly 80’s, platelet count 370,000, AST 30, ALT 33, creatinine 0.9 mg/ dl, urinalysis: negative for protein. Persistent, mild headache with some postural component. MRI: “no evidence of ischemic injury.”
Delayed eclampsia >48 hours following delivery, up to 4 weeks postpartum accounts for approximately 15% of cases of eclampsia. 63% had no antepartum hypertensive diagnosis. The most common presenting symptom was a headache, which occurred in about 70% of patients; other prodromal symptoms included shortness of breath, blurry vision, nausea or vomiting, edema, neurological deficit, and epigastric pain.
Delayed onset prevented the ability to predict this outcome. She did not have an indication for early follow up to see the provider. The only indicator was the headache. The patient could have been kept in the hospital longer to evaluate the headache, especially with her history of gestational hypertension. She also may have called her doctor or went to ED sooner if she had the proper education.
Preeclampsia is a complicated disease. It can have devastating consequences to the mother or fetus if not treated promptly and correctly. It is important for nurses and providers to know the facts about preeclampsia. It is also important for nurses to educate the woman so that she can advocate for her care as well.
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