case study on eclampsia scribd

Table of Contents

Introduction, case description, conclusions.

Makin MS (2021) Eclampsia at 20 Weeks of Gestation: A Case Report. Obstet Gynecol Cases Rev 8:201. doi.org/10.23937/2377-9004/1410201

Case Report | OPEN ACCESS DOI: 10.23937/2377-9004/1410201

Eclampsia at 20 weeks of gestation: a case report, mary sue makin *.

Daeyang Luke Hospital in Lilongwe, Malawi

A 23-year-old primigravida with unknown last menstrual period and 20 weeks gestation by ultrasound presented to Daeyang Luke Hospital in Lilongwe, Malawi with a history of headache, fever, vomiting and new-onset of convulsions. At the time of her admission the full blood count instrument at our hospital was out of service. A rapid blood test for malaria was positive. After an initial blood pressure of 164/127 and 3+ proteinuria on urinary dipstick the diagnosis of eclampsia was made. She was given magnesium sulfate by intravenous protocol and labor was induced with vaginal misoprostol. She delivered a nonviable premature infant after six hours. This case is presented because of the rarity of eclampsia at 20 weeks gestation [ 1 ] and to discuss some of the recent advances in the pathogenesis of preeclampsia especially as it pertains to early developmental changes in the maternofetal junctional zone.

Hypertensive disorders of pregnancy cause 14% of all maternal deaths globally, approximately 42,000 each year. 99% of these deaths occur in low resource settings [ 2 ]. According to WHO estimates, the incidence of preeclampsia in developing countries (2.8% of live births) is seven times higher than in developed countries (0.4% of live births). Eclampsia increases the risk of maternal death both in developed countries (0.4% of live births) and in developing countries (15%) [ 3 - 7 ]. Adequate obstetrical care in developing countries must include clinicians and facilities who are well versed and well prepared to care for preeclamptic and eclamptic patients.

The precise etiopathogenesis of preeclampsia is still a subject of extensive research, but most researchers believe it is multifactorial. Globally about 80% of all preeclamptic pregnancies occur after 34 weeks and are classified as “late onset”. These pregnancies have normally grown babies and no changes in blood flow in the umbilical arteries. Early onset preeclampsia makes up the rest of the affected pregnancies and is characterized by an inadequate and incomplete trophoblast invasion of maternal spiral arteries and clear signs of fetal growth restriction [ 8 ].

The pathogenesis of preeclampsia is complex with numerous genetic, immunologic and environmental factors interacting. Recently Hladunewich, et al. described preeclampsia as a two-stage process. The first stage is one of abnormal placental development occurring in the first trimester of pregnancy. This abnormal development results in placental insufficiency and the release of excessive amounts of placental materials into the maternal circulation. The second stage, the maternal syndrome, results from the failure of cytotrophoblast remodeling of uterine spiral arteries. This cytotrophoblastic failure is thought to release secreted factors that enter the maternal circulation resulting in the signs and symptoms of preeclampsia [ 7 , 8 ].

Extensive angiogenesis is necessary in human placentation to establish a suitable network for the supply of oxygen and nutrients to the fetus. Developing placentas secrete a variety of pro-and antiangiogenic factors. Placental angiogenesis has been found to be defective in preeclampsia as evidenced by the failure of the cytotrophoblasts to convert from an epithelial to an endothelial phenotype, based on cell surface marker studies [ 8 - 11 ].

In 2003 Maynard hypothesized that placental ischemia is an early event in preeclamptic pregnancies, leading to placental production of a soluble factor or factors that cause maternal endothelial dysfunction. He found that excess circulating sFlt1 secreted by the placenta in preeclampsia led to endothelial dysfunction, hypertension and proteinuria. He also found that rising levels of sFlt1 were accompanied by falling levels of vascular endothelial growth factor (VEGF), a signal protein produced by cells that stimulate angiogenesis, and falling levels of placenta growth factor (PlGF), a potent angiogenic factor of the VEGF family [ 12 , 13 ].

During implantation fetal trophoblast cells and maternal uterine tissues, which include endometrium and myometrium, come into intimate contact with each other. This results in a zone made up of fetal and maternal cells which can be called the maternofetal junctional zone. At the time of delivery part of the junctional zone adheres to the placenta and forms the bottom of the intervillous space, the basal plate. The remaining part of the junctional zone adheres to the uterine wall after delivery and makes up the placental bed [ 14 , 15 ].

The placental bed is that part of the decidua and adjoining myometrium which lies below the placenta. The function of this area is to maintain an adequate blood supply to the intervillous space of the placenta. Early in pregnancy spiral arteries from the placental bed are invaded by cytotrophoblasts that break down arterial endothelium, internal elastic lamina and the muscular layer of the vessel. These physiologic changes convert the vessels from muscular end arteries to wide mouthed sinusoids. A 5-10-fold dilation of the spiral arteries occurs resulting in a decrease in vascular resistance and an increase in blood flow to the fetus [ 14 - 16 ].

In normal pregnancies the physiologic changes described above involve the myometrial segment of the spiral arteries and these changes are completed by 20 weeks. In preeclampsia and intrauterine growth restriction the changes in the spiral arteries are limited to the decidual segment of the placental bed and the process does not extend into the myometrium [ 12 ].

Preeclampsia is classically described as the presence of hypertension and proteinuria in a previously normotensive pregnant woman after the 20 th week of pregnancy. This diagnosis is also applied in the absence of proteinuria if there is evidence of target organ damage [ 11 ].

The diagnosis of eclampsia should always be considered when convulsions occur in a pregnant woman after the 20 th week of gestation. Occurrence of eclampsia before 20 weeks is rare and a molar pregnancy should be considered. During management of a presumed eclamptic patient if convulsions continue to occur even after therapeutic dosages of magnesium sulfate have be administered, a cerebrovascular accident must be considered. Other conditions to be considered include expansive brain injury, toxic and metabolic encephalopathies, reversible cerebral vasoconstriction syndrome, thrombotic thrombocytopenic purpura, and central nervous system infection [ 14 ].

Convulsions without neurological deficits can be caused by metabolic abnormalities such as hypocalcemia, hyponatremia and hypoglycemia. Drug or alcohol withdrawal, infection (meningitis, encephalitis, sepsis) or recent head trauma should be considered. Disorders such as thrombotic thrombocytopenic purpura and uremic hemolytic syndrome can be triggered by pregnancy. A prior diagnosis of epilepsy should be ruled out [ 1 , 14 ].

A 23-year-old primigravida presented to the hospital with a history of headache, fever, vomiting and four episodes of convulsions the day of admission. Her mother described tonic-clonic movements lasting one to two minutes. She had no previous history of hypertension, convulsions or epilepsy. Admission blood pressure was 184/134, pulse 111, temperature 36.4 °C. A full blood count was not available at our hospital on admission, but the rapid test for malaria was positive and urine protein was 3+ on dipstick. Ultrasound revealed a viable intrauterine pregnancy with estimated gestational age 20 weeks. A lumbar puncture was done with benign results.

She was started on intravenous artesunate, intravenous magnesium sulfate and hydralazine per hospital protocols. Induction of labor with vaginal misoprostol was begun four hours after admission with the diagnosis of eclampsia at 20 weeks gestation. Twelve hours after induction she delivered a nonviable fetus and had an evacuation of retained products of conception in the theatre. Over the next 48 hours her blood pressures fluctuated between 150 and 174 systolic and 94 and 124 diastolic. She was discharged home on nifedipine 10 mg PO BD on her second postpartum day. Her blood pressure was 130/80 two weeks postpartum on no antihypertensives.

This case presentation is remarkable for the early gestational age of 20 weeks at which the convulsions occurred. 91% of all cases of eclampsia develop at or after 28 weeks gestation. 7.5% occur between 21 and 28 weeks. Only 1.5% occurs at 20 weeks or earlier [ 7 ].

This patient arrived at our hospital late in the afternoon at a time when our instrument for doing full blood counts was not functioning. With the elevated blood pressure and 3+ proteinuria the diagnosis of eclampsia was secure. The possibility of cerebral malaria was also considered. A lumbar puncture was performed to conclusively rule out meningitis. Because of the impossibility of survival for the fetus at this gestational age in a developing country like Malawi, the decision to induce labor was made. Even though we had no access to a full blood count, liver or kidney function tests, or cerebral imaging, the situation was considered critical to begin the induction of labor. Fortunately, the patient had an uneventful vaginal delivery and returned to a normal blood pressure by two weeks after the delivery.

• Sibai B (2005) Diagnosis, prevention and management of eclampsia. Obstet Gynecol 105: 402-410.
• Nakano K, Tsunemi T, Akasaka J, Shigemitsu A, Naruse K, et al. (2017) A case of very early onset eclampsia, placental abruption and intrauterine fetal death. Hypertens Res Pregnancy 5: 17-19.
• Tanaka M, Tsujimoto Y, Goto K, Kumahara K, Onishi S, et al. (2015) Preeclampsia before 20 weeks of gestation: A case report and review of the literature. CEN Case Rep 4: 55-60.
• Vousden N, Lawley E, Seed PT, Gidiri MF, Goudar S, et al. (2019) Incidence of eclampsia and related complications across 10 low- and middle-resource geographical regions: Secondary analysis of a cluster randomised controlled trial. PLoS Med 16: e1002775.
• Meazaw M, Chojenta C, Muluneh M, Loxton D (2020) Systematic and meta-analysis of factors associated with preeclampsia and eclampsia in sub-Sahara Africa. PLoS One 15: e0237600.
• World Health Organization (WHO) (2019) Trends in Maternal Mortality 2000 to 2017. Estimates by WHO, UNICEF, UNFPA, World Bank Group and the United Nations Population Division, Geneva, Switzerland.
• Lilungulu A, Bintabara D, Mujungu S, Chiwanga E, Chetto P, et al. (2020) Incidence and predictors of maternal and perinatal mortality among women with severe maternal outcomes: A tanzanian facility-based survey for improving maternal and newborn care. Obstet Gynecol Int 2020: 5390903.
• Huppertz B (2008) Placental origins of preeclampsia: Challenging the current hypothesis. Hypertension 51: 970-975.
• Hladunewich M, Karumanchi S, Lafayette R (2007) Pathopysiology of the clinical manifestations of preeclampsia. Clin J Am Soc Nephrol 2: 543-549.
• Zhou Y, Damsky C, Fisher S (1997) Preeclampsia is associated with failure of human cytotrophoblasts to mimic a vascular adhesion phenotype. J Clin Invest 99: 2139-2151.
• Peracoli J (2019) Pre-eclampsia/eclampsia. Rev Bras Ginecol Obstet 41: 318-322.
• Maynard S, Min J, Merchan J, Lim KH, Li J, et al. (2003) Excess placental soluble fms-like tyrosine kinase 1 (sFltl1) may contribute to endothelial dysfunction, hypertension and preeclampsia. J Clin Invest 111: 649-658.
• Valenzuela F, Perez-Sepulveda A, Torres M, Correa P, Repetto G, et al. (2012) Pathogenesis of preeclampsia: The genetic component. J Pregnancy 2012: 632732.
• Kaufmann P, Black S, Huppertz B (2003) Endovascular trophoblastic invasion: Implications for the pathogenesis of intrauterine growth restriction and preeclampsia. Biol Reprod 69: 1-7.
• Nobis P, Gautam H, Kathar K, Goswami P, Sharma J (2020) Spiral artery morphology in relation to hypertension in pregnancy and birthweight by placental bed biopsy: A retrospective analysis. Ann Clin Lab.
• Hennessy A, Makris A (2011) Preeclamptic nephropathy. Nephrology 16: 134-143.

Loading metrics

Open Access

Learning Forum

Learning Forum articles are commissioned by our educational advisors. The section provides a forum for learning about an important clinical problem that is relevant to a general medical audience.

See all article types »

A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria

• Andrea Luk,

* To whom correspondence should be addressed. E-mail: [email protected]

• Ching Wan Lam,
• Wing Hung Tam,
• Anthony W. I Lo,
• Enders K. W Ng,
• Alice P. S Kong,
• Wing Yee So,
• Chun Chung Chow
• Andrea Luk, 
• Ronald C. W Ma, 
• Ching Wan Lam, 
• Wing Hung Tam, 
• Anthony W. I Lo, 
• Enders K. W Ng, 
• Alice P. S Kong, 
• Wing Yee So, 

Published: February 24, 2009

• https://doi.org/10.1371/journal.pmed.1000037
• Reader Comments

Citation: Luk A, Ma RCW, Lam CW, Tam WH, Lo AWI, Ng EKW, et al. (2009) A 21-Year-Old Pregnant Woman with Hypertension and Proteinuria. PLoS Med 6(2): e1000037. https://doi.org/10.1371/journal.pmed.1000037

Copyright: © 2009 Luk et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Funding: The authors received no specific funding for this article.

Competing interests: RCWM is Section Editor of the Learning Forum. The remaining authors have declared that no competing interests exist.

Abbreviations: CT, computer tomography; I, iodine; MIBG, metaiodobenzylguanidine; MRI, magnetic resonance imaging; SDH, succinate dehydrogenase; SDHD, succinate dehydrogenase subunit D

Provenance: Commissioned; externally peer reviewed

Description of Case

A 21-year-old pregnant woman, gravida 2 para 1, presented with hypertension and proteinuria at 20 weeks of gestation. She had a history of pre-eclampsia in her first pregnancy one year ago. During that pregnancy, at 39 weeks of gestation, she developed high blood pressure, proteinuria, and deranged liver function. She eventually delivered by emergency caesarean section following failed induction of labour. Blood pressure returned to normal post-partum and she received no further medical follow-up. Family history was remarkable for her mother's diagnosis of hypertension in her fourth decade. Her father and five siblings, including a twin sister, were healthy. She did not smoke nor drink any alcohol. She was not taking any regular medications, health products, or herbs.

At 20 weeks of gestation, blood pressure was found to be elevated at 145/100 mmHg during a routine antenatal clinic visit. Aside from a mild headache, she reported no other symptoms. On physical examination, she was tachycardic with heart rate 100 beats per minute. Body mass index was 16.9 kg/m 2 and she had no cushingoid features. Heart sounds were normal, and there were no signs suggestive of congestive heart failure. Radial-femoral pulses were congruent, and there were no audible renal bruits.

Baseline laboratory investigations showed normal renal and liver function with normal serum urate concentration. Random glucose was 3.8 mmol/l. Complete blood count revealed microcytic anaemia with haemoglobin level 8.3 g/dl (normal range 11.5–14.3 g/dl) and a slightly raised platelet count of 446 × 10 9 /l (normal range 140–380 × 10 9 /l). Iron-deficient state was subsequently confirmed. Quantitation of urine protein indicated mild proteinuria with protein:creatinine ratio of 40.6 mg/mmol (normal range <30 mg/mmol in pregnancy).

What Were Our Differential Diagnoses?

An important cause of hypertension that occurs during pregnancy is pre-eclampsia. It is a condition unique to the gravid state and is characterised by the onset of raised blood pressure and proteinuria in late pregnancy, at or after 20 weeks of gestation [ 1 ]. Pre-eclampsia may be associated with hyperuricaemia, deranged liver function, and signs of neurologic irritability such as headaches, hyper-reflexia, and seizures. In our patient, hypertension developed at a relatively early stage of pregnancy than is customarily observed in pre-eclampsia. Although she had proteinuria, it should be remembered that this could also reflect underlying renal damage due to chronic untreated hypertension. Additionally, her electrocardiogram showed left ventricular hypertrophy, which was another indicator of chronicity.

While pre-eclampsia might still be a potential cause of hypertension in our case, the possibility of pre-existing hypertension needed to be considered. Box 1 shows the differential diagnoses of chronic hypertension, including essential hypertension, primary hyperaldosteronism related to Conn's adenoma or bilateral adrenal hyperplasia, Cushing's syndrome, phaeochromocytoma, renal artery stenosis, glomerulopathy, and coarctation of the aorta.

Box 1: Causes of Hypertension in Pregnancy

• Pre-eclampsia
• Essential hypertension
• Renal artery stenosis
• Glomerulopathy
• Renal parenchyma disease
• Primary hyperaldosteronism (Conn's adenoma or bilateral adrenal hyperplasia)
• Cushing's syndrome
• Phaeochromocytoma
• Coarctation of aorta
• Obstructive sleep apnoea

Renal causes of hypertension were excluded based on normal serum creatinine and a bland urinalysis. Serology for anti-nuclear antibodies was negative. Doppler ultrasonography of renal arteries showed normal flow and no evidence of stenosis. Cushing's syndrome was unlikely as she had no clinical features indicative of hypercortisolism, such as moon face, buffalo hump, violaceous striae, thin skin, proximal muscle weakness, or hyperglycaemia. Plasma potassium concentration was normal, although normokalaemia does not rule out primary hyperaldosteronism. Progesterone has anti-mineralocorticoid effects, and increased placental production of progesterone may mask hypokalaemia. Besides, measurements of renin activity and aldosterone concentration are difficult to interpret as the renin-angiotensin-aldosterone axis is typically stimulated in pregnancy. Phaeochromocytoma is a rare cause of hypertension in pregnancy that, if unrecognised, is associated with significant maternal and foetal morbidity and mortality. The diagnosis can be established by measuring levels of catecholamines (noradrenaline and adrenaline) and/or their metabolites (normetanephrine and metanephrine) in plasma or urine.

What Was the Diagnosis?

Catecholamine levels in 24-hour urine collections were found to be markedly raised. Urinary noradrenaline excretion was markedly elevated at 5,659 nmol, 8,225 nmol, and 9,601 nmol/day in repeated collections at 21 weeks of gestation (normal range 63–416 nmol/day). Urinary adrenaline excretion was normal. Pregnancy may induce mild elevation of catecholamine levels, but the marked elevation of urinary catecholamine observed was diagnostic of phaeochromocytoma. Conditions that are associated with false positive results, such as acute myocardial infarction, congestive heart failure, acute cerebrovascular event, withdrawal from alcohol, withdrawal from clonidine, and cocaine abuse, were not present in our patient.

The working diagnosis was therefore phaeochromocytoma complicating pregnancy. Magnetic resonance imaging (MRI) of neck to pelvis, without gadolinium enhancement, was performed at 24 weeks of gestation. It showed a 4.2 cm solid lesion in the mid-abdominal aorto-caval region, while both adrenals were unremarkable. There were no ectopic lesions seen in the rest of the examined areas. Based on existing investigation findings, it was concluded that she had extra-adrenal paraganglioma resulting in hypertension.

What Was the Next Step in Management?

At 22 weeks of gestation, the patient was started on phenoxybenzamine titrated to a dose of 30 mg in the morning and 10 mg in the evening. Propranolol was added several days after the commencement of phenoxybenzamine. Apart from mild postural dizziness, the medical therapy was well tolerated during the remainder of the pregnancy. In the third trimester, systolic and diastolic blood pressures were maintained to below 90 mmHg and 60 mmHg, respectively. During this period, she developed mild elevation of alkaline phosphatase ranging from 91 to 188 IU/l (reference 35–85 IU/l). However, liver transaminases were normal and the patient had no seizures. Repeated urinalysis showed resolution of proteinuria. At 38 weeks of gestation, the patient proceeded to elective caesarean section because of previous caesarean section, and a live female baby weighing 3.14 kg was delivered. The delivery was uncomplicated and blood pressure remained stable.

Following the delivery, computer tomography (CT) scan of neck, abdomen, and pelvis was performed as part of pre-operative planning to better delineate the relationship of the tumour to neighbouring structures. In addition to the previously identified extra-adrenal paraganglioma in the abdomen ( Figure 1 ), the CT revealed a 9 mm hypervascular nodule at the left carotid bifurcation, suggestive of a carotid body tumour ( Figure 2 ). The patient subsequently underwent an iodine (I) 131 metaiodobenzylguanidine (MIBG) scan, which demonstrated marked MIBG-avidity of the paraganglioma in the mid-abdomen. The reported left carotid body tumour, however, did not demonstrate any significant uptake. This could indicate either that the MIBG scan had poor sensitivity in detecting a small tumour, or that the carotid body tumour was not functional.

• PPT PowerPoint slide
• PNG larger image
• TIFF original image

https://doi.org/10.1371/journal.pmed.1000037.g001

https://doi.org/10.1371/journal.pmed.1000037.g002

In June 2008, four months after the delivery, the patient had a laparotomy with removal of the abdominal paraganglioma. The operation was uncomplicated. There was no wide fluctuation of blood pressures intra- and postoperatively. Phenoxybenzamine and propranolol were stopped after the operation. Histology of the excised tumour was consistent with paraganglioma with cells staining positive for chromogranin ( Figures 3 and 4 ) and synaptophysin. Adrenal tissues were notably absent.

The tumour is a well-circumscribed fleshy yellowish mass with maximal dimension of 5.5 cm.

https://doi.org/10.1371/journal.pmed.1000037.g003

The tumour cells are polygonal with bland nuclei. The cells are arranged in nests and are immunoreactive to chromogranin (shown here) and synaptophysin.

https://doi.org/10.1371/journal.pmed.1000037.g004

The patient was counselled for genetic testing for hereditary phaeochromocytoma/paraganglioma. She was found to be heterozygous for c.449_453dup mutation of the succinate dehydrogenase subunit D (SDHD) gene ( Figure 5 ). This mutation is a novel frameshift mutation, and leads to SDHD deficiency (GenBank accession number: 1162563). At the latest clinic visit in August 2008, she was asymptomatic and normotensive. Measurements of catecholamine in 24-hour urine collections had normalised. Resection of the left carotid body tumour was planned for a later date. She was to be followed up indefinitely to monitor for recurrences. She was also advised to contact family members for genetic testing. Our patient gave written consent for this case to be published.

https://doi.org/10.1371/journal.pmed.1000037.g005

Phaeochromocytoma in Pregnancy

Hypertension during pregnancy is a frequently encountered obstetric complication that occurs in 6%–8% of pregnancies [ 2 ]. Phaeochromocytoma presenting for the first time in pregnancy is rare, and only several hundred cases have been reported in the English literature. In a recent review of 41 cases that presented during 1988 to 1997, maternal mortality was 4% while the rate of foetal loss was 11% [ 3 ]. Antenatal diagnosis was associated with substantial reduction in maternal mortality but had little impact on foetal mortality. Further, chronic hypertension, regardless of aetiology, increases the risk of pre-eclampsia by 10-fold [ 1 ].

Classically, patients with phaeochromocytoma present with spells of palpitation, headaches, and diaphoresis [ 4 ]. Hypertension may be sustained or sporadic, and is associated with orthostatic blood pressure drop because of hypovolaemia and impaired vasoconstricting response to posture change. During pregnancy, catecholamine surge may be triggered by pressure from the enlarging uterus and foetal movements. In the majority of cases, catecholamine-secreting tumours develop in the adrenal medulla and are termed phaeochromocytoma. Ten percent of tumours arise from extra-adrenal chromaffin tissues located in the abdomen, pelvis, or thorax to form paraganglioma that may or may not be biochemically active. The malignant potential of phaeochromocytoma or paraganglioma cannot be determined from histology and is inferred by finding tumours in areas of the body not known to contain chromaffin tissues. The risk of malignancy is higher in extra-adrenal tumours and in tumours that secrete dopamine.

Making the Correct Diagnosis

The diagnosis of phaeochromocytoma requires a combination of biochemical and anatomical confirmation. Catecholamines and their metabolites, metanephrines, can be easily measured in urine or plasma samples. Day collection of urinary fractionated metanephrine is considered the most sensitive in detecting phaeochromocytoma [ 5 ]. In contrast to sporadic release of catecholamine, secretion of metanephrine is continuous and is less subjective to momentary stress. Localisation of tumour can be accomplished by either CT or MRI of the abdomen [ 6 ]. Sensitivities are comparable, although MRI is preferable in pregnancy because of minimal radiation exposure. Once a tumour is identified, nuclear medicine imaging should be performed to determine its activity, as well as to search for extra-adrenal diseases. I 131 or I 123 MIBG scan is the imaging modality of choice. Metaiodobenzylguanidine structurally resembles noradrenaline and is concentrated in chromaffin cells of phaeochromocytoma or paraganglioma that express noradrenaline transporters. Radionucleotide imaging is contraindicated in pregnancy and should be deferred until after the delivery.

Treatment Approach

Upon confirming the diagnosis, medical therapy should be initiated promptly to block the cardiovascular effects of catecholamine release. Phenoxybenzamine is a long-acting non-selective alpha-blocker commonly used in phaeochromocytoma to control blood pressure and prevent cardiovascular complications [ 7 ]. The main side-effects of phenoxybenzamine are postural hypotension and reflex tachycardia. The latter can be circumvented by the addition of a beta-blocker. It is important to note that beta-blockers should not be used in isolation, since blockade of ß2-adrenoceptors, which have a vasodilatory effect, can cause unopposed vasoconstriction by a1-adrenoceptor stimulation and precipitate severe hypertension. There is little data on the safety of use of phenoxybenzamine in pregnancy, although its use is deemed necessary and probably life-saving in this precarious situation.

The definitive treatment of phaeochromocytoma or paraganglioma is surgical excision. The timing of surgery is critical, and the decision must take into consideration risks to the foetus, technical difficulty regarding access to the tumour in the presence of a gravid uterus, and whether the patient's symptoms can be satisfactorily controlled with medical therapy [ 8 , 9 ]. It has been suggested that surgical resection is reasonable if the diagnosis is confirmed and the tumour identified before 24 weeks of gestation. Otherwise, it may be preferable to allow the pregnancy to progress under adequate alpha- and beta-blockade until foetal maturity is reached. Unprepared delivery is associated with a high risk of phaeochromocytoma crisis, characterised by labile blood pressure, tachycardia, fever, myocardial ischaemia, congestive heart failure, and intracerebral bleeding.

Patients with phaeochromocytoma or paraganglioma should be followed up for life. The rate of recurrence is estimated to be 2%–4% at five years [ 10 ]. Assessment for recurrent disease can be accomplished by periodic blood pressure monitoring and 24-hour urine catecholamine and/or metanephrine measurements.

Genetics of Phaeochromocytoma

Approximately one quarter of patients presenting with phaeochromocytoma may carry germline mutations, even in the absence of apparent family history [ 11 ]. The common syndromes of hereditary phaeochromocytoma/paraganglioma are listed in Box 2 . These include Von Hippel-Lindau syndrome, multiple endocrine neoplasia type 2, neurofibromatosis type 1, and succinate dehydrogenase (SDH) gene mutations. Our patient has a novel frameshift mutation in the SDHD gene located at Chromosome 11q. SDH is a mitochondrial enzyme that is involved in oxidative phosphorylation. Characteristically, SDHD mutation is associated with head or neck non-functional paraganglioma, and infrequently, sympathetic paraganglioma or phaeochromocytoma [ 12 ]. Tumours associated with SDHD mutation are rarely malignant, in contrast to those arisen from mutation of the SDHB gene. Like all other syndromes of hereditary phaeochromocytoma, SDHD mutation is transmitted in an autosomal dominant fashion. However, not all carriers of the SDHD mutation develop tumours, and inheritance is further complicated by maternal imprinting in gene expression. While it may not be practical to screen for genetic alterations in all cases of phaeochromocytoma, most authorities advocate genetic screening for patients with positive family history, young age of tumour onset, co-existence with other neoplasms, bilateral phaeochromocytoma, and extra-adrenal paraganglioma. The confirmation of genetic mutation should prompt evaluation of other family members.

Box 2: Hereditary Phaeochromocytoma/Paraganglioma Syndromes

• Von Hippel-Lindau syndrome
• Multiple endocrine neoplasia type 2A and type 2B
• Neurofibromatosis type 1
• Mutation of SDHB , SDHC , SDHD
• Ataxia-telangiectasia
• Tuberous sclerosis
• Sturge-Weber syndrome

Key Learning Points

• Hypertension complicating pregnancy is a commonly encountered medical condition.
• Pre-existing chronic hypertension must be considered in patients with hypertension presenting in pregnancy, particularly if elevation of blood pressure is detected early during pregnancy or if persists post-partum.
• Secondary causes of chronic hypertension include renal artery stenosis, renal parenchyma disease, primary hyperaldosteronism, phaeochromocytoma, Cushing's syndrome, coarctation of the aorta, and obstructive sleep apnoea.
• Phaeochromocytoma presenting during pregnancy is rare but carries high rates of maternal and foetal morbidity and mortality if unrecognised.
• Successful outcomes depend on early disease identification, prompt initiation of alpha- and beta-blockers, carefully planned delivery, and timely resection of the tumour.

Phaeochromocytoma complicating pregnancy is uncommon. Nonetheless, in view of the potential for catastrophic consequences if unrecognised, a high index of suspicion and careful evaluation for secondary causes of hypertension is of utmost importance. Blood pressure should be monitored in the post-partum period and persistence of hypertension must be thoroughly investigated.

Author Contributions

All authors participated in the management of the patient or writing of the article. AL and RCWM wrote the article, with contributions from all the authors.

• View Article
• Google Scholar

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• Geburtshilfe Frauenheilkd
• v.82(5); 2022 May

Language: English | German

Blood Pressure Levels and Maternal Outcome in Women with Preeclampsia – a Retrospective Study from a Large Tertiary Obstetric Centre

Blutdruckwerte und mütterliches outcome bei frauen mit präeklampsie – eine retrospektive studie aus einem perinatalzentrum level i, daniela willy.

1 Department of Obstetrics and Gynaecology, University Hospital Münster, Münster, Germany

Kevin Willy

2 Department of Cardiology, University Hospital Münster, Münster, Germany

Helen-Ann Köster

Janina braun, mareike möllers, marina sourouni, walter klockenbusch, ralf schmitz, kathrin oelmeier, associated data.

Introduction Patients with high blood pressure levels are at high risk for acute complications as well as serious long-term consequences. Women with preeclampsia often experience very high blood pressure levels during pregnancy and postpartum and are also known to have a higher cardiovascular risk in later life.

Material and Methods In our single-centre retrospective cohort study, we analysed 158 pregnancies complicated by preeclampsia in regard to maternal outcome. We divided the patient cohort into three subgroups according to the blood pressure levels during hospital stay.

Results Pre-existing arterial hypertension was significantly more common in patients with a hypertensive crisis (systolic blood pressure ≥ 180 mmHg and/or diastolic blood pressure ≥ 120 mmHg) during pregnancy than in patients with moderate or severe hypertension (p = 0.001). Women with a hypertensive crisis had an unfavourable outcome compared to women with lower blood pressure levels. These women developed a HELLP-syndrome significantly more often (p = 0.013). Moreover, most of the women with a hypertensive crisis during pregnancy were still hypertensive at hospital discharge (p = 0.004), even though they were administrated antihypertensive agents more often (p < 0.001) compared to women with lower blood pressure values.

Conclusion Preeclamptic women with hypertensive crises should be identified quickly and monitored closely to avoid further complications. Standardized follow-up programs are lacking, but especially these patients seem to be at high risk for persistent hypertension and increased cardiovascular morbidity and therefore should receive specialist follow-up, including hypertensiologists, cardiologists and gynaecologists. Large prospective trials are required for a better understanding of these interrelations and to develop a specific follow-up program.

Zusammenfassung

Einleitung Das Risiko für akute Komplikationen und schwerwiegende Langzeitfolgen ist höher bei Patientinnen mit Bluthochdruck. Frauen mit Präeklampsie haben oft sehr hohe Blutdruckwerte während der Schwangerschaft und postpartal und haben bekanntlich auch eine höheres Risiko für Herz-Gefäß-Erkrankungen im späteren Leben.

Material und Methoden Diese monozentrische retrospektive Kohortenstudie untersucht 158 Schwangerschaften mit Präeklampsie im Hinblick auf das mütterliche Outcome. Die Patientinnenkohorte wurde gemäß den Blutdruckwerten der Patientinnen während ihres Krankenhausaufenthalts in 3 Untergruppen aufgeteilt.

Ergebnisse Verglichen mit Patientinnen mit mittelschwerer oder schwerer Hypertonie hatten Patientinnen, die während der Schwangerschaft eine hypertensive Krise (systolischer Blutdruck ≥ 180 mmHg und/oder diastolischer Blutdruck ≥ 120 mmHg) erlitten, signifikant häufiger eine vorbestehende arterielle Hypertonie (p = 0,001). Frauen, die eine hypertensive Krise erlebten, hatten ein ungünstigeres Outcome verglichen mit Frauen mit niedrigerem Blutdruck. Diese Frauen entwickelten auch deutlich häufiger ein HELLP-Syndrom (p = 0,013). Außerdem hatten die meisten Frauen, die eine hypertensive Krise während der Schwangerschaft erlitten, immer noch hypertensive Blutdruckwerte zum Zeitpunkt ihrer Entlassung aus dem Krankenhaus (p = 0,004), obwohl sie öfters mit antihypertensiven Mitteln behandelt wurden (p < 0,001) als Frauen mit niedrigerem Blutdruck.

Schlussfolgerung Präeklamptische Frauen mit hypertensiven Krisen sollten rasch identifiziert und intensiv überwacht werden, um weitere Komplikationen zu verhindern. Es fehlt an standardisierten Nachsorgeprogrammen. Diese Patientinnen weisen ein besonders hohes Risiko für anhaltende Hypertonie und höhere kardiovaskuläre Morbidität auf und sollten daher eine fachärztliche Nachsorge durch Hypertensiolog*innen, Kardiolog*innen und Gynäkolog*innen erhalten. Große prospektive Studien sind nötig, um die Kenntnisse dieser Zusammenhänge zu verbessern und ein gezieltes Nachsorgeprogramm zu entwickeln.

Preeclampsia remains one of the most dangerous complications of pregnancy for mother and child 1 ,  2 . It is defined as hypertension in combination with proteinuria and/or onset of other organ dysfunction and/or fetal growth restriction. Preeclampsia is one of the main reasons for maternal and fetal morbidity and mortality worldwide and occurs in approximately 3 – 5% of all pregnancies 1 . Furthermore, it is known that women with a history of preeclampsia have a higher cardiovascular risk in later life 3 .

Until now, pathogenesis of preeclampsia is not fully understood. Several factors seem to play a role in its development, including shallow trophoblast invasion, an imbalance of pro- and anti-angiogenic factors, but also pre-existing maternal conditions such as arterial hypertension, diabetes mellitus or kidney disease, rheumatological disorders and autoimmune diseases 4 ,  5 .

Although it is known that women with a history of preeclampsia have a higher risk of severe cardiovascular events, e.g. stroke or acute coronary syndrome, currently no specific preventive care concept exists for this cohort 6 . However, in current national guidelines, a regular follow-up is recommended for women with early onset or severe course of preeclampsia 7 .

Moreover, factors predicting the progression of preeclampsia and onset of complications (e.g. HELLP-syndrome, eclampsia) are sparse. Especially in light of the very limited therapeutic options, with delivery as one and only causal therapy, predictors for severe complications would be very helpful for early and exact risk stratification and timing of delivery 8 ,  9 .

Current international guidelines on hypertension grade hypertensive blood pressure levels into different degrees of severity, as it is known that patients with higher blood pressure levels are at higher risk for acute and long-term complications 10 .

The aim of this study was to analyse maternal outcome in correlation with blood pressure levels in women with preeclampsia. We suspected that women with hypertensive crisis (systolic blood pressure ≥ 180 mmHg or diastolic blood pressure ≥ 120 mmHg) would have an unfavourable outcome compared to women with only moderate hypertension (systolic blood pressure up to 159 mmHg and diastolic blood up to 109 mmHg). Furthermore, blood pressure levels might guide risk stratification regarding necessity and frequency of medical follow-up after delivery and the need for further medical interventions to reduce the risk of cardiovascular morbidity in later life.

We conducted a retrospective cohort study at the University Hospital Münster, a tertiary obstetric centre. All deliveries at the University Hospital Münster from 1st January 2017 until 31st December 2020 were reviewed (5149 women) and included in the study if preeclampsia was diagnosed (158 women). A flow chart of patients screened and included in the study is shown in Fig.  S1 . The study was designed according to the Declaration of Helsinki and approved by the institutional review board.

The definition of preeclampsia, as described by the International Society for the Study of Hypertension in Pregnancy (ISSHP) and as defined in the current ACOG practice bulletin as well as in the current AWMF-guideline 7 ,  11 ,  12 , was applied as followed: hypertension (repeated blood pressure measurement ≥ 140/90 mmHg) plus at least one of the following in or after the 20th week of gestation:

• significant proteinuria (double positive urine test strip and/or elevated protein/creatinine ratio ≥ 30 mg/mmol)
• thrombocytopenia < 100 000/µl
• elevated liver enzymes (alanine transaminase ≥ twice the normal concentration)
• elevated serum creatinine > 1.0 mg/dl
• pulmonary oedema
• neurological dysfunction
• fetal growth restriction < 10th percentile

If these criteria of preeclampsia were not met or if data acquisition was incomplete, the patient was excluded from this study.

During the hospital stay, demographic data, medical history, blood pressure recordings, laboratory results, clinical symptoms, and obstetric outcome were recorded. The following clinical symptoms were recorded: epigastric pain, headache, visual sensations, hyperreflexia and other neurological symptoms (e.g. vomiting, hypaesthesia). Blood pressure was recorded either with an auscultatory or oscillometric semiautomatic or automatic sphygmomanometer with fitted cuff. All sphygmomanometers used were certified for use in pregnancy. Before blood pressure measurement was performed, patients were sitting for at least 5 minutes in a quiet environment and the cuff was positioned at heart level. Blood pressure was measured at least 4 – 6 times a day by medical staff only.

In conformity with current international guidelines for arterial hypertension, we divided the patients into three subgroups depending on their maximum blood pressure 10 ,  13 :

• patients with moderate hypertension: a systolic blood pressure up to 159 mmHg and a diastolic blood up to 109 mmHg
• patients with severe hypertension: a systolic blood pressure between 160 – 179 mmHg and/or a diastolic blood pressure between 110 – 119 mmHg
• patients with a hypertensive crisis: a systolic blood pressure ≥ 180 mmHg or a diastolic blood pressure ≥ 120 mmHg

According to the ESC/ESH guidelines on arterial hypertension and following the results of the SPRINT study, the blood pressure measurement at the day of hospital discharge was also divided into three groups 10 ,  14 :

• optimal blood pressure level: systolic blood pressure ≤ 120 and diastolic blood pressure ≤ 80 mmHg
• tolerable blood pressure level: systolic blood pressure 121 – 139 and/or diastolic blood pressure 81 – 89 mmHg
• hypertension: systolic blood pressure ≥ 140 or diastolic blood pressure ≥ 90 mmHg.

According to current national guidelines, antihypertensive treatment pre- as well as postnatal was initiated if repeated (≥ 3) blood pressure levels ≥ 150/100 mmHg were recorded 7 .

Statistical analysis

All statistical calculations were performed using SPSS Statistics, version 27 (IBM, Armonk, NY, USA). For descriptive data analysis of continuous variables we provided mean values and standard deviation, categorical data were expressed as frequencies/percentages. For comparison of two ordinally scaled variables, we used the chi-squared test after constructing contingency tables; we also used the chi-squared test for expressing oddʼs ratio, if indicated. To test for correlation between groups, one-way ANOVA was used (after having proven variance homogeneity with the Levene-test). Studentʼs t-test was used to compare the mean values between groups of normally-distributed metric variables.

A p-value < 0.05 was considered statistically significant, and significance levels were presented as follows: p-values < 0.05 are summarized with one asterisk (*), p-values < 0.01 with two asterisks (**) and p-values < 0.001 with three asterisks (***).

Patient characteristics

158 patients were included in this study. The mean maternal age was 31.9 ± 5.1 years. The majority of these women were primiparous (69.0%). Most patients were from Germany, 18.3% were from another country. Of these patients 15.8% had a history of preconceptual hypertension, 11.4% of coagulation disorders with 3.8% of thrombosis. 3.2% of women continued smoking during their pregnancy. 5.1% of included women had pre-existing diabetes. During pregnancy, about one fifth of patients developed a gestational diabetes: 13.9% of all patients developed gestational diabetes with dietary treatment and 5.7% of all patients developed insulin-depending gestational diabetes.

Only 30.4% of all patients did not take any form of medication during their pregnancy. 11.4% of pregnancies in our cohort were the result of fertility treatment. 45.6% of all patients had a positive family history for cardiovascular diseases.

We differentiated between women with moderate hypertension (n = 48, 30.4%), women with severe hypertension (n = 69, 43.7%) and women with hypertensive crises (n = 41, 25.9%) in accordance with the maximal prepartum blood pressure values during the hospital stay. Demographic data of the study population and study subgroups are displayed in Table 1 .

Table 1  Patient characteristics within hypertension subgroups.

Pre-existing hypertension was significantly associated with prepartum maternal blood pressure levels (p < 0.001), details are displayed in Fig. 1 .

 Frequency distribution of pre-existing hypertension between hypertension subgroups.

Moreover, we found that patients in the moderate hypertension group more often had a positive history for thrombosis than either of the other groups (p < 0.001).

Of all the symptoms assessed, only the occurrence of headaches correlated positively to the level of arterial hypertension (p = 0.025). None of the other symptoms showed a significant relationship to blood pressure levels. The sum of all symptoms reported did not show a significant correlation to blood pressure levels either.

Complications and severity of preeclampsia

We investigated the correlation between blood pressure levels and laboratory parameters. There was no significant relationship between blood pressure levels and serum creatinine, potassium levels, lactate dehydrogenase levels or thrombocytopenia. Furthermore, blood pressure levels did not correlate with the protein/creatinine-ratio. But we could show a significant positive association of the blood pressure level and uric acid and alanine transaminase levels (p = 0.049 and p = 0.003, respectively).

There was no significant correlation between blood pressure levels and occurrence of pre- or postnatal anaemia. However, we did see a tendency for severe postpartum anaemia in women with higher blood pressure levels (p = 0.068).

Laboratory findings within hypertension subgroups are displayed in Table S1 .

High blood pressure levels were a predictor for the development of HELLP-syndrome (p = 0.013). The higher the maternal blood pressure levels, the more often a HELLP-syndrome developed, as shown in Fig. 2 .

 Incidence of HELLP-syndrome in the three blood pressure groups.

High blood pressure levels also correlated positively with the administration of intravenous magnesium as prophylaxis for eclampsia (p = 0.001).

Severe complications of preeclampsia such as intracerebral haemorrhage and eclampsia were scarce. Of 158 patients, one developed pituitary haemorrhage and two patients abruptio placentae. All women were part of the severe hypertension group. No cases of posterior reversible encephalopathy syndrome or eclampsia were recorded.

Blood pressure at hospital discharge

A significant relationship between the highest blood pressure measured during the hospital stay and the blood pressure measured at hospital discharge was seen (p = 0.004). While patients with moderate hypertension were discharged with an optimal or acceptable blood pressure in 72.9% of the cases, this was the case for only 62.3% of the patients with severe hypertension and 36.5% of the patients with a hypertensive crisis during their hospital stay. The Oddʼs Ratio of being discharged with an insufficient blood pressure control was 4.7-fold higher in patients in the hypertensive crisis group than in patients with only moderate hypertension ( Table 2 ).

Table 2  Blood pressure levels at hospital discharge in the three blood pressure groups.

Patients with pre-existing arterial hypertension before pregnancy were discharged with optimal or acceptable blood pressure values in 46.2%, this was the case in 57.1% of patients without pre-existing hypertension (p = 0.15). Subgroup analysis regarding the three different blood pressure groups, pre-existing arterial hypertension and blood pressure levels at hospital discharge could not show a significant difference either.

Antihypertensive medication at discharge

We found that 83.3% of patients in the group with moderate hypertension were discharged without any blood pressure medication, while patients with a hypertensive crisis during pregnancy were discharged with at least one antihypertensive drug in 97.6% of the cases. In this group, 58.5% of patients were discharged with an antihypertensive monotherapy and 39.2% with a combination of antihypertensive agents underlining a highly significant association of highest blood pressure and medication at discharge (p < 0.001), see also Table 3 .

Table 3  Association of prepartum blood pressure levels in patients with preeclampsia and antihypertensive treatment at hospital discharge.

In our study, we could show that far beyond being a diagnostic criterion for preeclampsia, the level of hypertension in preeclamptic women can improve risk stratification in case of maternal deterioration and is an independent marker for poor maternal outcome. Succinctly, preeclamptic patients with a hypertensive crisis during pregnancy experience more complications and a more severe course of disease compared to women with blood pressure levels below 180/120 mmHg. Additionally, these patients are at higher risk of persistent hypertension at hospital discharge.

So far, little attention has been devoted to the severity of hypertension in preeclamptic patients and its significance for their clinical management. In most cases, a distinction is only made between preeclampsia with or without severe features, assigning all women with blood pressure levels ≥ 160/110 mmHg to the group of preeclampsia with severe features, without further differentiation 12 . In their study, Buchbinder and colleagues demonstrated that women with severe gestational hypertension had higher rates of adverse perinatal outcomes compared to women with mild preeclampsia. No significant differences were found between the normotensive/mild gestational hypertension and the mild preeclampsia group, underlining the importance of a differentiated blood pressure analysis in hypertensive diseases of pregnancy 15 .

Our study underlines the importance of a differentiated analysis of blood pressure levels in patients with preeclampsia as this particular parameter is paramount for clinical surveillance and antenatal monitoring. According to the severity of hypertension, patients can be stratified into different risk groups and managed accordingly. Antihypertensive medication should be initiated promptly in women with very high blood pressure levels to reduce the risk of severe complications, especially in the postpartum period.

After delivery, it is known that blood pressure levels normalize within the first week postpartum in many patients with hypertension during pregnancy, but women with chronic hypertension, preterm preeclampsia and/or very high blood pressure levels during pregnancy often remain hypertensive in the postpartum period and beyond 16 , 17 , 18 , 19 . Studies analysing the correlation of blood pressure levels during preeclampsia and cardiovascular morbidity in later life are sparse. In his review article, Aronow points out that women with a history of preeclampsia have a higher risk of developing persistent hypertension, but also for strokes, ischemic heart disease, kidney diseases and diabetes in later life 20 . Benschop and colleagues pointed out that women with a history of severe preeclampsia have a higher cardiovascular risk profile and that no uniform follow-up care program exists for women with a former hypertensive pregnancy disorder 6 . Recommendations on frequency and extent of follow-up examinations differ extensively between existing guidelines, if recommendations are specified at all 21 . Benschop et al. proposed a schedule of cardiovascular follow-ups after a pregnancy with hypertensive disorders, starting 6 – 8 weeks after delivery 6 . Muijsers and colleagues also pointed out that a standardized prevention guideline for patients with a history of preeclampsia is lacking and have started a clinical trial to improve detection and prevention of hypertension in women aged 40 – 60 years with a history of preeclampsia to reduce cardiovascular morbidity 22 . The current national guideline for Germany, Austria and Switzerland recommends an extensive assessment of the patientsʼ cardiovascular status and specific risk factors in the first 3 – 6 months after delivery and screening for cardiovascular risk factors every 5 years from then on 7 .

In our study, 41% of all patients were still hypertensive at hospital discharge, even though they were treated with antihypertensive agents. Although the patient cohort is young and most of the patients have few comorbidities, physicians should not restrain from prescribing antihypertensive medication and adjust the dosage, if necessary. In case a persistent hypertension remains untreated, there is a higher cumulative risk for complications due to the longer duration of hypertension and secondary damage to target organs 23 . Moreover, physicians should also determine the patientsʼ lipid status and recommend lifestyle changes and/or statin therapy, if indicated 6 . Polypills may increase acceptance and adherence to the antihypertensive therapy in young women, as these advantages have been shown extensively in other patient cohorts 24 ,  25 ,  26 . We conclude that especially in women with elevated blood pressure levels at discharge, a closer follow-up involving general practitioners and outpatient gynaecologists seems mandatory for monitoring and treatment of persistent arterial hypertension and should be organized with fixed appointments to achieve a higher therapy adherence. Particular attention should be given to women with pre-existent hypertension as it is obvious that these patients need a reliable permanent antihypertensive treatment. Women with former preeclampsia should receive a regular long-term follow-up, for example every five years 7 .

A limitation of this study is its retrospective approach and the risk for bias inherent in this study design. Since the University Hospital Münster is a tertiary obstetric centre, our patient cohort includes a high number of patients with pre-existing hypertension, which may influence outcome parameters. However, most women were young and healthy without any pre-existing medical conditions. Since management of patients at risk for preeclampsia is recommended to take place in obstetric centres, our results can be considered valid in this particular setting. Another point worth mentioning is that there were no measures to prevent bias such as white coat hypertension. However, as there were repeated daily blood pressure measurements, this risk can be deemed small.

One strength of this study is the differentiation between subgroups according to maternal blood pressure levels, and separate analysis of maternal outcome. We were able to show that in preeclampsia the nuanced quantification of hypertension enables patient stratification and can help identify patients at risk for an unfavourable outcome. To our knowledge, our study is the first to highlight the importance of a differentiated approach to the degree of arterial hypertension in pregnancy.

Current guidelines do not differentiate between different blood pressures levels, which may be a relevant shortcoming in the management of women with preeclampsia. Large prospective studies with a long-term follow-up including patients with a history of preeclampsia are needed in order to identify cardiovascular complications connected to preeclampsia and to develop a specific medical follow-up program.

This study could show that blood pressure levels correlate with maternal outcome in preeclampsia. Since preeclamptic women with hypertensive crisis have an unfavourable outcome, quantification of hypertension enables patient stratification in preeclampsia. This can help improve the clinical management and therefore potentially reduce maternal complications. Moreover, especially this patient cohort needs to be followed up closely to reduce future cardiovascular morbidity. Therefore, an interdisciplinary team of hypertensiologists, cardiologists and gynaecologists seems to be the most suitable option.

Supplements

Fig. S1: Flow chart of patients screened and included in the study.

Table S1: Laboratory findings within hypertension subgroups. Potassium, creatinine, uric acid, alanine transaminase (GPT) and lactate dehydrogenase (LDH) levels are shown as maximum levels, whereas haemoglobin levels and platelet counts are displayed as minimum levels. Presented are mean values ± standard deviation.

Conflict of Interest The authors declare that they have no conflict of interest.

Supporting Information

Academia.edu no longer supports Internet Explorer.

To browse Academia.edu and the wider internet faster and more securely, please take a few seconds to  upgrade your browser .

Enter the email address you signed up with and we'll email you a reset link.

• We're Hiring!
• Help Center

A CASE STUDY ON PREECLAMPSIA

this study shows the occurrence of pre-eclampsia, it's preventive measures, risk factors and management

Related Papers

Melissa Wilson

Preeclampsia remains a major problem worldwide for mothers and babies. It is estimated that yearly 50 000 women die in developing countries from preeclampsia. Careful maternal observation for the signs of preeclampsia and delivery of women with increasingly severe preeclampsia is the cornerstone of management (as it has been for the past 100 years). Maternal mortality is, therefore, much less in developed countries with the capacity for careful perinatal observation, but morbidity is considerable and remains the leading cause of admissions to intensive care for pregnant women. Also, the appropriate delivery of women who develop increasingly severe preeclampsia early in gestation accounts for 8% of all preterm births.

International Journal of Pharmaceutical Sciences Review and Research

Mohd Wasiullah

Classically most women who develop hypertension and proteinuria (Preeclampsia) present sometime after 20 weeks of gestation up to 48 hours postpartum. Recent data suggest that in some women preeclampsia and even eclampsia may develop in the absence of hypertension of proteinuria. Protein nutrients supply to placenta. Due to it the placenta becomes immature, poor plantation and some time it causes the death. In the preeclampsia the spirals arteries are becomes narrow due to fibrous depositions. Antihypertensive drugs and diuretics Anti-hypertensive drug treatment for mild to moderate hypertension during pregnancy. Preeclampsia risk is increase two or four times in women during women suffer from diabetes (TYPES-1 AND TYPES-2). Now days diabetes is also common disease or disorder but there is limited number of women whose get pregnant with pre-existing diabetes. Also suffer from preeclampsia. A Hypertensive disorder of pregnancy occurs in about 10% of all pregnant women around the worl...

Review Article

Preeclampsia is a pregnant hypertension condition. It has a significant negative impact on maternal and perinatal health and affects 2-8% of pregnancies worldwide. The disease's main features are hypertension and proteinuria, though systemic organ damage could follow. The aberrant placentation that precedes the release of antiangiogenic markers, which is predominantly mediated by soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin, is the first sign of the clinical condition.(sEng). Every maternal organ system, including the fetus, may be adversely affected by high levels of sFlt-1 and sEng due to endothelial dysfunction, vasoconstriction, and immunological dysregulation. With an emphasis on the mechanisms underlying the clinical symptoms, this article thoroughly investigates the pathogenesis of preeclampsia. The only permanent remedy is delivery. In high-risk populations, low-dose aspirin is advised for prophylaxis. There are few other therapy alternatives. The pathophysiology of this common disease has to be clarified in order to find possible therapeutic targets for better treatment and, ultimately, outcomes. The three most common causes of maternal morbidity and mortality worldwide are preeclampsia and eclampsia. Rates of eclampsia, maternal mortality, and maternal morbidity in wealthy nations have significantly decreased during the past 50 years. In contrast, maternal mortality, problems during pregnancy, and eclampsia rates are still high in developing nations. In industrialised nations, preeclampsia-eclampsia patients are properly managed, and prenatal care is widely accessible. These discrepancies are mostly attributable to these factors.

Journal of the Medical Sciences

Afreen Anwar

Background: Pre eclampsia and eclampsia is one of the leading causes of maternal morbidity and mortality worldwide. Eclampsia though still remains an obstetric enigma, and is a major problem in developing countries. Although the incidence of pre eclampsia and eclampsia is on the decline, still it remains major contributor to poor maternal outcome. In India-gestational hypertension continues to be responsible for the largest proportion of cases contributing to maternal morbidity and mortality. Aims & objectives: The main objective of the study is to analyse the case of pre eclampsia and eclampsia complicating pregnancy, its maternal outcome, study the consequences of hypertensive disorders contributing pregnancy and its management. Methods: All patients beyond 20 wks of pregnancy with hypertensive disorders complicating pregnancy admitted in Al Ameen Medical College Hospital, Bijapur during the two year three months study period were enrolled in the study. Results: Total hypertensive...

https://www.ijrrjournal.com/IJRR_Vol.5_Issue.10_Oct2018/Abstract_IJRR0039.html

International Journal of Research & Review (IJRR)

Preeclampsia/eclampsia is a potentially fatal disorder in pregnant women and remains one of the leading causes of maternal mortality and morbidity maternal and fetal mortality. Pre-eclampsia is 2-10% of all pregnancies and this may be higher in low resource settings. The databases searched included Pub Med, Science direct, and Trip database. To conduct this study the inclusive criteria we considered the population all over the world, pregnant women since 2011, research articles, association of certain factors with risk of preeclampsia, influence of certain drugs for those who are already at risk, pregnant women who are giving birth for the first time & second, obese patients. Exclusion criteria include patients who are previously diagnosed with Hypertension, Postpartum women, Diabetic women, Women having any habits (Smoking, alcohol), Postmenopausal women, and Healthy pregnant women. Data extraction included information about demographic details, Intervention, Participants, Search strategy &Type of study. The extraction was carried out from the studies that were identified for inclusion. Prevalence of pre-eclampsia was reported to be 2-10% of all pregnancies. Women who have a previous history of hypertension and LV diastolic dysfunction and those who are in treatment with various types of antidepressants are more likely to develop pre-eclampsia.

Annual Review of Medicine

jean marc Ayoubi

Noureen Nishtar

Objective: To identify and compile a list of important epidemiological risk factors of preeclampsia among pregnant women from observational studies.Methods:Review of published case control and cohort studies on risk factors of Preeclampsia (PE) by lit erature search from 1976 -2010 was conducted. 108 studies were selected using search engines of PubMed and Google Scholar. Findings: Most of the studies were case control studies. The factors identified most often were women with a previous history of preeclampsia , pre-existing diabetes, multiple (twin) pregnancy, nulliparity, family history , raised blood pressure (diastolic ≥80 mm Hg) at booking, raised body mass index before pregnancy, or increasing maternal age ≥40. In some individual studies the risk is also increased with an interval of 10 years or more since a previous pregnancy, autoimmune disease, renal disease and chronic hypertension.Conclusions :These factors and the underlying evidence base can be used to assess risk at b...

Journal of Nursing Care

yanti hermayanti

Preeclampsia is a danger sign for pregnant women, especially at 20 weeks gestation, marked by increased blood pressure. At this time, preeclampsia is the second largest contributor to deaths globally, with preeclampsia worldwide 10% -15%. In Indonesia, there is an increase of 2% every year, indicating that adequate treatment and prevention efforts are needed. At present, most research on the prevention and management of preeclampsia discusses pharmacological treatment, not discussing nursing interventions. This Literature review aims to find out various prevention efforts for preeclampsia that are developing at this time. The research method is a literature study of research results published in 2010-2019. The strategy used to search literature is to use keywords preeclampsia, prevention, treatment methods, and nursing interventions, using Google Scholar, PubMed, Pro-Quest, Science Direct database, which reviewed using The Joanna Briggs Institute Critical Appraisal tools. The study...

MIKIA: Mimbar Ilmiah Kesehatan Ibu dan Anak (Maternal and Neonatal Health Journal)

Herawati Mansur

Pre-eclampsia is a pregnancy complication characterized by high blood pressure. Many risk factors can influence the incidence of pre- clampsia, including maternal age, parity, gestational age, number of fetuses, number of ANC visits, and history of hypertension. This study aims to find out the risk factors that are correlated with the incidence of pre-eclampsia. The design used in this study is analytic with a retrospective approach. The population in this study were all pregnant women in the third trimester with a diagnosis of pre-eclampsia in RSUD &quot;Kanjuruhan&quot; Kepanjen with a sample of 231 respondents selected using saturated sampling. Collecting data using data collection sheets, registers, and patient status. From the results of multiple linear regression with 0.05, the probability is 0.333 – 0.923 &gt; 0.05, so there is no relationship between maternal age, parity, multiple pregnancies, history of hypertension, history of pre-eclampsia, and obesity on the incidence o...

International Journal of Gynecology & Obstetrics

RELATED PAPERS

IRJET Journal

Laura Schipor

Anais do Workshop de Computação Aplicada à Gestão do Meio Ambiente e Recursos Naturais (WCAMA)

Felipe Borella

Francesco Castelluccio

Milan Viturka

Journal of Applied Meteorology

Edwin X Berry

Nurhan Akaras

Archives of medical research

Ismet Burekovic

Naidea Nunes

Nasi Kotak Surabaya

Nasikotak Murahsurabaya

Journal of Photochemistry and Photobiology A: Chemistry

Amaresh Mishra

Bulletin of Electrical Engineering and Informatics

Dada Aborisade

Constance Leblanc

Advances in Dual Diagnosis

Walter Busuttil

Cell stress

stefanos kaplanis

Japanese Journal of Cardiovascular Surgery

Scientific reports

Gema Vallés

IEEE Transactions on Services Computing

Brazilian Journal of Animal and Environmental Research

Betina Galarza

Cuadernos de Literatura. Vol. 27,

Rosa García Gutiérrez

Journal of Southern History

Cheryll Cody

Procedia - Social and Behavioral Sciences

Axel Knicker

Şule İyigönül Atasağun

Journal of Pharmacology and Experimental Therapeutics

Tina Hinton

Brazilian Journal of Microbiology

Fernando Paolicchi

RELATED TOPICS

•   We're Hiring!
•   Help Center
• Find new research papers in:
• Health Sciences
• Earth Sciences
• Cognitive Science
• Mathematics
• Computer Science
• Academia ©2024

7 Preeclampsia & Gestational Hypertensive Disorders Nursing Care Plans and Management

Learn about the nursing care plan and management of patients with preeclampsia and gestational hypertensive disorders in this guide.

Table of Contents

What are hypertensive disorder of pregnancy, nursing problem priorities, nursing assessment, nursing diagnosis, nursing goals, 1. managing hypertension and maintaining effective cardiac output, 2. preventing fluid retention, 3. maintaining adequate tissue perfusion, 4. preventing injury, 5. promoting adequate nutrition, 6. initiating patient education and health teachings, 7. administer medications and provide pharmacologic support, recommended resources, references and sources.

Hypertensive disorders of pregnancy (also known as pregnancy-associated hypertensive disorders, pregnancy induced hypertension ) are the most common complications that occur during pregnancy and are a major cause of maternal and fetal morbidity and mortality. These disorders include gestational hypertension , preeclampsia, eclampsia, chronic hypertension, and chronic hypertension with superimposed preeclampsia. If left untreated, preeclampsia can lead to a life-threatening complication called HELLP (hemolysis, elevated liver enzymes, low platelet count) syndrome. It is estimated that preeclampsia alone complicates 2-8% of pregnancies globally. 

Hypertensive disorders in pregnancy include five categories of hypertension and are defined as such by the American College of Obstetricians and Gynecologists (ACOG): 

Gestational Hypertensive Disorders

• Gestational hypertension . Defined as a systolic blood pressure of 140 mm Hg or more, and/or diastolic blood pressure of 90 mm Hg or more on two blood pressure readings at least four (4) hours apart after 20 weeks of gestation in a woman with previously normal blood pressure. Gestational hypertension does not persist longer than 12 weeks postpartum and usually resolves after a week postpartum.
• Preeclampsia . Preeclampsia is a pregnancy-specific condition and is defined as a new-onset of hypertension that occurs most often after 20 weeks of gestation. Blood pressure is elevated more than 140 mm Hg systolic, more than 90 mm Hg diastolic. Hypertension is usually accompanied by new-onset proteinuria although other signs and symptoms of preeclampsia (thrombocytopenia, impaired liver function, pulmonary edema, visual disturbance) may present in some women in the absence of proteinuria.
• Eclampsia. Eclampsia is the onset of seizure activity or coma in a woman with preeclampsia with no history of preexisting pathology that can result in seizure activity. Seizure leads to severe maternal hypoxia, injury , and aspiration pneumonia . Eclampsia has an increased maternal mortality rate especially in settings with low resources. 

Chronic Hypertensive Disorders

• Chronic hypertension . Chronic hypertension as hypertension diagnosed or present before pregnancy or before 20 weeks of gestation. It is more prevalent with increasing late childbearing and in persons with obesity. Additionally, hypertension that is diagnosed for the first time during pregnancy and that does not resolve postpartum is also classified as chronic hypertension. 
• Chronic hypertension with superimposed preeclampsia. Preeclampsia is considered superimposed when it complicates preexisting chronic hypertension. About half of women with chronic hypertension may develop superimposed preeclampsia. It is associated with increased maternal or fetal mortality.

Nursing Care Plans and Management

Nursing care planning and management for pregnant clients with hypertensive disorders or preeclampsia involve early detection, thorough assessment , and prompt treatment of preeclampsia. Another priority is to ensure the mother’s safety and deliver a healthy newborn as close to a full term as possible. 

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

• Blood pressure management. Monitoring and managing elevated blood pressure levels to prevent complications associated with preeclampsia and gestational hypertensive disorders.
• Fetal monitoring. Regularly assessing fetal well-being through non-stress tests, ultrasounds, or other appropriate methods to ensure the baby’s health and detect any signs of distress.
• Maternal health evaluation . Assessing and managing the overall health of the mother, including monitoring organ function, assessing for signs of severe preeclampsia, and addressing any pre-existing medical conditions.
• Proteinuria monitoring. Regularly testing urine for the presence of protein to assess the severity of preeclampsia and monitor renal function.
• Medication management. Prescribing and monitoring the appropriate medications, such as antihypertensive drugs, to control blood pressure and manage preeclampsia or gestational hypertensive disorders.
• Fluid balance. Monitoring and maintaining appropriate fluid balance to prevent dehydration or fluid overload , especially in cases of preeclampsia with edema or decreased urine output.
• Prevention of complications. Implementing measures to prevent complications associated with preeclampsia, such as eclampsia or HELLP syndrome, by closely monitoring symptoms and providing appropriate interventions.
• Delivery planning. Collaborating with obstetric specialists to determine the optimal timing and mode of delivery based on the severity of preeclampsia, gestational age, and maternal and fetal conditions.
• Maternal education and support. Providing education to the mother regarding preeclampsia, its signs and symptoms, and the importance of self-monitoring and seeking medical attention for any concerning changes.
• Postpartum care. Ensuring appropriate postpartum monitoring and care to address any lingering effects of preeclampsia, manage blood pressure, and support maternal recovery.

Assess for the following subjective and objective data:

• See nursing assessment cues under Nursing Interventions and Actions.

Following a thorough assessment, a nursing diagnosis is formulated to specifically address the challenges associated with preeclampsia & gestational hypertensive disorders based on the nurse ’s clinical judgment and understanding of the patient’s unique health condition. While nursing diagnoses serve as a framework for organizing care, their usefulness may vary in different clinical situations. In real-life clinical settings, it is important to note that the use of specific nursing diagnostic labels may not be as prominent or commonly utilized as other components of the care plan. It is ultimately the nurse’s clinical expertise and judgment that shape the care plan to meet the unique needs of each patient, prioritizing their health concerns and priorities.

Goals and expected outcomes may include:

• The client remains normotensive throughout the remainder of the pregnancy.
• The client reports absence and/or decreased episodes of dyspnea .
• The client alters activity level as the condition warrants.
• The client adheres to the therapeutic regimen and participates in the monitoring, as indicated.
• The client verbalizes understanding of the need for close monitoring of weight, BP, urine protein, and edema.
• The client is free of signs of generalized, pulmonary, and cerebral edema (i.e., epigastric pain , headaches, confusion , dyspnea, nausea /vomiting)
• The client exhibits hemoglobin and hematocrit values and protein levels within normal limits.
• The client exhibits physiological edema with no signs of pitting.
• The client demonstrates normal central nervous system (CNS) reactivity on a nonstress test (NST).
• The client is free of late decelerations.
• The client has no decrease in FHR on the contraction stress test/ oxytocin challenge test (CST/OCT).
• The client is full-term, appropriate for gestational age (AGA).
• The client participates in treatment and/or environmental modifications to protect herself and enhance safety.
• The client is free of signs of cerebral ischemia (visual disturbances, headache, changes in mentation).
• The client displays normal levels of clotting factors and liver enzymes.
• The client maintains a treatment regimen to control or eliminate seizure activity.
• The client verbalizes understanding of individual dietary needs.
• The client demonstrates knowledge of proper diet as evidenced by developing a dietary plan within their own financial resources.
• The client maintains or regains weight as indicated by the individual situation.
• The client is free of edema.
• The client identifies signs/symptoms requiring medical evaluation.
• The client maintains BP within individually acceptable parameters.
• The client performs the necessary procedures correctly.
• The client verbalizes understanding of the disease process and appropriate treatment plan.
• The client initiates lifestyle/behavior changes as indicated.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with preeclampsia & gestational hypertensive disorders may include:

A decrease in circulating blood volume due to the shifting of fluid from the intravascular to the interstitial spaces occurs in a pregnant client with a hypertensive disorder due to the decrease of the circulating blood volume and the total vascular volume and an increase in the systemic vascular resistance, the heart rate decreases as well as the stroke volume. These mechanisms lead to a decrease in cardiac output seen among clients with hypertensive disorders in pregnancy.

Assess blood pressure and pulse every one (1) hour or as indicated. Accurate measurement of blood pressure is essential for the early detection of hypertensive disorders. Hypertension is defined as a systolic blood pressure greater than 140 mm Hg or diastolic blood pressure greater than 90 mm Hg. Blood pressure may be elevated because of the increase in systemic vascular resistance whereas decreased cardiac output may also be reflected by diminished peripheral pulses. Rising blood pressure indicates the progression of preeclampsia. Use a consistent and standardized method when taking blood pressure measurements to maintain accuracy. 

Assess the mean arterial pressure (MAP) at 11-13 and 20-24 weeks gestation. A pressure of 90 mm Hg is considered predictive of preeclampsia. Mean arterial pressure (MAP) is the average arterial pressure throughout one cardiac cycle and is influenced by cardiac output and systemic vascular resistance. MAP prediction is best when measured during 11-13 weeks and at 20-24 weeks than at only one of these gestational ranges. MAP is increased from the first trimester in pregnancies developing preeclampsia (Gallo et al., 2014). Women with early-onset preeclampsia have higher mean arterial blood pressure levels at 20 weeks of gestation (Mayrink et al., 2019). 

Assess for crackles, wheezes, and dyspnea; note respiratory rate/effort. Note client snoring. Pulmonary edema may transpire with modification in peripheral vascular resistance and a drop in plasma colloid osmotic pressure. Fluid from the intravascular spaces shifts to the interstitial spaces, depleting the circulating blood volume but overwhelming the important organs of the body, especially the lungs . Pregnancy-onset snoring may also be a risk factor for developing gestational hypertension and preeclampsia (O’Brien et al., 2012). 

Auscultate for the apical pulse and assess the client’s heart rate and rhythm. Tachycardia may be present when the body compensates for the decrease in circulating volume that can hardly reach the peripheries and distant tissues.

Assess the client’s neurological status. Decreased cardiac output can precipitate alternations in the sensorium due to inadequate cerebral perfusion. Neurologic complications associated with preeclampsia may also manifest. These symptoms include cerebral edema, hemorrhage , irritability, headaches, hyperreflexia, seizures. 

Assess the client for visual disturbances. Alteration in the sensorium may indicate inadequate cerebral perfusion secondary to decreased cardiac output. Vision changes are due to arteriolar vasospasms and decreased blood circulation to the retina. These symptoms may include dimming of vision, blind or dark spots in the visual speed, blurring of vision, double vision. 

Assess the client for indications for an earlier delivery. Worsening preeclampsia that may progress to eclampsia warrants the need for an emergency early delivery. The fetal blood supply can be cut off, resulting in fetal distress and ultimately fetal death if delivery is not hastened (Sinkey et al., 2020; Espinoza 2012). These symptoms include uncontrolled severe-range blood pressure, refractory headaches, upper abdominal pain, visual disturbances, stroke . 

Monitor and measure the client’s urine output as per protocol. Maintain strict intake and output . In preeclampsia, the kidneys respond to reduced cardiac output by retaining water and sodium . Intrarenal vasospasms cause oliguria in severe preeclampsia due to a reduction in glomerular filtration rate . Contraction of the intravascular space secondary to vasospasms worsens renal sodium and water retention (ACOG, 2020). 

Monitor and measure the client’s 24-hour urine for proteinuria. Proteinuria is ideally determined by the evaluation of a 24-hour urine collection. However, current guidelines state that massive proteinuria is not considered a severe feature of preeclampsia. Reduced kidney perfusion causes renal deterioration and damages glomerular endothelial cells allowing protein molecules to pass into the urine, causing proteinuria. In some instances where it may be difficult to collect a 24-hour urine sample, preeclampsia may be diagnosed as hypertension with either thrombocytopenia, renal insufficiency, impaired liver function, pulmonary edema. 

Provide frequent rest periods with bed rest . Restrict activity rather than instituting complete bed rest. Improves venous return, cardiac output, and renal-placental perfusion. Help the client understand the importance of reduced activity and frequent rest periods and plan ways to manage them. Activity diverts blood from the placenta , reducing the infant’s oxygen supply. Although frequently recommended by healthcare providers, no evidence has been found that complete bed rest improves pregnancy outcomes. Rather, prolonged bed rest can increase the risk of complications due to immobility (e.g., muscle atrophy, weight loss, cardiovascular deconditioning, psychologic stress, etc.). Therefore, restricted activity rather than complete bed rest is recommended (Ghulmiyyah et al., 2012).

Instruct the client to elevate legs when sitting or lying down. Elevating the legs decreases venous stasis and may also reduce the incidence of thrombus and embolus formation in the client on bed rest.

Monitor the client’s BP and instruct monitoring of BP at home. Monitor BP every 15 minutes during the critical phase and every 1 to 4 hours as the client’s condition improves. If the client is an outpatient, instruct both the client and a family member to monitor the BP two to four times per day in the same arm and the same position. A family member must be taught the technique to ensure accurate measurements. Rising blood pressure levels may indicate worsening preeclampsia. 

Record and graph vital signs, especially BP and pulse. The client with preeclampsia does not display the normal cardiovascular response to pregnancy (left ventricular hypertrophy, increased plasma volume, vascular relaxation with decreased peripheral resistance). Hypertension (the second manifestation of preeclampsia after edema) occurs due to increased sensitization to angiotensin II, which increases BP and promotes aldosterone release to increase sodium/water reabsorption from the renal tubules constricts blood vessels.

Monitor for invasive hemodynamic parameters such as cardiac output, as indicated. Provides a precise picture of vascular changes and fluid volume. Prolonged vascular constriction, increased hemoconcentration, and fluid shifts decrease cardiac output.

Administer low-dose aspirin as indicated. When initiated before 16 weeks gestation, low-dose aspirin effectively prevents preeclampsia, severe preeclampsia, preterm birth, and intrauterine growth restriction in patients with high-risk pregnancies (Fantasia, 2018; Xu et al., 2015). It is recommended that daily dose aspirin therapy be initiated late in the first trimester for women who have a history of early-onset preeclampsia and subsequent preterm birth at less than 34 weeks of gestation or a history of preeclampsia in more than one previous pregnancy. 

Administer antihypertensive medications as ordered. Observe for side effects of antihypertensive drugs. If blood pressure does not respond to conservative measures, short-term medication may be needed with other therapies (e.g., fluid replacement, magnesium sulfate). Antihypertensive treatment should be initiated as soon as reasonably possible for acute-onset severe hypertension that persists (ACOG, 2020). Antihypertensive drugs work directly on arterioles to promote relaxation of cardiovascular smooth muscles and help increase blood supply to the cerebrum, kidneys, uterus, and placenta (Lightstone, 2013). Intravenous hydralazine, or labetalol , and oral nifedipine are three agents commonly used to control hypertension in pregnancy. See Pharmacologic Management

Prepare for the birth of fetus by cesarean delivery, labor when severe preeclamptic or eclamptic condition is stabilized, but vaginal delivery is not feasible. If conservative treatment is ineffective and labor induction is ruled out, then surgical procedure is the only means of halting the hypertensive problems. Delivery of the fetus is the cure for preeclampsia. If preeclampsia is severe, the fetus is often in greater danger from being in the uterus because its oxygen and nutritional supply may be cut off or its growth can be restricted. Fetal death sometimes can occur.

In a normal pregnancy, fluid retention is a common and expected feature. However, when pregnancy-induced hypertension is a concern, low placental perfusion causes a decrease in GFR and altered glomerular permeability, resulting in protein loss through the kidneys. The loss of intravascular protein results in a decrease in intravascular osmolality and loss of fluid to the interstitial spaces resulting in edema and excessive extravascular fluid retention. 

Assess lung sounds and respiratory rate and effort. Dyspnea and crackles may mean pulmonary edema, which needs immediate treatment. In preeclampsia, the loss of intravascular protein allows fluid to seep out of the intravascular spaces, overwhelming other nearby organs, in this case, the lungs. Orthopnea and paroxysmal nocturnal dyspnea may occur due to an excessive venous return of fluid from the lower extremities that may reach the lungs.

Weigh the client regularly during hospital visits. Advise the client to record weight at home in-between visits. Weight measurement should be on the same scale, in the same type of clothing, and at the same time of day. Abrupt, notable weight gain (e.g., more than 3.5 lb (1.8 kg) per week in the second or third trimester reflects fluid retention and may indicate preeclampsia. Fluid shifts from the vascular to the interstitial space, resulting in generalized edema.

Assess the client’s vital signs, closely monitoring blood pressure and pulse. A rise in blood pressure may happen in response to catecholamines, vasopressin, prostaglandins, and, as recent findings suggest, decreased levels of prostacyclin. Increased pulse rate can be due to low intravascular colloid-osmotic pressure caused by increased capillary permeability. This creates higher fluid retention and decreased hydrostatic pressure, inhibiting fluid circulation and congesting the lungs (Froes, 2020).

Assess for the presence of edema and degree of pitting edema. The presence of pitting edema (mild, 1+ to 2+; severe, 3+ to 4+) of face, hands, legs, sacral area, or abdominal wall, or edema that does not disappear after 12 hours of bed rest is vital. Edema is assessed for distribution, pitting, and degree. Edema may be present on the most dependent body parts where hydrostatic pressure is greatest. It may also be more evident in the feet and ankles of the ambulatory pregnant woman. 

Assess for signs of progressive or excessive edema. Assess for possible eclampsia. Signs for possible eclampsia include epigastric pain, cerebral symptoms, nausea, vomiting. Edema and intravascular fibrin deposition (in HELLP syndrome) within the encapsulated liver are manifested by right upper quadrant pain; dyspnea, indicating pulmonary involvement; cerebral edema, possibly leading to seizures; and nausea, and vomiting, indicating GI edema.

Note alterations in hematocrit/hemoglobin levels. Identifies degree of hemoconcentration caused by fluid shift. If hematocrit is less than three times hemoglobin level, hemoconcentration exists. Hemoconcentration occurs due to an increase in plasma volume which is higher than the increase in erythrocyte production.

Monitor intake and output. Note urine color, and measure specific gravity as indicated. Urine output is a sensitive indicator of circulatory blood volume. Decreased blood flow to the kidneys reduces urine production. Oliguria and specific gravity of 1.040 indicate severe hypovolemia and kidney involvement. Administering magnesium sulfate can cause a transient increase in urine output. 

Encourage the client to increase protein intake. Proper nutrition decreases the incidence of prenatal hypovolemia and hypoperfusion; insufficient protein/calories increases the risk of edema formation and preeclampsia. Intake of 80–100 g of protein may be required daily to replace losses. Protein becomes depleted as the glomeruli become damaged and cannot prevent it from being excreted through the urine. 

Review moderate sodium intake of up to 6 g/day. Advise clients to read food labels and avoid foods high in sodium. Some sodium intake is necessary because levels below 2–4 g/day result in greater dehydration in some clients. High sodium foods include processed meat such as bacon, luncheon meats, hot dogs, potato chips, etc. However, excess sodium may increase edema formation and increase the risk for hypertension.

Schedule prenatal visit every 1-2 weeks if mild preeclampsia; weekly if severe. Important to monitor changes more closely for the well-being of the client and fetus. BP monitoring twice weekly combined with fetal non-stress test, amniotic fluid index evaluation, and laboratory evaluations may be indicated (Luger & Knight, 2021).

Educate the client and family members or significant others on home monitoring/day-care programs, as appropriate. Some mildly hypertensive clients without proteinuria may be managed on an outpatient basis if adequate surveillance and support are provided, and the client/family actively participates in the treatment regimen.

Substitute fluids orally or parenterally via an infusion pump, as indicated. Fluid replacement treats hypovolemia yet must be given cautiously to prevent overload, especially if interstitial fluid is drawn back into circulation when activity is reduced. With renal involvement, fluid intake is restricted; i.e., if the output is reduced (less than 700 ml/24 hr), total fluid intake is restricted to approximate output plus insensible loss. The use of an infusion pump allows more accurate control delivery of IV fluids .

Respond to questions and review rationale for avoiding the use of diuretics to treat edema. Diuretics further increase the chances of dehydration by decreasing intravascular volume and placental perfusion, and they may cause thrombocytopenia, hyperbilirubinemia , or alteration in carbohydrate metabolism in fetus/newborn. Diuretics may be useful in treating pulmonary edema.

Examine clean-catch, first-voided urine specimen for protein each visit, or daily/hourly as appropriate if hospitalized. Report readings of 2+ or greater. Aids in identifying the degree of severity/progression of the condition. A 2+ reading implies glomerular edema or spasm. Proteinuria affects fluid shifts from the vascular tree. Urine contaminated by vaginal secretions may test positive for protein, or dilution may result in a false-negative result. In addition, preeclampsia may be present without significant proteinuria.

Collaborate with a dietitian as indicated. A nutritional consult may be beneficial in determining individual needs/dietary plans. Dietary sodium and potassium intake are believed to significantly contribute to the changes in blood pressure in the general and hypertensive population (Lu et al., 2018). 

When the fluid deficit is severe, and the client is hospitalized:

Insert indwelling catheter if kidney output is reduced or is less than 50 ml/hr. Allows more accurate monitoring of output/renal perfusion. Decreased cardiac output results in impaired kidney perfusion, sodium and water retention, and reduced urine output.

Assist with insertion of lines and monitoring of invasive hemodynamic parameters, such as central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP). Gives a more precise measurement of fluid volume. In normal pregnancy, plasma volume increases by 30%–50%, yet this increase does not occur in preeclampsia clients.

Monitor serum uric acid and creatinine levels and blood urea nitrogen (BUN). Uric acid clearance is decreased, but serum uric acid levels increase. Elevated uric acid levels indicate impaired kidney function, worsening maternal condition, and poor fetal outcome. Elevated serum uric acid is also a biomarker for preeclampsia and contributes to the pathogenesis of maternal and fetal manifestations (Johnson et al., 2011). 

Administer platelets, fibrinogen, or fresh, frozen plasma (FFP) as indicated. Clients with HELLP syndrome awaiting delivery of the fetus may benefit from transfusion of platelets when the count is below 5,000 u/L with active bleeding or hemorrhage risk. In the case of coagulopathy, the coagulation factors must be corrected with fibrinogen and fresh, frozen plasma (El Allani et al., 2020). 

Hypertensive disorders of pregnancy cause a reduction in the maternal blood and nutrition flow through the placenta and decrease the oxygen available to the fetus. The fetus may have intrauterine growth restriction, and fetal death may sometimes occur. 

Evaluate fetal growth through McDonald’s measurement; measure progressive fundal growth at each office visit or periodically during home visits, as appropriate. Reduced placental functioning may accompany pregnancy-induced hypertension, resulting in intrauterine growth restriction (IUGR). Blood and nutrition flow through the placenta is reduced, decreasing the oxygen available to the fetus. Chronic intrauterine stress and uteroplacental insufficiency decrease the amount of fetal contribution to the amniotic fluid pool.

Assess fetal heart rate (FHR) manually or electronically, as indicated. Helps evaluate fetal well-being. An elevated FHR may show a compensatory response to hypoxia, prematurity, or abruptio placentae .

Assess fetal response to biophysical profile (BPP) criteria or contraction stress test (CST), as maternal status indicates. BPP helps evaluate fetus and fetal environment on five specific parameters to assess CNS function and fetal contribution to the amniotic fluid volume. CST assesses placental functioning and reserves.

Assess for amniotic fluid volume (AFV), as indicated. Assessment of AFV allows the detection of oligohydramnios . AFV can be assessed with ultrasound measurements or by amniotic fluid index. Abnormal placentation occurs due to the failure of appropriate remodeling of the spiral arteries, resulting in higher resistance to placental blood flow and hypoperfusion of the placenta. These processes can result in oligohydramnios, fetal hypoxia, and fetal distress (Fox et al., 2019).

Advise bedrest and restriction of activities. Activity restriction allows blood that would be circulated to the skeletal muscles to be conserved for circulation to the mother’s vital organs and the placenta. The woman should remain on reduced activity with frequent rest periods lying on her side to improve blood flow to the placenta. 

Educate the mother and family members about the home assessment or identifying daily fetal movements and when to seek immediate medical attention. Decrease in placental blood flow results in reduced gas exchange and impaired healthy functioning of the placenta. Potential outcomes of poor placental perfusion include a malnourished, low birth weight infant, and prematurity associated with early delivery, abruptio placentae, and fetal death. Reduced fetal activity means fetal compromise. 

Identify and educate the mother and family members about fetal activity factors . Cigarette smoking, medications, drug use, serum glucose levels, environmental sounds, time of day, and the sleep -wake cycle of the fetus can increase or decrease fetal movement. The woman should report a decrease in movements or if none occur during 3 hours. 

Report signs of abruptio placentae (i.e., vaginal bleeding, uterine tenderness, abdominal pain, and decreased fetal activity). Immediate attention and intervention increase the likelihood of a positive outcome. Placental abruption occurs when there is a compromise of the vascular structures supporting the placenta. These vascular structures deliver oxygen and nutrients to the fetus (Schmidth et al., 2021).

Present contact number for the client and family members to direct questions, address changes in daily fetal movements and maternal condition. Provides a chance to address concerns and misconceptions and intervene promptly, as indicated.

Note the fetal response to medications such as magnesium sulfate (MgSO4), phenobarbital, and diazepam. Depressant effects of medication reduce fetal respiratory and cardiac function and fetal activity level, even though placental circulation may be adequate.

Assist with assessing fetal maturity and well-being using lecithin-sphingomyelin (L/S) ratio, prostaglandins, estriol levels, fetal breathing movements, and sequential sonography beginning at 20–26 weeks’ gestation. In the event of declining maternal/fetal condition, risks of delivering a preterm infant are weighed against the risks of continuing the pregnancy, using results from evaluative studies of lung and kidney maturity, fetal growth, and placental functioning. Intrauterine growth restriction (IUGR) is associated with reduced maternal volume and vascular changes.

Assist with assessing maternal plasma volume at 24–26 weeks’ gestation using Evans’ blue dye when indicated. Identifies fetus at risk for IUGR or intrauterine fetal demise associated with reduced plasma volume and reduced placental perfusion.

Assist in Doppler ultrasound of the fetal umbilical artery. The use of umbilical artery Doppler ultrasound for fetal surveillance in high-risk pregnancies is supported by several RCTs and systematic reviews. Doppler ultrasound of the fetal umbilical artery measures the blood flow patterns through the artery as an indicator of placental perfusion. If the umbilical artery flow is absent or reversed during end-diastole, this illustrates abnormally high placental resistance, reducing fetal blood flow (Fox et al., 2019).

Utilizing ultrasonography assist with the assessment of placental size. Reduced placental function and size are associated with preeclampsia. A common pathological feature of preeclampsia is the failure of the maternal arteries supplying the placenta to undergo the physiological adaptations of a normal pregnancy that facilitate adequate placental perfusion (Schmidt et al., 2021).

Administer a single course of corticosteroid ( dexamethasone , betamethasone) IM for at least 24–48 hr, but not more than seven days before delivery, when severe preeclampsia necessitates premature delivery between 26 and 34 weeks gestation. Corticosteroids are thought to induce fetal pulmonary maturity (surfactant production) and prevent respiratory distress syndrome , at least in a fetus delivered prematurely because of condition or inadequate placental functioning. Best results are obtained when the fetus is less than 34 weeks gestation and delivery occurs within a week of corticosteroid administration.

Vasospasm and decreased organ perfusion are the main characteristics of preeclampsia, which can lead to cerebral vasospasm. Endothelial dysfunction occurs at the site of the uterus and at the cerebral endothelium, which leads to neurological disorders, including eclampsia. Progression to eclampsia occurs when the woman has one or more generalized tonic-clonic seizures. An eclamptic seizure may result in cerebral hemorrhage, abruptio placentae, fetal compromise, or death of the mother or fetus.

Assess for central nervous system (CNS) involvement. Cerebral edema and vasoconstriction can be evaluated in terms of symptoms, behaviors, or retinal changes. Elevated blood pressure from preeclampsia causes dysfunction of autoregulation of the cerebral vasculature, which causes hypoperfusion, endothelial damage, or edema. These symptoms include headache, irritability, visual disturbances, or changes on fundoscopic examination. 

Assess for alterations in level of consciousness. In progressive preeclampsia, vasoconstriction and vasospasms of cerebral blood vessels reduce oxygen consumption by 20% and cerebral ischemia.

Assess the client’s deep tendon reflexes (3+ to 4+) and ankle clonus. Deep tendon reflexes become hyperactive because of central nervous system irritability. Ankle clonus is generally accompanied by hyperreflexia. To assess for ankle clonus, the nurse supports the leg with the knee flexed with one hand. Using the other hand, the nurse sharply dorsiflexes the foot and holds the position for a moment, and then releases the foot. Normal response (negative clonus) is elicited when no rhythmic oscillations are felt while the foot is held in dorsiflexion. Abnormal response (positive clonus) is recorded when the nurse feels and sees the oscillations against this pressure. Video for sustained ankle clonus can be watched here . 

Assess for signs of labor at every visit. Ask the client if she feels any signs of contractions, vaginal bleeding, or leaking of fluid. Prenatal care is performed to determine any pregnancy complications and perform early interventions, as indicated.

Assess the client’s vital signs. A client with systolic blood pressure greater than or equal to 140 mmHg and diastolic blood pressure greater than 90 mmHg meets the criteria for new-onset hypertension. Additionally, shortness of breath may suggest pulmonary edema, which is concerning for the development of preeclampsia.

Assess for the presence of epigastric or RUQ pain. Assess the client for any complaints of epigastric pain, RUQ pain, or even heartburn. Liver ischemia is caused by decreased organ perfusion leading to pain in the epigastric area, nausea and vomiting, and elevated liver enzymes.

Perform fundoscopic examination regularly. It helps to evaluate changes or severity of retinal involvement. Visual disturbances such as blurring of vision, scotoma, and photopsia are common in women with preeclampsia and eclampsia. Vasoconstriction causes retinal arteriolar spasm, which in turn results in visual disturbances. 

Palpate for uterine tenderness or rigidity; check for vaginal bleeding—review history of other medical problems. These signs may indicate abruptio placentae, especially if a pre-existing medical problem, such as diabetes mellitus or a renal or cardiac disorder, causes vascular involvement.

Emphasize the importance of the client promptly reporting signs/symptoms of CNS involvement. Delayed treatment or progressive onset of symptoms may result in tonic-clonic convulsions or eclampsia. Symptoms that commonly precede a convulsion are severe, persistent headaches, blurred vision, photophobia, epigastric pain, or heartburn.

Establish measures to lessen the likelihood of seizures. Keeping the room quiet and dimly lit, limiting visitors, planning and coordinating care, and promoting rest lessen environmental factors that may stimulate irritable cerebrum and cause a convulsive state.

Review test results of clotting time, prothrombin time (PT), partial thromboplastin time (PTT), and fibrinogen levels. These tests can indicate depletion of coagulation factors and fibrinolysis and may suggest disseminated intravascular coagulation (DIC), which indicates a worsening of preeclampsia. As the blood vessels constrict, the formation of clots occurs to repair the endothelial damage until the body’s platelet supply is diminished.

Enforce seizure precautions per protocol. If a seizure does occur, a seizure protocol reduces the risk of injury.

Advise the client to maintain strict bedrest if prodromal signs or aura are experienced and explain the necessity for these actions. Explain that eclampsia is usually preceded by prodromal signs such as persistent headache, blurring of vision, severe epigastric pain, altered mental status, and abdominal pain. The client may feel restless during the aural phase. Understanding the importance of providing for own safety needs may enhance client cooperation. 

In the event of a seizure, ensure a patent airway and promote client safety. 

Stay with the client during and after a seizure. Do not leave the bedside and call for assistance. Promotes client safety and reduces the sense of isolation during the event. 

Keep padded side rails up pillows or folded blankets. Set the bed in the lowest position. Women with eclampsia are prone to sustaining fractures from falling out of bed during seizures. Minimizes injury should frequent or generalized seizures occur while the client is in bed. 

Do not attempt to restrain or restrict the client’s movements during the seizure. Cradle the client’s head, place it on a soft area and assist to the floor if out of bed. Gentle guiding of extremities reduces risk or physical injury when the client lacks voluntary muscle control. If an attempt is made to restrain the client during the seizure, erratic movements may increase, and the client may injure themselves or others. 

Note the time of onset and duration of the seizure. Document motor involvement, duration of seizure, and post-seizure behavior. Helps localize the cerebral area of involvement and may be useful in helping the client and family members manage seizure activity.

Turn the client’s head on the side; insert airway/bite block per facility protocol only if the jaw is relaxed; suction nasopharynx, as indicated. Helps ensure a patent airway and reduces the risk of oral trauma but should not be “forced” or inserted when teeth are clenched because dental and soft-tissue damage may result.

Check for the patency of the intravenous line. Restart the IV line immediately if infiltrated. Check whether the IV line is still patent after seizure activity. Start a new line with a gauge 18 needle and administer magnesium sulfate as ordered. See interventions for magnesium sulfate administration below. 

Administer oxygen 10 L/min by a non-rebreather face mask. Monitor pulse oximetry. After convulsions, administration of supplementary oxygen treats postictal hypoxemia . 

Observe for signs and symptoms of labor or uterine contractions. Assess uterine activity, cervical status, and fetal status. Convulsions increase uterine irritability, becoming hypercontractile and hypertonic. As a result, the membranes may have ruptured, or the cervix may have dilated rapidly. Labor and birth may ensue after seizure activity. 

Assess fetal well-being, noting fetal heart rate (FHR). During seizure activity, fetal bradycardia may occur, including late decelerations. The placental blood flow can be cut off, which will lead to fetal distress and death.

Monitor for signs of disseminated intravascular coagulation (DIC), easy/spontaneous bruising, prolonged bleeding, epistaxis, GI bleeding. Abruptio placentae with the release of thromboplastin predispose the client to DIC. DIC occurs when platelets rush to repair the endothelial damage until their numbers are diminished, resulting in bleeding in the woman.

Be prepared to assist with birth when the client is stable. Following an eclamptic seizure and after stabilizing the client and fetus, a decision is made regarding the timing and method of birth. Eclampsia, by itself, is not an indication of immediate cesarean birth . The route and timing of birth depending on the condition of the mother and fetus, gestational age of the fetus, presence of labor, and cervix score. 

Administer magnesium sulfate (MgSO4) intramuscularly or IV using an infusion pump. Magnesium sulfate is the drug of choice for treating eclamptic seizures and preventing repeated seizures. MgSO4 is a CNS depressant that decreases acetylcholine release, blocks neuromuscular transmission, and prevents seizures. It has a transient effect of lowering BP and increasing urine output by altering vascular response to pressor substances. Although IV administration of MgSO4 is easier to regulate and reduces the risk of a toxic reaction, some facilities may still use the IM route if continuous surveillance is not possible or if appropriate infusion apparatus is not available (He, Chen et al., 2020). Note: Adding 1 ml of 2% lidocaine to the IM injection may reduce associated discomfort. Current research suggests the use of phenytoin infusion may be effective in treating eclampsia without the adverse side effects, such as respiratory depression and tocolytic effect on uterine smooth muscle, which can impede labor intrapartum therapy (Khooshideh et al., 2017) .

Monitor BP before, during, and after magnesium sulfate (MgSO4) administration. Note serum magnesium levels in conjunction with respiratory rate, patellar/deep tendon reflex (DTRs), and urine output. A therapeutic level of MgSO4 is achieved with serum levels of 4.0–7.5 mEq/L or 6–8 mg/dL. Adverse/toxic reactions develop above 10–12 mg/dL, with loss of DTRs occurring first, respiratory paralysis between 15–17 mg/dL, or heart block occurring at 30–35 mg/dL.

Prepare calcium gluconate. Give 10 ml (1 g/10 ml) over 3 minutes as indicated. It serves as an antidote to counteract the adverse/toxic effects of MgSO4. Magnesium toxicity can present in several ways, including diminished deep tendon reflexes, cardiopulmonary arrest, and respiratory depression (Chakraborty & Can, 2021).

Administer amobarbital (Amytal) or diazepam (Valium), as indicated. Depresses cerebral activity; has a sedative effect when MgSO4 does not control convulsions. These are usually not recommended as first-line therapy because they depress the gag reflex , and their sedative effects also affect the fetus. 

Review the results of sequential platelet count. Avoid amniocentesis if the platelet count is less than 50,000/mm3. If thrombocytopenia is present during the operative procedure, use general anesthesia . As indicated, transfuse with platelets, packed red blood cells, fresh frozen plasma, or whole blood. Rule out HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome. Thrombocytopenia may arise because of platelet adherence to disrupted endothelium or reduced prostacyclin levels (a potent inhibitor of platelet aggregation). Invasive procedures or anesthesia requiring needle puncture (such as spinal/epidural) could result in excessive bleeding.

Monitor liver enzymes and bilirubin; note hemolysis and presence of Burr cells on peripheral smear. An elevated liver enzyme (aspartate transaminase [AST], alanine transaminase [ALT]) and bilirubin levels, microangiopathic hemolytic anemia , and thrombocytopenia may indicate the presence of HELLP syndrome, signifying a need for immediate cesarean delivery if the condition of the cervix is unfavorable for induction of labor.

Hospitalize if central nervous system (CNS) involvement is present. Immediate introduction of therapy helps to ensure safety and limit complications.

Prepare for cesarean birth if preeclampsia is severe, placental functioning is compromised, and cervix is not ripe or responsive to induction. When fetal oxygenation is severely reduced owing to vasoconstriction within the malfunctioning placenta, immediate delivery may be necessary to save the fetus.

With hypertensive disorders of pregnancy, the reduced placental perfusion of the pregnant woman causes endothelial disruption that leads to vasoconstriction and water and sodium retention. Local vasospasm in the kidneys causes glomerular damage leading to oliguria and proteinuria. The loss of protein can cause malnutrition and muscle wasting in pregnant women. Additionally, vascular permeability is compromised due to the loss of protein, allowing water to shift from the intravascular space to the interstitial spaces, resulting in generalized edema.

Assess the client’s nutritional status, dietary intake, condition of hair and nails, and height, and pregravid weight. Establishes guidelines for determining dietary needs and educating the client. Malnutrition may be a contributing factor to the onset of preeclampsia, specifically when the client follows a low-protein diet, has insufficient caloric intake, and is overweight or underweight by 20% or more before conception.

Assess the client’s weight daily, preferably in the morning before breakfast. Weigh the client on the same weighing scale, with the same amount of clothes, and at the same time of the day to increase the accuracy of results. Changes in excess of 0.5 kg (1.1 lb) may reflect shifts in fluid balance.

Provide information about normal weight gain in pregnancy, adjusting the information to meet the client’s needs. The underweight client with a BMI of less than 18.5 should gain 28-40 pounds and may need a diet higher in calories throughout the pregnancy. The obese client with a BMI of 25.0 to 29.9 should gain 15 to 25 pounds and should avoid dieting throughout the pregnancy because it places the fetus at risk for ketosis (CDC, 2021).

Educate the client and family members about the action and uses of protein and its role in the development of preeclampsia. Regular intake of 80–100 g/day (1.5 g/kg) of protein is sufficient to replace proteins lost in the urine and allow for normal serum oncotic pressure. The DASH Trial (Dietary Approaches to Stop Hypertension) and the OmniHeart (Optimal Macronutrient Intake Trial to Prevent Heart Disease) were two large-scale interventional studies seeking to evaluate the effect of implementing healthy dietary patterns in adults, and the overall results from both trials confirmed the health benefit associated with greater plant protein consumption (Abais-Battad et al., 2018).

Advise the client to have frequent rest periods and limit activity to conserve protein requirements. Decreasing metabolic rate through bed rest and limited activity reduces protein needs. Additionally, the fetal demands can also take a toll on maternal nutrient needs. Therefore, rest and an appropriate dietary plan can help conserve protein requirements.

Advise the pregnant woman to increase consumption of protein-containing foods, as indicated. Ensure a balanced diet with adequate fluid intake. Protein is abundant in lean meat, vegetables, eggs, and fish. As indicated by a dietitian, the client may add more protein by consuming these foods. During pregnancy, poor nutrition practice is linked with gestational weight gain and preeclampsia (Zelalem et al., 2017).

Monitor laboratory studies, such as BUN, sodium, and potassium. Indicators of nutritional needs, restrictions, and the necessity for and effectiveness of therapy.

Collaborate with a dietitian, as indicated. Helpful in creating individual dietary plans incorporating specific needs/restrictions. Nutrition education during pregnancy about a healthy diet and a healthy lifestyle can be the right time to encourage adequate daily iron, folic acid intake, and other pregnancy-specific foods (Zelalem et al., 2017). 

The pregnant client with a hypertensive disorder may not be aware of the processes that can lead to the development of the disease and how it could be prevented or managed. Furthermore, the client and the family members need an understanding of the interventions that are appropriate for this disease process.

Assess the client’s or family member’s knowledge of the disease process. Provide information about the pathophysiology of preeclampsia, implications for mother and fetus. Establishes a database and provides information. Provide information about areas in which learning is needed. The pathophysiology of pregnancy-induced hypertension is related to a mechanism of reduced placental perfusion inducing systemic vascular endothelial dysfunction. This arises due to the inability of the uterine spiral arteries to vasodilate, decreasing the fetus’ blood and nutrient supply and increasing the mother’s blood pressure (Braunthal & Brateanu, 2019).

Assess the client’s or family member’s knowledge about the rationales for interventions, procedures, and tests, as needed. Taking information can improve understanding and reduce fear , helping to facilitate the treatment plan for the client. Note: Current research in progress may provide additional treatment options, such as using low-dose (60 mg/day) aspirin to reduce thromboxane generation by platelets, limiting the severity/incidence of preeclampsia (Pradhan et al., 2020).

Provide information about signs/symptoms indicating worsening of the condition, and instruct the client when to notify the healthcare provider. Helps ensure that the client seeks timely treatment and may prevent worsening of preeclamptic state or additional complications. Instruct the client to report any signs of headaches, new-onset visual changes, new-onset epigastric or RUQ pain, decreased fetal movement, and severe dyspnea. These symptoms are indicative of severe preeclampsia that may progress to eclampsia, and therefore needs immediate intervention.

Inform the client of health status, results of tests, and fetal well-being. Fears and anxieties can be compounded when the client or family members do not have adequate information about the state of the disease process or its impact on the client and fetus. When the client understands the consequences of inadequate intervention and is motivated to achieve health, the client typically participates in treatment interventions.

Educate the client on monitoring her weight at home and notify the healthcare provider if the gain is more than 2 lbs (0.9 kg)/wk, or 0.5 lb (0.23 kg)/day. A gain of 3.5 lbs (1.59 kg) or greater per month in the second trimester or 1 lb (0.45 kg) or greater per week in the third trimester suggests preeclampsia.

Educate and assist family members in learning the procedure for home monitoring of blood pressure. Encourages cooperation in the treatment regimen, allows immediate intervention as needed, and may reassure that efforts are beneficial. Blood pressure monitoring should be taught to family members two to four times per day in the same arm and the same position.

Review techniques for stress management and diet restriction. Strengthens the importance of the client’s responsibility in treatment. Healthcare personnel must examine a pregnant woman’s stress levels and recommend practical stress management strategies based on their particular stressors and conditions. Mental stress during pregnancy has associated an increase in the risk for gestational hypertension (Rasouli et al., 2019; Leener et al., 2009).

Educate the client with possible or mild preeclampsia and ensure enough protein in the diet. Loss of protein through the urine is common among clients with preeclampsia because of glomerular damage, leading to excessive protein excretion. Protein is essential for intravascular and extravascular fluid regulation.

Instruct the client to follow the prescribed dietary regimen that includes a diet low in sodium, saturated fat, and cholesterol. Excess saturated fats, cholesterol, sodium, and calories have been defined as nutritional risks in preeclampsia. A diet low in fat and high in polyunsaturated fat reduces BP.

Review self-testing of urine for protein. Reinforce rationale for and implications of testing. A test result of 2+ or greater is vital and needs to be reported to a healthcare provider. Urine specimens contaminated by vaginal discharge or red blood cells may produce positive test results for protein.

Reinforce the importance of adhering to treatment regimens and keeping follow-up appointments. Lack of engagement in the treatment plan is a common reason for the failure of antihypertensive therapy. Ongoing evaluation for client participation is critical to successful treatment.

Explain prescribed medications and their rationale, dosage, expected and adverse side effects, and particular traits. Adequate information and understanding about the side effects can enhance the client’s commitment to the treatment plan.

Administering medications and providing pharmacologic support in patients with preeclampsia and gestational hypertensive disorders play a critical role in managing these conditions and mitigating potential complications. Healthcare providers closely monitor the patient’s response to medication, including blood pressure levels, renal function, and potential side effects.

1. Hydralazine (Apresoline, Neopresol).  Administered intravenously, hydralazine reduces blood pressure by relaxing the smooth muscles. The vasodilating effect reduces 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 decreases peripheral vascular resistance without significant change in cardiac output or causing tachycardia. Contraindicated with asthma and congestive heart failure . Closely monitor blood pressure after administration. 

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

4. Nifedipine (Adalat).  Calcium channel blocker that dilates arterioles and decreases systemic vascular resistance by relaxing arterial smooth muscle. Nifedipine can potentiate the CNS effects of magnesium sulfate. Closely monitor blood pressure after administration. 

5. Sodium Nitroprusside (Nitropress). Used in rare scenarios where other antihypertensive agents have failed to control blood pressure.

• Patient must exhibit a normal blood pressure of 120/70 mmHg.
• No presence of protein should be detected in her urine.
• Edema should be minimized or confined to the lower extremities only.

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy .

Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care We love this book because of its evidence-based approach to nursing interventions. This care plan handbook uses an easy, three-step system to guide you through client assessment, nursing diagnosis, and care planning. Includes step-by-step instructions showing how to implement care and evaluate outcomes, and help you build skills in diagnostic reasoning and critical thinking.

Nursing Care Plans – Nursing Diagnosis & Intervention (10th Edition) Includes over two hundred care plans that reflect the most recent evidence-based guidelines. New to this edition are ICNP diagnoses, care plans on LGBTQ health issues, and on electrolytes and acid-base balance.

Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales Quick-reference tool includes all you need to identify the correct diagnoses for efficient patient care planning. The sixteenth edition includes the most recent nursing diagnoses and interventions and an alphabetized listing of nursing diagnoses covering more than 400 disorders.

Nursing Diagnosis Manual: Planning, Individualizing, and Documenting Client Care  Identify interventions to plan, individualize, and document care for more than 800 diseases and disorders. Only in the Nursing Diagnosis Manual will you find for each diagnosis subjectively and objectively – sample clinical applications, prioritized action/interventions with rationales – a documentation section, and much more!

All-in-One Nursing Care Planning Resource – E-Book: Medical-Surgical, Pediatric, Maternity, and Psychiatric-Mental Health   Includes over 100 care plans for medical-surgical, maternity/OB, pediatrics, and psychiatric and mental health. Interprofessional “patient problems” focus familiarizes you with how to speak to patients.

Other recommended site resources for this nursing care plan:

• Nursing Care Plans (NCP): Ultimate Guide and Database MUST READ! Over 150+ nursing care plans for different diseases and conditions. Includes our easy-to-follow guide on how to create nursing care plans from scratch.
• Nursing Diagnosis Guide and List: All You Need to Know to Master Diagnosing Our comprehensive guide on how to create and write diagnostic labels. Includes detailed nursing care plan guides for common nursing diagnostic labels.

Other care plans related to the care of the pregnant mother and her baby:

• Abortion (Termination of Pregnancy) | 8 Care Plans
• Cervical Insufficiency (Premature Dilation of the Cervix) | 4 Care Plans
• Cesarean Birth | 11 Care Plans
• Cleft Palate and Cleft Lip | 7 Care Plans
• Gestational Diabetes Mellitus | 8 Care Plans
• Hyperbilirubinemia (Jaundice) | 4 Care Plans
• Labor Stages, Induced, Augmented, Dysfunctional, Precipitous Labor | 45 Care Plans
• Neonatal Sepsis | 8 Care Plans
• Perinatal Loss (Miscarriage, Stillbirth) | 6 Care Plans
• Placental Abruption | 4 Care Plans
• Placenta Previa | 4 Care Plans
• Postpartum Hemorrhage | 8 Care Plans
• Postpartum Thrombophlebitis | 5 Care Plans
• Prenatal Hemorrhage (Bleeding in Pregnancy) | 9 Care Plans
• Preeclampsia and Gestational Hypertension  | 6 Care Plans
• Prenatal Infection | 5 Care Plans
• Preterm Labor | 7 Care Plans
• Puerperal & Postpartum Infections  | 5 Care Plans
• Substance Abuse in Pregnancy | 9 Care Plans

References and sources for this nursing care plan for hypertensive disorders in pregnancy.

• Abais-Battad, J. M., Lund, H., Fehrenbach, D. J., Dasinger, J. H., Alsheikh, A. J., & Mattson, D. L. (2018, 31 December). Parental Dietary Protein Source and the Role of CMKLR1 in Determining the Severity of Dahl Salt-Sensitive Hypertension . Hypertension, 73(2).
• American College of Obstetricians and Gynecologists (ACOG) Committee on Obstetric Practice. (2020). Practice Bulletin #222: Gestational Hypertension and Preeclampsia . Obstetrics & Gynecology , 135 , 237-260.
• Arulkumaran, N., & Lightstone, L. (2013). Severe pre-eclampsia and hypertensive crises . Best Practice & Research Clinical Obstetrics & Gynaecology, 27(6), 877-884.
• Benigni, A., Gregorini, G., Frusca, T., Chiabrando, C., Ballerini, S., Valcamonico, A., … & Remuzzi, G. (1989). Effect of low-dose aspirin on fetal and maternal generation of thromboxane by platelets in women at risk for pregnancy-induced hypertension . New England Journal of Medicine, 321(6), 357-362.
• Braunthal, S., & Brateanu, A. (2019, April 10). Hypertension in pregnancy: Pathophysiology and treatment . SAGE, 7.Chakraborty, A., & Can, A. S. (2021, July 2). Calcium Gluconate – StatPearls. NCBI. Retrieved December 14, 2021.
• El Allani, L., Benlamkaddem, S., Berdai, M. A., & Harandou, M. (2020, June 9). A case of massive hepatic infarction in severe preeclampsia as part of the HELLP syndrome . The Pan African Medical Journal, 36(78).
• Espinoza, J. (2012). Uteroplacental ischemia in early‐and late‐onset preeclampsia: a role for the fetus? . Ultrasound in obstetrics & gynecology, 40(4), 373-382.
• Fantasia, H. C. (2018). Low-dose aspirin for the prevention of preeclampsia . Nursing for women’s health, 22(1), 87-92.
• Fox, R., Kitt, J., Leeson, P., Aye, C. Y.L., & Lewandowski, A. J. (2019, October 4). Preeclampsia: Risk Factors, Diagnosis, Management, and the Cardiovascular Impact on the Offspring . Journal of Clinical Medicine , 8 (10), 5-6. MDPI.
• Fróes, N. B. M., Lopes, M. V. D. O., Pontes, C. M., Ferreira, G. L., & Aquino, P. D. S. (2020). Middle range theory for the nursing diagnosis Excess Fluid Volume in pregnant women . Revista Brasileira de Enfermagem , 73 .
• Gallo, D., Poon, L. C., Fernandez, M., Wright, D., & Nicolaides, K. H. (2014, April 15). Prediction of Preeclampsia by Mean Arterial Pressure at 11–13 and 20–24 Weeks’ Gestation . Fetal Diagnosis and Therapy.
• Ghulmiyyah, L., & Sibai, B. (2012, February). Maternal mortality from preeclampsia/eclampsia . In Seminars in perinatology (Vol. 36, No. 1, pp. 56-59). WB Saunders.
• He, G., Chen, Y., Chen, M., He, G., & Liu, X. (2020, November 13). Efficacy and safety of low dose aspirin and magnesium sulfate in the treatment of pregnancy-induced hypertension A protocol for systematic review and meta-analysis . Medicine (Baltimore) , 99 (46).
• Johnson, R. J., Kanbay, M., Kang, D.-H., Lozada, L. G. S.-., & Feig, D. (2011, August 29). Uric Acid A Clinically Useful Marker to Distinguish Preeclampsia From Gestational Hypertension . Hypertension, 58(4), 704-708.
• Khooshideh, M., Ghaffarpour, M., & Bitarafan, S. (2017, July 6). The comparison of anti-seizure and tocolytic effects of phenytoin and magnesium sulfate in the treatment of eclampsia and preeclampsia: A randomised clinical trial. Iranian Journal of Neurology , 16 (3), 125-129.
• Leeners, B., Wagner, P. N.-., Kuse, S., Stiller, R., & Rath, W. (2009, July 07). Emotional Stress and the Risk to Develop Hypertensive Diseases in Pregnancy . Hypertension in Pregnancy , 26 (2), 211-226.
• Leifer, G. (2018). Introduction to Maternity and Pediatric Nursing (8th ed., Vol. 1). Elsevier.
• Lu, Y., Chen, R., Cai, J., Huang, Z., & Hong Yuan. (2018, October 29). The management of hypertension in women planning for pregnancy . British Medical Bulletin, 128(1), 75-84.
• Luger, R. K., & Knight, B. P. (2021, October 9). Hypertension In Pregnancy . Statpearls. Retrieved December 8, 2021.
• Mayrink, J., Souza, R. T., Feitosa, F. E., Rocha Filho, E. A., Leite, D. F., Vettorazzi, J., … & Cecatti, J. G. (2019). Mean arterial blood pressure: potential predictive tool for preeclampsia in a cohort of healthy nulliparous pregnant women . BMC pregnancy and childbirth, 19(1), 1-8.
• O’Brien, L. M., Bullough, A. S., Owusu, J. T., Tremblay, K. A., Brincat, C. A., Chames, M. C., … & Chervin, R. D. (2012). Pregnancy-onset habitual snoring, gestational hypertension, and preeclampsia: prospective cohort study . American journal of obstetrics and gynecology, 207(6), 487-e1. 
• Pradhan, M., Kishore, S.V., & Champatiray, J. (2020, April 4). Effect of low dose aspirin on maternal outcome in women at risk for developing pregnancy-induced hypertension . International Journal of Reproduction, Contraception , Obstetrics and Gynecology, 9(4), 1590+.
• Perry, S. E., Hockenberry, M. J., Lowdermilk, D. L., Wilson, D., Alden, K. R., & Cashion, M. C. (2017).  Maternal child nursing care-E-Book . Elsevier Health Sciences.
• Rasouli, M., Pourheidari, M., & Gardesh, Z. H. (2019, February 12). Effect of Self-care Before and During Pregnancy to Prevention and Control Preeclampsia in High-risk Women . International Journal of Preventive Medicine, 10(21).
• ​​Schiff, E., Peleg, E., Goldenberg, M., Rosenthal, T., Ruppin, E., Tamarkin, M., … & Mashiach, S. (1989). The Use of Aspirin to Prevent Pregnancy-Induced Hypertension and Lower the Ratio of Thromboxane A2 to Prostcyclin in Relatively High-Risk Pregnancies . New England Journal of Medicine, 321(6), 351-356.
• Schmidt P, Skelly CL, Raines DA. Placental Abruption . [Updated 2021 Jul 5]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing.
• Sinkey, R. G., Battarbee, A. N., Bello, N. A., Ives, C. W., Oparil, S., & Tita, A. T.N. (2020, August 27). Prevention, Diagnosis, and Management of Hypertensive Disorders of Pregnancy: a Comparison of International Guidelines . Current Hypertension Reports, 22(66), 2. Topical Collection on Preeclampsia.
• Weight Gain During Pregnancy | Pregnancy | Maternal and Infant Health. (2021, May 26). CDC.
• Wisner, K. (2019). Gestational hypertension and preeclampsia . MCN: The American Journal of Maternal/Child Nursing , 44 (3), 170.
• Xu, T. T., Zhou, F., Deng, C. Y., Huang, G. Q., Li, J. K., & Wang, X. D. (2015). Low‐Dose aspirin for preventing preeclampsia and its complications: a meta‐analysis . The Journal of Clinical Hypertension, 17(7), 567-573. 
• Zelalem, A., Endeshaw, M., Ayenew, M., Shiferaw, S., & Yirgu, R. (2017, July 25). Effect of Nutrition Education on Pregnancy Specific Nutrition Knowledge and Healthy Dietary Practice among Pregnant Women in Addis Ababa . Clinics in Mother and Child Health.

Updated and reviewed by M. Belleza, R.N. and M. Vera, BSN, R.N.

4 thoughts on “7 Preeclampsia & Gestational Hypertensive Disorders Nursing Care Plans and Management”

Well done your knowledge is greatly appreciated

Thanks very interesting

Thanks for well searched management of hypertension, pre-eclampsia and eclampsia.

Happy to help, you’re welcome Ogwang!