pregnancy induced hypertension essay

The Pregnancy-Induced Hypertension Essay

Pregnancy-induced hypertension (PIH) is among the major causes of maternal mortality and a significant contributor to maternal and perinatal morbidity. Preeclampsia is characterized by hypertension that develops throughout pregnancy and disappears after birth, suggesting that the placenta is a critical player in the condition. Reduced placental perfusion, which leads to extensive malfunction of the maternal vascular endothelium, is an initial PIH event (Osman, 2019). There is a variety of processes that contribute to decreased placental perfusion in PIH, but most studies point to abnormal cytotrophoblast invasions of spiral arterioles as a critical component.

There are greater odds of developing PIH when a woman is connected to nulliparity, extreme maternal ages, numerous pregnancies, gestational diabetes, chronic hypertension, fetal deformity, obesity, or history of PIH in the past pregnancies. Chronic diseases such as renal disease and diabetes mellitus, cardiovascular problems, unrecognized chronic hypertension, and PIH in family history are precipitating PIH factors. In addition, alcohol use, rheumatoid arthritis, extreme underweight and overweight, mental stress, asthma, and low socioeconomic status are also risk factors for PIH.

The most typical symptoms of PIH are increased blood pressure, protein in the urine, edema, abrupt weight gain, visual abnormalities, nausea, upper right abdominal discomfort or pain around the stomach, and reduced amounts of urine. However, each woman has distinct symptoms that are related to PIH. A physician determines the precise therapy for PIH based on a woman’s pregnancy, general health and medical history, the severity of the condition, tolerance for certain drugs, and expectations for the disease’s course. The primary objective of therapy is to prevent the illness from becoming worse and from leading to secondary consequences. Bedrest, magnesium sulfate, fetal monitoring, and regular urine and blood tests to detect changes that may suggest worsening of PIH are some of the treatments for PIH. Furthermore, drugs such as corticosteroids may aid in the maturation of the fetus’s lungs. If therapy fails to manage PIH or if the fetus or mother is in danger, delivery of the infant may be considered, with cesarean delivery being suggested in such circumstances.

Osman, O. (2019). Pregnancy induced hypertension (PIH): Beyond pregnancy. Frontiers in Women’s Health , 4 (3). Web.

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Article Contents

Mean arterial pressure and urinary protein excretion responses to chronic reductions in uterine perfusion pressure (rupp) in pregnant rats. all data are expressed as mean ± sem., vascular responses to acetylcholine are reduced in pregnant rats with chronic reductions in uterine perfusion pressure (rupp). all data are expressed as mean ± sem., glomerular filtration rate and renal plasma flow responses to chronic reductions in uterine perfusion pressure (rupp) in pregnant rats. all data are expressed as mean ± sem., does a reduction in renal nitric oxide synthesis mediate the abnormal pressure natriuresis and elevation in arterial pressure during pih, does enhanced endothelin synthesis contribute to the elevation in arterial pressure during pih, does enhanced thromboxane and/or reduced prostacyclin synthesis mediate the renal and cardiovascular abnormalities in pih.

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Pathophysiology of pregnancy-induced hypertension

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Joey P. Granger, Barbara T. Alexander, William A. Bennett, Raouf A. Khalil, Pathophysiology of pregnancy-induced hypertension, American Journal of Hypertension , Volume 14, Issue S3, June 2001, Pages 178S–185S, https://doi.org/10.1016/S0895-7061(01)02086-6

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Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of all pregnancies in the United States. Despite being the leading cause of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH have not yet been fully elucidated. Studies during the past decade, however, have provided a better understanding of the potential mechanisms responsible for the pathogenesis of PIH. The initiating event in PIH appears to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as nitric oxide and prostacyclin. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during PIH is still unclear. Investigators are also attempting to elucidate the placental factors that are responsible for mediating activation/dysfunction of the maternal vascular endothelium. Microarray analysis of genes within the ischemic placenta should provide new insights into the link between placental ischemia and hypertension. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood. Am J Hypertens 2001;14:178S–185S © 2001 American Journal of Hypertension, Ltd.

Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of all pregnancies in the United States. 1–4 Despite being one of the leading causes of maternal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH are unclear. Hypertension associated with preeclampsia develops during pregnancy and remits after delivery, implicating the placenta as a central culprit in the disease. An initiating event in PIH has been postulated to be reduced placental perfusion that leads to widespread dysfunction of the maternal vascular endothelium by mechanisms that remain to be defined. 1–4 The mechanisms leading to reduced placental perfusion in PIH may be multiple, but most studies in humans suggest abnormal cytotrophoblast invasion of spiral arterioles as an important factor. 1–5

Several lines of experimental evidence support this hypothesis. For example, studies in various animal models, including sheep, dog, rabbit, and rat have shown that reductions in uteroplacental blood flow leads to a hypertensive state that closely resembles PIH in women. 6 , 7 Additional support for this concept derives from studies in humans that indicate increased circulating fibronectin and factor VIII antigen, both markers of endothelial cell injury. 1–4 , 8–10 Decreases in the production of endothelial-derived relaxing factors, such as nitric oxide and prostacyclin, increase production of endothelin and thromboxane, and enhanced vascular reactivity to angiotensin II in women with PIH also suggest abnormal endothelial function. 1–4 , 11

During normal pregnancy, significant changes in cardiovascular and renal function occur to meet the metabolic needs of the mother and the fetus. 1–3 For example, maternal cardiac output and blood volume increase by approximately 40% to 50%, whereas total peripheral resistance and arterial blood pressure (BP) tend to decrease. 1–3 In addition, there are marked changes in renal function such as elevations in renal plasma flow and glomerular filtration rate of approximately 30% to 40%. 12 Renin concentration, renin activity, and angiotensin II levels are elevated; however, the vascular responsiveness to angiotensin II appears to be reduced. 13 The mechanisms that are involved in mediating these significant cardiovascular and renal changes during pregnancy have been studied extensively, and it appears that endothelial factors such as nitric oxide play an important role. 1–3 , 14 , 15

The marked hemodynamic and renal changes that normally occur during pregnancy do not manifest themselves in women who develop PIH. Pregnancy-induced hypertension is associated with significant elevations in total peripheral resistance, enhanced responsiveness to angiotensin II, and marked reductions in renal blood flow and glomerular filtration rate and proteinuria. 1–3 Although the physiologic mechanisms that mediate the alterations in cardiovascular and renal function have been extensively studied during normal pregnancy, information regarding the mediators of the reduction in renal and cardiovascular function during PIH has been limited because of the difficulty in performing mechanistic studies in pregnant women. Although several animal models have been developed to study PIH, information on the mechanisms involved in mediating the long-term reduction in kidney function and increase in arterial pressure is lacking. Experimental induction of chronic uteroplacental ischemia appears to be the most promising animal model to study potential mechanisms of PIH, as reductions in uteroplacental blood flow in a variety of animal models lead to a hypertensive state that closely resembles PIH in women. 1–3 , 6 , 7 , 16

Chronic reductions in uteroplacental perfusion pressure in gravid rats after day 14 of gestation, as reported by Eder and MacDonald 17 and Abitbol, 18 lead to significant increases in arterial pressure and proteinuria. We have recently begun to work with this model to examine potential pathophysiologic mechanisms that mediate the hypertension during chronic reductions in uteroplacental perfusion pressure. 19 We reduced uterine perfusion pressure in the gravid rat by approximately 40% by placing a silver clip around the aorta below the renal arteries. Because this procedure has been shown to cause an adaptive increase in uterine blood flow through the ovarian artery, we also placed a silver clip on both the right and left uterine arcade at the ovarian end just before the first segmental artery. 20 We found that reducing uteroplacental perfusion with this approach results in significant and consistent elevations in arterial pressure of 20 to 30 mm Hg as compared to control pregnant rats at day 19 of gestation (Fig. 1) . Our data also indicate that this hypertension is associated with proteinuria, reductions in renal plasma flow and glomerular filtration rate (Figs. 1 and 2 ), and a hypertensive shift in the pressure natriuresis relationship. 20 , 67 Moreover, our data indicate that endothelial function (Fig. 3) is significantly altered in response to chronic reductions in uteroplacental perfusion pressure in the pregnant rat. 21 , 22 Finally, we have found intrauterine growth restriction in response to chronic reductions in uteroplacental perfusion pressure in the pregnant rat, as the average pup size in this group is smaller than in normal pregnant rats. 20 Thus, a chronic reduction in uteroplacental perfusion pressure in the pregnant rat has many of the features of PIH in women. The role of various endothelial, autacoid, and hormonal factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure produced by chronic reductions in uteroplacental perfusion pressure will be the main focus of the remaining portion of this brief review.

One potential mechanism for the reduction in pressure natriuresis and elevation in arterial pressure in response to a chronic reduction in uteroplacental perfusion pressure in the pregnant rat is a reduction in renal nitric oxide (NO) synthesis. 23–26 Nitric oxide is synthesized from L-arginine by a family of enzymes known as NO synthases (NOS). Nitric oxide synthase is readily inhibited by L-arginine analogs such as N -methyl-arginine (L-NMMA), N -nitro-L-arginine (L-NNA), and N -nitro-L-arginine methyl ester (L-NAME). Studies from our laboratories and others have indicated that NO plays an important role in the regulation of renal function and arterial pressure under various physiologic and pathophysiologic conditions. 24 , 27–33 Of particular relevance to PIH is the finding that reducing NO synthesis results in a hypertensive shift in the pressure natriuresis relationship. 28 , 33 This impairment in pressure natriuresis is also associated with reductions in renal plasma flow and glomerular filtration rate and an inability to transmit renal perfusion pressure into the renal interstitium. 28 , 33

Substantial evidence indicates that NO production is elevated in normal pregnancy. 14 , 15 Plasma and urinary levels of cGMP, the second messenger of NO, increase during pregnancy in rats. 14 , 15 Marked increases in 24-h urinary nitrate/nitrite excretion have also been reported to be normal during pregnancy in the rat. 14 , 15 Studies have also shown that pregnancy increases activity of calcium-dependent NOS in uterine artery and heart in early and late pregnancy. 14 , 15 Increased expression of mRNA levels for both constitutive NOS isoforms have been observed in a variety of tissues in late pregnancy. 14 , 15 Plasma arginine levels are also reduced in pregnancy. These findings presumably reflect increased utilization of substrate in response to increased formation of NO.

Increases in NO production appear to play an important role in the renal vasodilatation of pregnancy. 14 , 15 Recent studies by Conrad 14 and other researchers 15 clearly demonstrated that the renal vasodilatation in the pregnant rat is due to an increased NO production. Because NO appears be an important physiologic vasodilator in normal pregnancy, NO deficiency during preeclampsia might be involved in the disease process. Studies from several laboratories have found that chronic NOS inhibition in pregnant rats produces a hypertension associated with peripheral and renal vasoconstriction, proteinuria, intrauterine growth retardation, and increased fetal morbidity, a pattern that closely resembles the symptoms of human pregnancy-induced hypertension. 22 , 34 , 35 However, whether there is a reduction in NO production during pregnancy-induced hypertension is unclear. Much of the uncertainty originates from the difficulty in directly assessing the activity of the NO system in a clinical setting. 1–3 Assessment of whole body NO production by measurement of 24-h nitrate/nitrite excretion has yielded variable results due to difficulties in controlling for factors such as nitrate intake. We have recently reported that normal pregnancy in the rat is associated with significant increases in whole body NO production and renal protein expression of neuronal and inducible NOS. 36 We also recently determined whether whole body and renal NO production is reduced in a rat model of PIH produced by chronically reducing uterine perfusion pressure. 20 Chronic reductions in uterine perfusion pressure resulted in increases in arterial pressure of 20 to 25 mm Hg, decreases in renal plasma flow and glomerular filtration rate, but no difference in urinary nitrite/nitrate excretion relative to control pregnant rats. In contrast, reductions in uterine perfusion pressure in virgin rats resulted in no significant effects on arterial pressure. Renal endothelial and inducible NOS protein expression did not decrease significantly in the chronically reduced uterine perfusion pressure rats relative to normal pregnant rats; however, significant reductions in neuronal NOS were observed. The results of this study indicate that the increase in arterial pressure observed in response to chronic decreases in uterine perfusion pressure in pregnant rats is associated with no change in whole body NO production and a decrease in renal protein expression of neuronal NOS. Whether the reduction in renal protein expression of neuronal NOS occurs as a result of the hypertension or the reduction in renal protein expression of neuronal NOS plays a role in mediating the reduction in renal hemodynamics and elevation in arterial pressure remains to be determined.

Another endothelial-derived factor that may play a role in PIH is the vasoconstrictor endothelin. In 1988, Yanagisawa and co-workers 37 characterized an endothelial-derived vasoconstrictor, a 21-amino-acid peptide subsequently called endothelin. Endothelin is derived from a 23-amino-acid peptide precursor preproendothelin that is cleaved after translation to form proendothelin. In the presence of a converting enzyme located within the endothelial cells, proendothelin or big endothelin is cleaved to produce the 21-amino-acid peptide endothelin. Endothelin receptor-binding sites have been identified throughout the body with the greatest number of receptors in the kidneys and lungs. 38 The vasoconstrictor effects of endothelin are mediated by endothelin A receptors on the vascular smooth muscle. In addition, evidence is accumulating that endothelin B receptors located on vascular smooth muscle also contribute to the vasoconstrictor effects of this peptide. 39 Endothelin B receptors located on endothelium are thought to release NO and prostacyclin. Endothelin reduces renal hemodynamic and sodium excretory function and plays an important role in mediating the altered pressure natriuresis and other hemodynamic changes in several models of hypertension including the deoxycorticosterone salt hypertensive rat and the Dahl salt-sensitive hypertensive rat. 39–41

Because endothelial damage is a known stimulus for endothelin synthesis, increases in the production of endothelin may participate in PIH. Plasma concentration of endothelin has been measured in a number of studies involving normal pregnant women and women with pregnancy-induced hypertension. 42–45 Most investigators have found higher plasma concentrations of endothelin of approximately two- to threefold in women with PIH. 42–45 Typically, plasma levels of endothelin are highest during the latter stage of the disease, suggesting that endothelin may not be involved in the initiation of PIH, but rather in the progression of disease into a malignant phase. 42–45 Although the elevation in plasma levels of endothelin are only two- or threefold above normal during PIH, we found that this level of plasma endothelin can have significant long-term effects on systemic hemodynamics and arterial pressure regulation. 46 , 47 We found that increasing the plasma levels of endothelin within the two- to threefold range for 2 to 3 h had no effect on arterial pressure, whereas increasing endothelin levels for 7 days resulted in significant reductions in renal hemodynamics, renal pressure natriuresis, and significant elevations in mean arterial pressure. 46 , 47 The increase in mean arterial pressure was also associated with significant reductions in cardiac output and renal plasma flow and elevations in total peripheral resistance. 46 , 47 Thus, long-term elevations in plasma levels of endothelin comparable to those measured in patients with PIH could play a role in mediating the reductions in renal function and elevations in arterial pressure observed in women with PIH.

Although some studies have reported no significant changes in circulating levels of endothelin during PIH, a role for endothelin as a paracrine or autocrine agent in PIH remains worthy of consideration. Many of the experimental and genetic rat models of hypertension are not associated with elevations in plasma endothelin. 39 Yet, elevations in endothelin synthesis have been reported in specific tissues including the kidney. 39 For example, investigators have reported enhanced expression of preproendothelin in vascular tissues from various organ systems, including the kidney. 38 , 39 Several studies have also reported an increase in local production of endothelin in women with PIH. 42–44 Whether increased synthesis of endothelin occurs within the kidney during PIH remains uncertain, as some investigators have found no differences between preeclamptic and normal pregnant women in urinary excretion of endothelin—a measure of local renal synthesis. 42–44

We recently examined the role of endothelin in mediating the hypertension in response to chronic reductions in uterine perfusion pressure in conscious, chronically instrumented pregnant rats. 48 Renal expression of preproendothelin was significantly elevated in both the medulla and in the cortex of the pregnant rats with chronic reductions in uterine perfusion pressure as compared to control pregnant rats. Chronic administration of the selective endothelin type A receptor antagonist (ABT-627, 5 mg/kg/day for 10 days) markedly attenuated the increase in mean arterial pressure observed in the pregnant rats with chronic reductions in uterine perfusion pressure (Fig. 4) . However, endothelin type A receptor blockade had no significant effect on BP in the normal pregnant animals. These findings suggest that endothelin plays a major role in mediating the hypertension produced by chronic reductions in uterine perfusion pressure in pregnant rats.

Mean arterial pressure in response to chronic reductions in uterine perfusion pressure (RUPP) in control pregnant rats and pregnant rats pretreated with an ET A receptor antagonist (+ET A ). All data are expressed as mean ± SEM.

Several lines of evidence suggest that changes in the prostaglandin system may play a role in mediating the renal dysfunction and increase in arterial pressure during PIH. Significant alterations in prostacyclin and thromboxane production occur in women with PIH. 49–52 Plasma and urine levels of thromboxane are elevated in women with PIH, whereas syntheses of prostaglandins, such as prostacyclin, are reduced. 49–52 Additional evidence for a potential role of thromboxane in PIH derives from a study by Woods. 53 She demonstrated that short-term increases in systemic arterial pressure produced by acute reductions in uterine perfusion in pregnant dogs can be prevented by thromboxane receptor antagonism. Further evidence of a potential role for thromboxane is supported by studies in humans, indicating that low dose aspirin attenuates the development of PIH in women at risk for the disease. 1–3

Although some studies suggest a potential role for thromboxane in PIH, the quantitative importance of this substance in mediating the long-term reduction in renal hemodynamics and elevation in arterial pressure produced by chronic reductions in uterine perfusion pressure in pregnant rats is still uncertain. Thromboxane is not only produced by platelets and macrophages, but also by multiple renal cells. 54 , 55 Furthermore, the receptor for thromboxane appears to be abundant within the vasculature of the kidney. 54 , 55 Finally, there is considerable evidence that thromboxane-induced constriction contributes to the renal vasoconstriction in several experimental models of hypertension, 54 , 55 Whether thromboxane mediates the renal hemodynamic and arterial pressure changes observed in the rat model of PIH is unknown. In preliminary experiments, however, we found that urinary excretion of thromboxane B 2 was higher in the hypertensive pregnant rats with chronic reductions in uterine perfusion pressure than normal pregnant rats at day 19 of gestation. 56

Is the renin-angiotensin system important in mediating the reduction in renal function and increase in arterial pressure during PIH?

The renin-angiotensin system plays an important role in the long-term regulation of renal function and arterial pressure during a variety of physiologic and pathophysiologic conditions. 57 During normal pregnancy, plasma renin concentration, renin activity, and angiotensin II (Ang II) levels are all elevated; however, the vascular responsiveness to Ang II appears to be reduced. 1–3 The importance of the renin-angiotensin in the regulation of renal function and arterial pressure during PIH is unclear. Although some studies have reported that reductions in uterine perfusion pressure enhances uteroplacental renin release, most animal studies have reported decreased or normal plasma renin activity and Ang II concentrations. 1–3 In addition, most investigators have observed that in established human preeclampsia, plasma renin activity and Ang II levels are usually low or normal. 1–3 Although circulating levels of Ang II may be normal during PIH, it is possible that reducing uteroplacental perfusion pressure could increase the renal sensitivity to Ang II through reductions in NO or prostacyclin synthesis or by enhanced formation of thromboxane. Consistent with this suggestion are studies indicating enhanced vascular responsiveness to Ang II in vessels from animals or humans with PIH. 1–3 Furthermore, previous studies from our laboratory and others have found that, unlike normal conditions, the preglomerular vessels of the renal circulation become extremely sensitive to the vasoconstrictor actions of Ang II when the renal synthesis of NO or prostacyclin is reduced or when thromboxane synthesis is elevated. 29 , 30 , 57 Increased vascular Ang II responsiveness during PIH, however, does not prove Ang II as an important endogenous mediator of the vasoconstriction or hypertension in experimental models of PIH, as increased responsiveness may only reflect low endogenous Ang II formation. Thus, the importance of increased Ang II to the control of renal function and BP during PIH is unclear. A previous study by Woods and Brooks, 58 however, indicates that Ang II may not be important in mediating the acute rise in arterial pressure during short-term reductions in uterine perfusion pressure in dogs. They demonstrated that the increase in arterial pressure in response to reduced uterine perfusion pressure was unaltered in animals whose renin-angiotensin system had been fixed by prior infusion of captopril plus Ang II infusion. Although the results from this acute study suggest that the renin-angiotensin system might not be involved in mediating increases in systemic arterial pressure during acute reductions in uteroplacental blood flow, the mechanisms causing hypertension under acute conditions may not necessarily be the same as those that contribute to the chronic hypertension induced by long-term reductions in uteroplacental perfusion pressure.

We recently determined the importance of Ang II in mediating the long-term reduction in renal hemodynamic and the hypertension produced by chronic reductions in uterine perfusion pressure in pregnant rats. 59 Chronic oral administration of a converting enzyme inhibitor (enalapril, 250 mg/L for 6 days) decreased mean arterial pressure to a similar extent in pregnant rats with reduced uterine perfusion pressure (RUPP) and normal pregnant rats. Blockade of the renin-angiotensin system (RAS), however, had no significant effect on the BP response to chronic reductions in uterine perfusion pressure as the differences in BP between the normal pregnant and RUPP rats were similar in control and converting enzyme inhibitor-treated groups. These findings suggest that the RAS does not play a major role in mediating the hypertension produced by chronic reductions in uterine perfusion pressure in pregnant rats. 59

Is maternal endothelial activation/dysfunction in preeclampsia due to enhanced cytokine production in response to placental ischemia?

Although reductions in blood flow to the uteroplacental unit are known to result in cardiovascular and renal abnormalities consistent with the pathophysiologic features of human PIH, the physiologic mechanisms linking placental ischemia with the abnormalities in the maternal circulation are unclear. 60 Several lines of evidence support the hypothesis that the ischemic placenta contributes to endothelial cell activation/dysfunction of the maternal circulation by enhancing the synthesis of cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1). 60 TNF-α and IL-1 are inflammatory cytokines that have been shown to induced structural as well as functional alterations in endothelial cells. 61 These inflammatory cytokines also enhance the formation of a number of endothelial cell substances such as endothelin and reduce acetylcholine-induced vasodilatation. 60–62 Also supporting a potential role of TNF-α in preeclampsia are findings that plasma levels of TNF-α are significantly elevated in women with preeclampsia by approximately twofold. 60 , 63 Furthermore, IL-6, which is activated by TNF-α, has also been reported to be elevated in preeclamptic women. 60 Although high levels of TNF-α, as observed during septic shock or after lipopolysaccharide administration, activate gene expression of inducible nitric oxide synthase, modest levels of TNF-α have been shown to destabilize the mRNA of endothelial nitric oxide synthase. 64

Whether chronic and modest increases in plasma TNF-α can activate the endothelium during pregnancy and lead to reduced kidney function, high BP, and other features of PIH is unknown. Consistent with a potential role of cytokine activation in PIH is the recent study by Faas and colleagues. 65 They reported that an intravenous infusion of a high dose of lipopolysaccharide (LPS) decreased BP in pregnant rats, whereas a very low dose infusion of the endotoxin resulted in significant and long-term increases in BP and urinary albumin excretion and significant platelet aggregation in conscious pregnant rats. Although LPS is known to activate TNF-α, it is unclear whether the effects of low dose LPS on cardiovascular and kidney function were mediated through TNF-α or IL-1, as these cytokines were not measured in that study.

Although plasma levels of TNF-α are elevated by two- to threefold in women with PIH, the importance of TNF-α in mediating the systemic and renal hemodynamic changes associated with this disease is unclear. To determine the long-term effects of a two- to threefold elevation in plasma TNF-α on renal and systemic hemodynamics in pregnant rats we recently infused TNF-α for 5 days at a rate of 50 ng/day during days 14 to 19 of gestation in pregnant rats. 66 Plasma levels doubled in the TNF-α-treated pregnant rats. Arterial pressure was significantly higher in the TNF-α-treated pregnant rat as compared to pregnant controls at day 19 of gestation. A twofold elevation in plasma TNF-α in pregnant rats also caused a significant reduction in renal hemodynamics. These data suggest that elevated plasma levels of TNF-α observed in preeclamptic women may play an important role in the pathogenesis of PIH.

Although these preliminary findings with TNF-α support the cytokine hypothesis, finding the link between placental ischemia and maternal endothelial and vascular abnormalities remains an important area of investigation. Microarray analysis of genes within the ischemic placenta of women with preeclampsia and in animal models of chronic reductions in uterine perfusion pressure should provide new insights into the link between placental ischemia and hypertension. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood.

Studies during the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of PIH. The initiating event in PIH has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles (Fig. 5) . Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to Ang II, and decreased formation of vasodilators such as NO and prostacyclin. These endothelial abnormalities, in turn, cause chronic hypertension by impairing renal pressure natriuresis and increasing total peripheral resistance. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during PIH is still unclear. Results from ongoing basic and clinical studies, however, should provide new and important information regarding the physiologic mechanisms responsible for the elevation in arterial pressure in women with preeclampsia. More effective strategies for the prevention of preeclampsia should be forthcoming once the underlying pathophysiologic mechanisms that are involved in PIH are completely understood.

Potential mechanism whereby chronic reductions in uteroplacental perfusion may lead to hypertension. ET = endothelin; TBX = thromboxane; PGI 2 = prostacyclin; NO = nitric oxide; ANG II = angiotensin II.

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• epoprostenol
• hypertension, pregnancy-induced
• nitric oxide
• pre-eclampsia
• hypertension
• hemodynamics
• excretory function
• angiotensin ii
• thromboxane
• vascular endothelium
• vasodilators
• endothelins
• endothelium
• maternal mortality
• arterial pressure
• perinatal period
• cytotrophoblast

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Complication of Pregnancy: Pregnancy Induced Hypertension (PIH)

Teaching plan, additional sources.

Pregnant women are prone to complications, which threaten their lives and that of the infants. Pregnancy-induced hypertension is one of the complications that pregnant women experience. To prevent or manage complications, parents usually attend childbirth classes.

The childbirth class, which was held at Sibley Memorial Hospital taught parents how to handle experiences that they undergo during the first, second, and third trimesters. Despite the fact that the instructor covered extensive topics, she did not cover the topic of pregnancy-induced hypertension. Hence, the teaching plan focused on signs and symptoms, the nature of the complication, risk factors, and applicable interventions.

On February 7, 2015, I attended a boot camp for childbirth class that was hosted at Sibley Memorial Hospital. The session of the childbirth class started at 9am and ended at 5pm. The instructor’s name was Rosemarie Antunes, a registered nurse with the experience of 30 years in obstetric, labor, and delivery nursing acquired from different hospitals in different states.

She obtained her licenses as a registered nurse (RN) from the Virginia Department of Health Professions in 2004 and State of Connecticut, Department of Public Health in 1980. She has also received professional certification from Prepared Childbirth Educators in 2006 and Certified Labor Doula in 2009. Rosemarie took her diploma education for RN at Saint Francis Hospital School in 1977-1980.

Currently, she works for Fauquier Health System, a family birthing center, since 2004. She also works for Labor and Delivery, Postpartum, and Normal Newborn as a certified childbirth educator with experience of 10 years in preparing expectant mothers and their partners for what is ahead of them. Rosemarie is a mother of six children with 10 grandchildren (R. Antunes, personal communication, February 7, 2015).

The instructor employed constructivism as a teaching philosophy because she aided the participants to understand experiences that they expect during pregnancy and delivery by using questions and demonstrations. To construct the foundation of teaching, the instructor told the participants to ask questions that they might have before she commences each session.

Moreover, the instructor informed the participants that she would stop at any time during presentation to allow them to ask questions. To enhance understanding among the participants, the instructor demonstrated her teachings using various methods. The teaching methods that the instructor employed in demonstrations are videos, PowerPoint presentation, handouts, dolls, and birth balls.

The childbirth class took place on February 7, 2015 at Sibley Memorial Hospital in one of their lecture halls from 9am to 5pm. The childbirth class comprised of Caucasian couples, African couples, and Asians couples. Interestingly, during their introduction, all of them indicated that they were expecting their babies in March 2015.

From the introduction, it became apparent that half of the couples were married while the remaining couples were just partners. The participants were young adults between the ages of 20 to 30 years, who were expecting their babies for the first time. The couples were ready for the childbirth lessons as they brought with them pillows, birth balls, and blankets.

The topics covered in childbirth class aimed at enhancing the understanding of pregnancy (3 rd trimester), labor, Christina Birth story, comfort techniques, medical procedures, cesarean birth, newborn procedures, postpartum, and labor rehabilitation. The instructor covered anatomy and physiology of pregnancy from first trimester to the third trimester, and hormonal proliferations that happen during pregnancy.

To improve their health, the instructor encouraged the pregnant women to eat food high in fiber, drink water at all times, and call HCP whenever they experience pain during urination. The instructor also covered signs of labor and expected medical emergencies such as induction and cesarean births, which are essential in saving babies and mothers.

She taught the participants how to employ exercise, relaxation, massage, and music in improving the birth of the newborn in a natural way. The instructor also mentioned postpartum and gave healthcare instructions for newborn, such as safety and breastfeeding techniques.

Pregnancy-Induced Hypertension (PIH)

Although the instructor extensively covered diverse areas of childbirth, I noted that she did not delve deep into complications of pregnancy, and thus, she should have examined the topic of pregnancy-induced hypertension (PIH).

Pregnant women are susceptible to PIH or gestational hypertension owing to changes in their bodies. Essentially, PIH has medical importance because it threatens the lives of the baby and the mother. Therefore, I will explore the topic of PIH with a view of equipping the participants with the appropriate knowledge that is critical in prevention, treatment, and management of the complication.

Summary of Teaching

The first objective of teaching pregnant women is to enable them to identify signs and symptoms of PIH. As PIH requires early detection for treatment and management interventions to be effective, pregnant women need to understand how to identify the signs and symptoms of PIH very early.

Excessive swelling of hands and feet, dizziness, excessive nausea, rapid heartbeat, severe headaches, drowsiness, fever, blurred vision, and pain in the abdomen are some of the signs and symptoms of PIH, which pregnant women need to watch so that they can seek early medical attention.

According to Jwa et al. (2013), early detection of PIH is critical for fetal and maternal health because it enhances the effectiveness of treatment and management interventions. As teaching methods, I will employ PowerPoint presentation, brochures, handouts, and discussion.

In teaching about PIH, the second objective is to enable the participating couples to understand the nature of PIH. Given that pregnant women experience diverse forms of hypertension, PIH is a unique form of hypertension because it only happens after the 20th week of pregnancy and can be either transient or chronic (Sajith et al., 2014).

When blood pressure of a pregnant woman is higher than 140/90 in two different occasions, and her urine contains no proteins, the differential diagnosis indicates PIH. As a teaching method, I will demonstrate diagnosis of PIH by measuring blood pressure of the pregnant women and undertaking urinalysis to determine the presence of proteins in urine.

The third objective is to enable the participating couples to understand risks of PIH. The common risk factors for PIH are women with the first-time pregnancy, increased maternal age, family history, multiple gestations, proteinuria, hypertension, and diabetes mellitus (Jwa et al., 2013).

Moreover, nutrition also has other risk factors for PIH because an increased consumption of vitamin E and mono- and poly-unsaturated fatty acids increases the risk for PIH, while an increased consumption of magnesium, potassium, and vitamin C reduces the risk for PIH (Kazemian et al., 2012).

Sleep disturbance is also a possible risk factor for PHI because it correlates with hypertension (Haney, Buysse, & Okun, 2011). To expose these findings, I will employ PowerPoint presentation, brochures, handouts, and discussion.

The fourth objective of teaching is to enhance understanding of available treatment and management interventions of PIH. When pregnant women know the nature of available interventions, they can discuss with their doctors and choose the best intervention that fits them, hence, promote therapeutic adherence.

Sajith et al. (2014) state that both mono- and combined therapies of antihypertensive drugs are used in the treatment and management of PIH because they are safe for mothers and infants. Kazemian et al., (2012) recommends the application of nutrition in the prevention, treatment, and management of PIH.

Moreover, Haney, Buysse, and Okun (2011) recommend that alleviation of sleep disturbance reduces blood pressure, and hence, prevents the occurrence of PIH. The methods of teaching will comprise the use of the PowerPoint presentation, brochures, handouts, and discussion.

Pregnancy-Induced Hypertension

What is pregnancy-induced hypertension.

Pregnancy-induced hypertension refers to the high blood pressure, which women experience when they are pregnant.

Why is it important for pregnant women?

Pregnancy-induced hypertension affects pregnant women because their body changes during pregnancy. If doctors do not detect and treat pregnancy-induced hypertension, the mother and the baby will die. Therefore, pregnant women need to understand this disease so that they can seek medical attention whenever they experience signs and symptoms and save themselves and the unborn babies.

Signs and Symptoms

The common signs and symptoms of pregnancy-induced hypertension are excessive swelling of hands and feet, severe morning sickness, dizziness, fast heartbeat, severe headaches, drowsiness, high temperature, poor vision, and pain in the abdomen.

Nature of Pregnancy-Induced Hypertension

Pregnancy-induced hypertension is different from other types of hypertensions because it affects women only, occurs after 20 weeks of pregnancy, and there are no proteins in the urine. However, when not treated, it progresses into a disease called preeclampsia, which causes urine to appear in urine.

Risk Factors

The risk factors for pregnancy-induced hypertension are first-time pregnancy, age of the mother, bloodline with this disease, proteins in urine, many pregnancies, diabetes, nutrition, high blood pressure, and sleep disturbance.

Treatment and Management Interventions

• Use medications that reduce high blood pressure (antihypertensive drugs).
• Control food intake by reducing the amount of oils while increasing the amount of potassium, magnesium, and vitamin C.
• Avoid disturbance during sleep and have peace of mind.

Haney, A., Buysse, D., & Okun, M. (2011). Sleep and pregnancy-induced hypertension: A possible target for intervention? Journal of Clinical Sleep Medicine, 9 (12), 1349-1356.

Jwa, S., Arata, N., Sakamoto, N., Watanabe, N., Aoki, H., Kurauchi-Mito, A., Dongmei, Q., Ohya, Y., Ichihara, A., & Kitagawa. (2011). Prediction of pregnancy-induced hypertension by shift of blood pressure class according to the JSH 2009 guidelines. Hypertension Research, 34 (1), 1203-1208.

Kazemian, E., Dorosti-Motiagh, A., Sotoudeh, G., Eshraghian, M., & Ansary, S. (2012). The nutritional status of women with gestational hypertension compared to normal pregnant women. Women’s Health Care, 1 (10), 1-6.

Sajith, M., Nimbargi, V., Modi, A., Sumariya, R., & Pawar, A. (2014). Incidence of pregnancy induced hypertension and prescription pattern of antihypertensive drugs in pregnancy. International Journal of Pharma Sciences and Research, 5 (4), 163-170.

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Preeclampsia and human reproduction. An essay of a long term reflection

Affiliation.

• 1 Neonatology, Center Hospitalier Sud-Reunion, BP 350, 97448 Saint-Pierre cedex, Reunion, France. [email protected]
• PMID: 12896815
• DOI: 10.1016/s0165-0378(03)00040-8

Hypertensive disorders of pregnancy (HDP: pregnancy-induced hypertension, preeclampsia, eclampsia) affect approximately 10% of human births. Women are at increased risk for HDP during their first conception; and/or when the conception is with a new partner (new paternity); when conception occurs very shortly after the beginning of their sexual relationship. A primary cause of preeclampsia is the defect of the normal human-specific deep endovascular invasion of trophoblast, which is a consequence of the nutritional demands of growth of the human fetal brain. The occurrence of preeclampsia represents a reproductive disadvantage unique to humans compared with other mammals. As such, it may have played a significant role in shaping human reproduction and, therefore, human sexuality. This deep implantation/preeclampsia phenomenon may explain many anthropological mysteries of human sexuality that do not exist in other mammalian species (and primates). These include: very low fertility rate, concealed ovulation, all year long 'apparent-waste-of-efficiency' sexuality, absence of sperm competition in human females at the time of conception, and the unexplained testicle size in human males compared with relevant primates. Further, this deep trophoblastic implantation (and its failure in preeclampsia) in humans might be a decisive condition of hominization between great apes and all the other Homo genuses. This frontier might even have occurred inside these Homo lineages: because of their relatively small brains, the first species of Homo might not have presented the deep trophoblastic invasion described in Homo sapiens.

• Adaptation, Physiological
• Blood Pressure
• Eclampsia / physiopathology*
• Embryo Implantation*
• Maternal-Fetal Exchange
• Pre-Eclampsia / physiopathology*
• Reproduction*
• Sexual Behavior
• Trophoblasts / physiology

Sample details

Hypertension

• Words: 1031

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• Cardiovascular disease
• Dengue fever
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Pregnancy Induced Hypertension

Pregnancy Induced Hypertension (PIH) and Pre eclampsia A. Discussion of disease/condition 1. Incidence Pregnancy Induced Hypertension (PIH) is a multi-organ disease process that develops as a result of pregnancy and regresses in the postpartum period. It usually develops after 20 weeks of gestation in a woman who had normal blood pressure. It is defined as an elevation of systolic and diastolic pressures equal to or above 140/90 mm Hg. In clinical practice, the terms PIH and pre eclampsia are used interchangeable, but in pre eclampsia the woman also has protein in her urine indicating that there is renal involvement as well.

The only know cure for pre eclampsia is delivery of the fetus. It is a relatively common problem of pregnancy and affects about 8% of all pregnancies. (Murray, p680) 2. Risk factors There are many factors that increase a woman’s risk. Those include women who are having their first baby, those under 17 years old, women who are obese, having diabetes mellitus, chronic hypertension, or pre-existing vascular disease and women with multi-fetal gestation. Also a woman is more likely to have pre eclampsia if the mother or sister has the disorder. (Murray, p681) 3.

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Etiology and Pathophysiology Pre eclampsia is due to generalized vasospasm. In natural pregnancy, vascular volume and cardiac output increase significantly, but despite these increases, blood pressure does not rise in normal pregnancy. This is because pregnant women resistance to the effects of vasoconstrictors such as angiotension. However, in pre eclampsia, peripheral vascular resistance increase because some women are sensitive to angiotension Vasospasm decrease the diameter of blood vessels which results in endothelia cell damage, impeded blood flow and elevated blood pressure.

As a result of this circulation to all body organs, including the kidneys, liver, brain and placenta, is decreased. This will cause many changes such as decreased venal perfusion, glomerular damage, impaired liver function, small cerebral haemorrhages, pulmonary oedema, and dyspnoea and decreased placental circulation. Decrease placental circulation can result in infarctions that increase the risk for abruptio placentae. Also when maternal blood flows hrough the placenta is decreased, the fetus is likely to experience intrauterine growth restriction and persistent fetal hypoxemia and acidosis (Murray, p679-681) 4. Signs and Symptoms Hypertension, generalized oedema and proteinuria are the three classic signs of pre eclampsia. The first sign is that a pregnant woman may notice is oedema and a rapid weight gain which are due to fluid retention. Hypertension is defined as sustained blood pressure equal to or above 140/90.

Blood pressure should be taken in the sitting position with the arm supported in a horizontal position at hear level. Proteinuria usually develops later than hypertension an oedema. The combination of proteinuria and hypertension indicates a worsening disease process. Additional signs include vascular constriction and narrowing of small arteries (e. g. when the retina is examines). Deep tendon reflexes may be very brisk (hyperreflexia) and clonus may be present. This may suggest cerebral irritability. Pre eclampsia is dangerous for the woman and fetus for 2 reasons.

The first reason it develops and progresses so rapidly and secondly the earliest manifestation are not noticed by the woman. Certain symptoms are not noticed by the woman. Certain symptoms include headache, drowsiness, or mental confusion indicate poor cerebral perfusion and may be precursors indicate arterial spasms and oedema in the retina. Numbness or tingling of the hands or feet also happens when nerves are compressed or “upset stomach” are particularly ominous because they indicate distension of the hepatic capsule and often warn that a seizure is imminent.

Decreased urinary output indicates poor perfusion of the kidneys and may precede acute renal failure. (Murray, p682-683). 5. Medical and Nursing Management The only cure for pre eclampsia is delivery of the baby. Home care is possible for many women if the condition is mild and in stable condition with a reassuring fetal status. She must be able to adhere to a prescribed treatment plan which may include bed rest and home blood pressure monitoring. Also, she has to visit the physician twice a week.

She must also do fetal surveillance such as daily kick counts. If the disease is severe that is when blood pressure is higher than 160/110 mmHg proteinuria is higher than 5 gm, and oliguria occurs (500ml or less in 24 hours), then the woman is hospitalized. If it is very severe, the baby is delivered, regardless of gestation, because of comprised placental circulation. Goals of management are to increase placental blood flow, fetal oxygenation and to prevent seizures and other maternal complications such as stroke so she is stabilized before delivery.

For bed rest, the woman is placed on her lateral position and her environment is kept quiet. External stimuli such as lights and noise that may precipitate antihypertensive drugs are used; the fetal rate must be closely monitored because a sudden drop in maternal blood pressure may precipitate fetal distress. Example of some drugs are Hydralazine (Apresoline), nifedipine (Procardia) or labetalol (Normodyne). The anticonvulsant medication given in the USA is magnesium sulphate (MgSo). It prevents seizures and precipitate seizures.

A paediatrician, neonatologist or neonatal nurse must be available to care for the newborn at birth. The next day, proper pre-natal care with attention to pattern weight gain and monitoring of blood pressure and urinary protein may lessen maternal and fetal morbidity and mortality by allowing early detection of the problem. (Murray, p685). When given MgSo, the nurse determines the woman’s respiratory rate hourly, level of consciousness and reflexes). Urine is checked for protein every four hours. She should assess the woman’s stress level and help her with ways to lessen it.

Signs that the woman is recovering from pre eclampsia include urinary output of 4-6 litre/day, decreased or no protein in urine and a return of normal blood pressure within 2 weeks. (Murray, p. 685) B How does your patient fit this textbook picture? My patient, LC, fit this textbook picture in many ways. Theses include this is her first baby, she is obese, have diabetes mellitus (on her 14th week of pregnancy). She also had protein in her urine on 10/09/03 and her BP was 145/90 and so she was diagnosed with PIH and told to stay on her bed rest at home. On 10/09/03, she was diagnosed with pre eclampsia.

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Despite equal hypertension awareness as white Americans, African Americans have a significantly higher hypertension prevalence and poorer control rates. Furthermore, the overall age-adjusted death rate related to hypertension in blacks is almost twice that than any other U.S. racial/ethnic subgroup [1,2]. Moreover, with the adoption of recent systolic/diastolic hypertension designation of greater than 130/80, the

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Mr. Jones, a 59-year-old African-American male, who has no history of alcohol use and who denies smoking cigarettes. On the weekends, he coaches a basketball team, Mr. Jones consumes high sodium food like hot dogs and nachos following basketball games. Mr. Jones is being monitored for HTN and previously reported a blood pressure of 168/92

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Preeclampsia: Recent Advances in Predicting, Preventing, and Managing the Maternal and Fetal Life-Threatening Condition

Kai-jung chang.

1 Department of Obstetrics and Gynecology, Taipei Tzu-Chi Hospital, The Buddhist Tzu-Chi Medical Foundation, Taipei 231, Taiwan

Kok-Min Seow

2 Department of Obstetrics and Gynecology, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111, Taiwan

3 Department of Obstetrics and Gynecology, National Yang-Ming Chiao-Tung University, Taipei 112, Taiwan

Kuo-Hu Chen

4 School of Medicine, Tzu-Chi University, Hualien 970, Taiwan

Associated Data

Not applicable.

Preeclampsia accounts for one of the most common documented gestational complications, with a prevalence of approximately 2 to 15% of all pregnancies. Defined as gestational hypertension after 20 weeks of pregnancy and coexisting proteinuria or generalized edema, and certain forms of organ damage, it is life-threatening for both the mother and the fetus, in terms of increasing the rate of mortality and morbidity. Preeclamptic pregnancies are strongly associated with significantly higher medical costs. The maternal costs are related to the extra utility of the healthcare system, more resources used during hospitalization, and likely more surgical spending due to an elevated rate of cesarean deliveries. The infant costs also contribute to a large percentage of the expenses as the babies are prone to preterm deliveries and relevant or causative adverse events. Preeclampsia imposes a considerable financial burden on our societies. It is important for healthcare providers and policy-makers to recognize this phenomenon and allocate enough economic budgets and medical and social resources accordingly. The true cellular and molecular mechanisms underlying preeclampsia remain largely unexplained, which is assumed to be a two-stage process of impaired uteroplacental perfusion with or without prior defective trophoblast invasion (stage 1), followed by general endothelial dysfunction and vascular inflammation that lead to systemic organ damages (stage 2). Risk factors for preeclampsia including race, advanced maternal age, obesity, nulliparity, multi-fetal pregnancy, and co-existing medical disorders, can serve as warnings or markers that call for enhanced surveillance of maternal and fetal well-being. Doppler ultrasonography and biomarkers including the mean arterial pressure (MAP), uterine artery pulsatility index (UtA-PI), and serum pregnancy-associated plasma protein A (PAPP-A) can be used for the prediction of preeclampsia. For women perceived as high-risk individuals for developing preeclampsia, the administration of low-dose aspirin on a daily basis since early pregnancy has proven to be the most effective way to prevent preeclampsia. For preeclamptic females, relevant information, counseling, and suggestions should be provided to facilitate timely intervention or specialty referral. In pregnancies complicated with preeclampsia, closer monitoring and antepartum surveillance including the Doppler ultrasound blood flow study, biophysical profile, non-stress test, and oxytocin challenge test can be arranged. If the results are unfavorable, early intervention and aggressive therapy should be considered. Affected females should have access to higher levels of obstetric units and neonatal institutes. Before, during, and after delivery, monitoring and preparation should be intensified for affected gravidas to avoid serious complications of preeclampsia. In severe cases, delivery of the fetus and the placenta is the ultimate solution to treat preeclampsia. The current review is a summary of recent advances regarding the knowledge of preeclampsia. However, the detailed etiology, pathophysiology, and effect of preeclampsia seem complicated, and further research to address the primary etiology and pathophysiology underlying the clinical manifestations and outcomes is warranted.

1. Introduction

Hypertensive disorder during pregnancy poses a substantial threat to both maternal and fetal health conditions [ 1 ]. Preeclampsia is one of the most well-known medical conditions that belong to this disease spectrum, which also accounts for one of the most common documented gestational complications, with a prevalence of approximately 2 to 15% of all pregnancies [ 2 , 3 ]. It is depicted as a gestational condition with a hypertensive disorder diagnosed after 20 weeks of gestation and coexisting proteinuria or generalized edema, and certain forms of hematologic disorders such as thrombocytopenia or signs of end organ damage including renal impairment, abnormal liver function, pulmonary edema, and cerebral and visual disturbance [ 4 , 5 ]. The definitions of gestational hypertension (pregnancy-induced hypertension) and preeclampsia are shown in Figure 1 . Serious or long-term complications may result when preeclampsia turns into a severe type or is left without being sufficiently treated. Multiorgan involvement may be seen in such cases, and the impairment of uteroplacental perfusion could potentially lead to gestational complications and poor fetal outcomes including intrauterine fetal growth restriction and preterm delivery. As the situation worsens, it may become life-threatening for both the mother and the fetus, in terms of increasing the rate of mortality and morbidity [ 5 ].

The definitions of gestational hypertension (pregnancy-induced hypertension) and preeclampsia.

One straightforward way to categorize preeclampsia is to subdivide it into early-onset and late-onset groups in accordance with the gestational age (GA). The cutoff point is usually set as GA 34 weeks or GA 37 weeks, and we can subcategorize preeclampsia into the early-onset (GA < 34 weeks), late-onset (GA ≥ 34 weeks), preterm (GA < 37 weeks), and term (GA ≥ 37weeks) subgroups ( Table 1 ). The diagnoses made at different timings during the pregnancy course may suggest different pathophysiologic and etiologic pathways [ 6 ].

Classification of preeclampsia according to gestational age.

Preeclampsia should be viewed as a disease spectrum in which different subtypes may vary greatly in disease mechanisms and clinical presentations. The status of a previously normotensive pregnant woman developing new onset of hypertension after GA 20 weeks is termed “gestational hypertension” or “pregnancy induced hypertension”. If aside from gestational hypertension, a patient is also noted with proteinuria, thrombocytopenia, impairment in renal or liver function, cerebral symptoms, visual symptoms, or pulmonary edema, then she meets the diagnostic criteria of preeclampsia ( Figure 1 ). In terms of severity, preeclampsia could be classified as “nonsevere” or “severe” types ( Table 2 ), with the latter group exhibiting clinical features including blood pressure exceeding 160/100 mmHg, headache, visual disturbances, upper abdominal pain, oliguria, elevated serum creatinine, thrombocytopenia (<100,000/µL), elevated level of liver enzymes, fetal growth restriction, pulmonary edema, onset at an early gestational age, and the presence of convulsion (eclampsia) [ 7 ].

Classification of preeclampsia according to severity.

Although the definite cause of preeclampsia remains unknown to date, several hypotheses have been made to explain its pathophysiology. One of the most commonly accepted theories is the two-stage model, which proposes that inadequate trophoblast invasion would lead to shallow placentation and subsequent poor uteroplacental perfusion (stage I), thus causing widespread endothelial dysfunction and systemic clinical manifestations (stage II) [ 8 ]. The window between the first and second stages provides an optimal opportunity for prediction during the subclinical phase [ 5 ]. Known as a safe and effective drug in the prevention of pregnancy-related vascular disorders including but not limited to preeclampsia, aspirin has been applied for preeclampsia prevention with a low dosage starting as early as before GA 16 weeks and until approximately GA 36 weeks [ 9 ]. Nevertheless, non-pregnant women throughout the world enjoy the privilege of early prevention and intervention. Even if they do, sometimes preeclampsia may still develop. The only definite solution for preeclampsia is the delivery or termination of pregnancy. When a diagnosis is made, antihypertensive medication is, however, one of the most important treatments before delivery. Fluid control, prevention, and treatment for end organ damage should be applied as well [ 10 ].

Due to the notable prevalence and influence of preeclampsia in pregnancy, an understanding of preeclampsia, as thorough as possible, is crucial. The review aimed to summarize existing studies in the literature to explore the epidemiology, etiology (risk factors), socioeconomic burdens, pathophysiologic mechanisms, prediction, prevention, and treatment of preeclampsia. The cutting-edge studies will be analyzed and integrated into this review to provide state-of-the-art knowledge.

2. Materials and Methods

Searching terms and strategies in the literature.

The literature was searched to identify basic and clinical studies, which investigated the epidemiology, etiology (risk factors), socioeconomic burdens, and underlying pathophysiological mechanisms of preeclampsia, along with its prediction, prevention, and treatment. Figure 2 illustrates the flowchart of database searching, screening, and inclusion of the references that we selected from the literature. In this review, all of the articles were retrieved from the databases Medline and PubMed using the search terms “preeclampsia”, “gestational hypertension”, and “pregnancy induced hypertension” for the research topic. For screening and selection in the next stage, only full-text articles were considered for inclusion in further analysis. In the second stage, the articles published before 1983 were excluded to ensure the novelty of the current review. Duplicated articles were also excluded. From a total of 152 articles identified in the screening process, 126 potential articles (1983–2022) met the criteria for inclusion.

Flowchart of database searching, screening, and inclusion of the references selected from the literature.

Hereafter, two experts in the field independently inspected the contents of articles including demographics, research designs, and outcomes, and identified eligible basic and clinical studies for inclusion. The solicited articles with poor research designs, questionable sampling methods, or mismatched outcomes would be excluded at this stage. The discrepancies between the experts were discussed via mutual communication to reach a consensus. All eligible studies were included in the review using the search terms and strategies (identification from the database, screening of the studies, selection of potential articles, and final inclusion). Finally, a total of 103 articles were collected for review from 152 articles identified in the initial search.

3. Epidemiology, Etiology (Risk Factors), and Economic Burden of Preeclampsia

3.1. epidemiology and risk factors.

Preeclampsia is a gestational disorder affecting women worldwide from different nations, ethnicities, age groups, etc. Overall, a prevalence rate of approximately 2 to 15% of pregnant women is documented, with an average prevalence rate of approximately 4.6% [ 2 , 3 , 11 ]. The pathophysiology of preeclampsia is complex and remains incompletely unveiled, which makes it sensible that its prevalence and traits would vary under different circumstances. In other words, different populations with preeclampsia may display different prevalence, patterns, or distribution of risk factors and pregnancy outcomes. The study of its epidemiology and risk factors could thereby demonstrate its complexity and heterogeneity. Table 3 presents a list of risk factors for preeclampsia.

A brief summary of risk factors for preeclampsia.

3.2. Race and Ethnicity

In a cross-sectional study conducted by Yang et al., a thorough comparison between the characteristics of preeclampsia among the Chinese and Swedish populations was made. The study included a total of 634,689 pregnancies, among which the Chinese and the Swedish exhibited similar prevalence rates of approximately 2 to 3%. However, there were marked variabilities in the other descriptive results. The maternal age, mean body mass index (BMI), and obesity rates were higher in Sweden, while more nulliparous women and cesarean deliveries were identified in their Chinese counterparts. The disease extent and pregnancy outcomes also differed. Mild preeclampsia was more common in the Swedish population, while there were more severe cases in China. The Chinese also had overall higher rates of stillbirth, preterm birth, and low birth weight. Ethnicity, lifestyle, metabolic perturbations, genetic factors, and seeking medical help may all contribute to these variabilities [ 11 ]. While race is a potential contributory factor, it may not be completely persuasive in this scenario since the Swedish comprised relatively richer ethnicities whereas the Chinese were primarily Hans.

The role of race in preeclampsia has been investigated in various studies. A review article written by Zhang et al. pointed out that African Americans had a higher rate and severity of preeclampsia, which was likely related to, if not directly resulting from, multifactorial causes including previous history of preeclampsia, system lupus erythematosus, sickle cell anemia, gestational diabetes mellitus, and a history of chronic hypertension [ 12 ]. Another study conducted by Ghosh et al. suggested that non-Hispanic women had higher odds of developing preeclampsia and had greater severity of disease, compared with Hispanic women and Asian/Pacific Islanders. An expert review written by Johnson also mentioned a higher risk of preeclampsia among Black, Native American, and Native Alaskan races. Nevertheless, it is worth noting that research focusing on the role of race or ethnicity in the disparities of preeclampsia shares some common limitations. Firstly, race or ethnicity is not a scientifically biological or genetic trait; rather, it is more often self-reported and thus may become subjective. Secondly, a person could belong to more than one racial or ethnic group instead of being assigned to one single category. Thirdly, a standardized method of classification used in medical research may fail to reflect the cultural, lingual, or historical origins and distributions in reality. Instead of serving as a direct or independent factor, the role that race or ethnicity plays in preeclampsia may correspond to the reflection or marker for the influence of cultural, socioeconomic, or healthcare resources, etc. [ 13 ].

Many real-world statistics suggest that advanced or extremely young maternal age is an important risk factor for preeclampsia. Furthermore, these mothers at risk may also face more adverse maternal and neonatal outcomes and hence should raise special concerns throughout their pregnancy courses.

A cohort study that included preeclamptic individuals from 1998–2014 in the U.S. suggested that women at extreme ages (<25 years or >45 years) tended to develop severe morbidities. Women younger than 25 years of age had a significantly higher rate of developing eclampsia. On the other hand, women more than 45 years old were more likely to suffer from acute heart failure and acute kidney injury (acute renal failure). The results suggested that both extremely young and elderly mothers were exposed to a greater threat during gestation but possibly from different perspectives [ 14 ].

Some studies focused mainly on the advanced maternal age (AMA) groups. A registry-based study in Finland suggested that women older than 35 years exhibited more preeclampsia, early and late preterm deliveries, cesarean deliveries, and poorer neonatal outcomes [ 15 ]. In a retrospective cross-sectional study in Indonesia conducted in 2016-2017, preeclamptic women over 35 years of age developed more severe complications in general, with postpartum hemorrhage in particular, while no significant increase in the developments of HELLP syndrome, visual disturbances, pulmonary edema, or eclampsia was identified. Regarding neonatal outcomes, there were more preterm deliveries (GA < 37 weeks), intrauterine growth restrictions, neonatal asphyxia, and neonatal infections in the group of advanced-age women [ 16 ].

3.4. Parity

Nulliparity has long been classified as a risk factor, as it may triple the risk for preeclampsia [ 17 ]. Some studies have concluded that nulliparous women were found with a higher percentage of preeclampsia compared to other cohorts [ 18 ]. Many hypotheses attribute this to immunological reasons. A feasible explanation is that a suboptimal maternal adaptation to fetal or paternal alloantigens may indirectly result in impaired uteroplacental perfusion, which accounts for the pathogenesis of preeclampsia [ 19 ]. Nulliparous women were also proposed to endure an “angiogenic imbalance”, manifested as a higher circulating sFlt1 level and sFlt1/PIGF ratio, which may also contribute to their tendency of developing preeclampsia [ 20 ]. From a fundamental viewpoint, meanwhile, there may be little difference between nulliparous and multiparous women regarding other risk factors including AMA, diabetes mellitus, multifetal gestations, etc. [ 21 ].

3.5. Obesity

Obesity is an alarming issue in the modern world and has proven to confer many hazards to human health. With time, it has raised concerns in both developed and developing countries. As one of the leading attributable risk factors, the mechanism of how obesity could potentially lead to preeclampsia has been studied. Obesity is known to be associated with systemic inflammatory reactions, insulin resistance, and oxidative stress. The pathways through which obesity could result in hypertensive disorder include increased oxidative stress, increased sympathetic tone, and increased expression of angiotensinogen [ 22 ]. Insulin resistance, on the other hand, is linked to reduced cytotrophoblast migration and consequent placental ischemia [ 23 ].

For pregnant women, maternal obesity, maternal overweight, and even a BMI increase within the normal range may indicate an increased risk of maternal and fetal morbidities, including preeclampsia. Accordingly, obese or overweight pregnant women should be advised to lose weight through diet control, a moderate amount of physical activity, and lifestyle modification.

3.6. Other Maternal Conditions

One of the most important risk factors for preeclampsia is a history of preeclampsia in a previous pregnancy. Women with preeclampsia in their first pregnancies have a notably higher risk of developing it again in their second pregnancies. Many cohort studies have demonstrated this phenomenon. [ref. Risk factors for pre-eclampsia at antenatal booking: systematic review of controlled studies]. Aside from her own medical history, a woman’s family history of preeclampsia should warrant special concerns as well, as a positive family history is also a powerful indicator of preeclampsia at all stages of the pregnancy course [ 24 , 25 ].

Multifetal gestation is associated with a three- to four-fold increased risk for preeclampsia. This may be more related to the gestation itself because multifetal gestation imposes a greater burden on the cardiovascular system. Individuals with multifetal gestations are frequently excluded from general studies, as they are often viewed as a special population. For these women who are diagnosed with preeclampsia, it may be confusing whether some of the adverse outcomes such as preterm deliveries are related to preeclampsia or multifetal gestation per se. Nevertheless, the fact that women with multifetal gestations are more prone to preeclampsia and serious complications should raise more attention, and allow an opportunity for screening, prevention, or early intervention [ 26 ].

Preeclamptic patients with pre-pregnancy chronic hypertension are classified to have “superimposed preeclampsia”. Chronic hypertension accounts for approximately 4% of pregnancies and is often associated with adverse gestational outcomes such as preeclampsia, preterm delivery, intrauterine fetal growth restriction, and placenta abruption. Approximately 20% of these patients eventually develop preeclampsia and tend to do so even earlier than the normotensive population. Poorer pregnancy outcomes are observed concurrently [ 27 ].

Both pre-existing type I and type II diabetes mellitus have been shown to possess a higher risk of preeclampsia. Statistically, 10–20% of diabetic women develop preeclampsia during pregnancy, which is a significantly higher percentage compared to their non-diabetic counterparts. On the other hand, gestational diabetes mellitus (GDM) is also considered to be an independent risk factor for preeclampsia by some researchers, while more investigations are required to determine whether GDM and preeclampsia share a common etiologic pathway [ 28 ].

While preeclamptic patients have an increased long-term risk of developing an end-stage renal disease, the renal disease itself may also serve as a risk factor for preeclampsia. To be more specific, microalbuminuria, diabetic nephropathy, and chronic kidney disease may predispose to preeclampsia [ 29 ]. This may be related to impaired glycocalyx integrity and alterations in the complement and renin-angiotensin-aldosterone systems [ 30 ].

Other than the aforementioned risk factors, mostly involving but not limited to pre-pregnancy health conditions, there are numerous other risk factors that could be mentioned. Aside from pre-existing hypertension, diabetes mellitus, and renal disease, particular medical conditions including autoimmune disease, periodontal disease, and antidepressant exposure have all been proven to play a part in this “disease of theories”. [ 31 , 32 , 33 ].

3.7. Socioeconomic Burden

Preeclampsia is one of the top causes of adverse maternal and fetal outcomes globally, and hence a short-term special medical care program is often required to take care of preeclamptic patients. This makes it not only a health-related issue but also a socioeconomic one, as greater manpower or resource consumption and extra spending in the healthcare system would be inevitable. Yet, few studies have aimed to make estimates of the potentially enormous socioeconomic burden related to preeclampsia. Relevant studies have made limited conclusions to date.

Jing Hao et al. conducted a retrospective study to investigate the economic burden of preeclampsia using data from the United States. Three cohorts were defined in this study: Women who had uncomplicated pregnancies until term, women with hypertension but not preeclampsia, and women diagnosed with preeclampsia. The maternal and infant costs were estimated from GA 20 weeks until 6 weeks postpartum for the former and 12 months post-delivery for the latter. The mean care cost of the preeclamptic group was $41,790 USD, which was significantly higher than the uncomplicated group ($13,187 USD) and the group with hypertension but without preeclampsia ($24,182 USD). The cost difference was largely dependent on the infant costs [ 34 ].

Another retrospective study focused on a similar issue in the United States was conducted by Warren et al. The maternal costs were estimated from 6 months before birth and 12 months afterward, while the infant costs were calculated until 12 months of age. The results suggested an estimated increased cost of $6583 USD per birth in the maternal model. On the other hand, the increased cost of the infant model was substantially influenced by the gestational age at birth. Costs devoted to the infant accounted for 26% of total healthcare costs at term delivery, and a tremendously increased percentage of 91% with deliveries at GA < 28 weeks. As a result of preeclampsia and preterm deliveries, these high costs were more closely related to adverse fetal or infant outcomes, including intraventricular hemorrhage, bronchopulmonary dysplasia, periventricular leukomalacia, and infant death [ 35 ].

An Irish study using data from the SCOPE (Screening for Pregnancy End Points) study disclosed a doubling average cost (5243 EUR) in preeclampsia-complicated pregnancies. The study included data from the initial antepartum visit until 12 months postpartum and drew the conclusion that these costs were primarily related to postpartum care, followed by antepartum and peripartum care, respectively. The increased medical costs were related to more and higher-level health services including antepartum examinations, more maternal hospitalization spending, longer infantile NICU stays, etc. [ 36 ].

Despite the lack of abundant research, present economic studies on preeclampsia in different parts of the world seem to have reached the consensus that preeclamptic pregnancies are strongly associated with significantly higher medical costs for both the mother and her baby. The maternal costs are related to the extra utility of the healthcare system, more resources used during hospitalization, and likely more surgical spending due to an elevated rate of cesarean deliveries. The infant costs also contribute to a large percentage of the expenses as the babies are prone to preterm deliveries and relevant or causative adverse events. Although studies cannot reflect the accurate amount of preeclampsia-related healthcare costs in reality, there is no doubt that preeclampsia imposes a considerable financial burden on our societies. It is important for healthcare providers and policy-makers to recognize this phenomenon and allocate enough economic budgets, medical, and social resources accordingly.

4. Pathophysiology of Preeclampsia

4.1. brief summary.

Preeclampsia has been termed a “disease of theories” by some as numerous studies have aimed to propose different concepts to explore its complex etiology and pathophysiology. Previous findings have suggested that the triggers of preeclampsia include placental factors and other predisposing maternal factors. The mechanisms of early- and late-onset preeclampsia may not be completely the same. Based on the current understanding of preeclampsia, the revised “two-stage model” has become one of the most widely accepted theories regarding its formation.

The classical two-stage model was first described in 1991, innovatively introducing the idea that preeclampsia should be viewed as a trophoblastic disease rather than merely a hypertensive disorder. In this model, the first stage of preeclampsia is described as the “placental stage”, in which deficient remodeling of spiral arteries results in impaired placental perfusion and placental ischemia. As the disease progresses with time and clinical maternal syndrome develops, it reaches the second stage [ 37 ]. The clinical manifestations of preeclampsia will be further discussed in the next section.

Ever since the initial proposal of the two-stage theory, ongoing research has expanded and refined our knowledge of the development of preeclampsia. Stage 1 is focused on the revised idea of impaired uteroplacental perfusion with or without poor placentation and subsequent spiral artery insufficiency. Stage 2 surrounds the concept that general endothelial dysfunction and vascular inflammation would lead to a systemic clinical response. Figure 3 displays the contributing factors and the two-stage models of preeclampsia.

Contributing factors and the two-stage models of preeclampsia.

4.2. Stage 1

In the current revised model, stage 1 is initiated when reduced placental perfusion develops. Poor placentation and the resultant deficient spiral artery remodeling in the intervillous space is one of the causes for this phase but may not be the sole mechanism. In addition to the impairment of placental perfusion, maternal factors are essential so as to result in the development of systemic maternal pathophysiological changes [ 37 ]. Stage 1 usually occurs in the first trimester, at the period of time when the deep invasion of the extravillous trophoblast (EVT) takes place. The migration of EVT cells into the decidua leads to the remodeling of maternal spiral arteries, which is a key element to uteroplacental perfusion and fetal blood supply. The process may initiate as early as before GA 8 weeks, while the establishment of uteroplacental circulation is completed at approximately GA 12 weeks. Hence, it is believed that stage 1 takes place before GA 12 to 20 weeks [ 38 ].

The differentiation and invasion of EVTs are regulated by various factors including cytokines, growth factors, chemokines, cell adhesion molecules, placental oxygen tension, extracellular matrix (ECM)-degrading enzymes, and membrane-bound cell surface peptidases. These factors are either directly or indirectly related to the differentiation and decidual invasion of EVT cells and may serve as markers for the first stage of preeclampsia formation [ 38 ]. When defective trophoblast invasion and insufficient transformation of the maternal uterine vasculature emerge, decreased maternal uterine blood flow follows, which may be detected and quantified by uterine artery Doppler studies. Persistent high vessel resistance in early pregnancy may suggest that the aforementioned phenomenon has occurred. Existing studies have demonstrated that the placental endothelial cells in women with high-resistance uterine arteries are more sensitive to TNFα and thus are more susceptible to cell injury and apoptosis.

In the normal process of trophoblast invasion, the resistance of uterine artery blood flow decreases, and the uterine artery blood flow increases in the term. The placenta is typically developed in the first trimester. If a relatively hypoxic environment is noted, the latter placental tissues may exhibit an altered balance of antioxidant enzyme activity. However, the histopathology findings of the placenta are nonspecific and not limited to preeclamptic pregnancies. These changes to the placenta can also be induced by other microscopic insults or toxins [ 39 ].

4.3. Stage 2

Stage 2 features the scenario where impaired uteroplacental perfusion interacts with other various maternal constitutional factors. Pathophysiological changes in the liver, kidney, and cardiovascular system are compatible with the concept of insufficient blood supply. Systemic endothelial dysfunction and injury are possible explanations for the maternal clinical manifestations and have been proven to be present in preeclamptic women.

One important issue that attracts interest is how the first stage links to or leads to the second stage. The clinical value of discovering the answer lies in the fact that it may shed light on a way to “prevent” the formation of preeclampsia, which will be further discussed in the article. One proposal suggests that microparticle particles produced during syncytiotrophoblast apoptosis may directly or indirectly result in endothelial dysfunction. An increased amount and concentration of inflammatory cells and substances have been found in women with preeclampsia, and they could potentially alter the systemic endothelial function. The renin-angiotensin system may also play a role in the process. In addition, some recent findings have suggested that vascular endothelial growth factor (VEGF) and placental growth factor (sFlt-1) could be involved in the linkage as well. Moreover, oxidative stress accumulated during the process may provide another possible explanation [ 40 ]. Table 4 lists the possible pathways and explanations of mechanisms underlying preeclampsia.

Possible pathways and explanations of mechanisms underlying preeclampsia.

Various factors contribute to the regulation of artery compliance during pregnancy. A failure of maternal vascular adaptation can cause hypertensive disorders such as preeclampsia. Some circulating cytokines and growth factors at abnormal levels may inhibit normal calcium signaling events, thereby damaging cell-to-cell contacts of the endothelium and leading to endothelial dysfunction. Important markers include endothelin-1 (ET-1), interleukin-8 (IL-8), ELAM, and the endothelial leukocyte adhesion molecule-1 [ 41 ]. There is also sound evidence of decreased production or bioavailability of nitric oxide (NO)—a stimulant of smooth muscle relaxation—in preeclamptic pregnancies [ 42 ]. Other potential influential vasodilators include prostacyclin (PGI2) and the endothelium-derived hyperpolarizing factor (EDHF) [ 41 ].

As mentioned above, the dysregulation of the renin-angiotensin system (RAS) may participate in the pathogenesis of preeclampsia. In 2007, Florian Herse et al. published a study that included preeclamptic and non-preeclamptic women who had undergone cesarean deliveries. Genetic characteristics and histopathological results of the maternal and placental tissues of the participants were investigated. A 4-fold increase in the angiotensin II type 1 (AT1) receptor in the decidua was found in preeclamptic pregnancies. Increases in corresponding gene and protein expression were also confirmed by RT-PCR and immunohistochemistry studies. Circulating agonistic autoantibodies (AAs) targeting the AT1 receptor have been described previously, with the ability to cross the placenta and enter fetal circulation. AT1-AAs could induce calcium signaling and initiate events that would later lead to preeclampsia [ 43 ]. Roxanna A. Irani et al. published a study with similar findings in 2010. Animal experiments showed that pregnant mice with AT1-AA injections developed preeclamptic features and also had increased levels of antiangiogenic factors such as soluble fms-like tyrosine kinase 1 (sFlt-1) and endoglin. Additionally, AT1-AA might be associated with increased TNF-α, indirectly causing damage to the endothelium and end organs [ 44 ].

Oxidative stress describes the imbalance between the formation of oxidative reactive species (ROS) and the antioxidant capacity of the body [ 45 ]. A causal role of oxidative stress in hypertension has been demonstrated in previous research, with multiple possible pathogenic pathways including the alteration of NO bioavailability or signaling. A reduction of oxidative stress has been observed in hypertensive cases who received antihypertensive treatment [ 46 ]. Oxidative stress in the healthy placenta may be important for its organogenesis, but excess levels in the impaired placenta would lead to increased circulating placenta debris, damaging the maternal endothelial cells in the term. As a major source of ROS production, the mitochondria have been found to be swollen in the trophoblasts of preeclamptic animal models, which plays a crucial role in cell apoptosis. Altogether, any errors in the maintenance of the oxygen pressure may bring about placental diseases and maternal complications, such as preeclampsia [ 46 ].

4.4. Limitations of the Placenta Model

Even though the two-stage theory is the mainstream explanation of the origin of preeclampsia, some argue that further evaluation is needed to determine the causative relation between trophoblast development and spiral artery transformation. For instance, previous case reports have pointed out similar findings of the uterine artery Doppler waveforms in extra-uterine pregnancies, suggesting that the resistance of uterine artery blood flow may not accurately reflect the consequences of trophoblast invasion [ 47 ].

Some have suggested that the result of Doppler studies may be a reflection of systemic vascular resistance changes but not on the uterine artery itself. The argument is based on the paradox that a “de-transformation” of spiral arteries does not occur when the vascular resistance of the uterine artery is noted in the third trimester [ 48 ]. In the meantime, while it is fairly certain that impaired uteroplacental perfusion is associated with subsequent endothelial dysfunction, almost all the supporting evidence of different hypotheses of its linkage raises some challenges. To date, it is believed that many potential mechanisms underlie preeclampsia, and the disease is caused by complicated interactions between maternal and environmental factors, and potentially more than that. The incomplete understanding of its pathogenesis continues to provoke further research.

5. Systemic Manifestations of Preeclampsia

Preeclampsia is a systemic disorder that may present with various symptoms and signs. The manifestation of preeclampsia is widely perceived to be centered around hypertension and proteinuria, but clinical presentations could be variable in essence. Different organs and systems could all be influenced by preeclampsia. Systemic manifestations of preeclampsia are shown in Figure 4 .

Systemic manifestations of preeclampsia.

According to the two-stage theory, preeclampsia proceeds into the clinical stage once the systemic vascular response and inflammation have taken place as a result of endothelial dysfunction. This aptly explains why preeclampsia is a global syndrome as the endothelium is distributed all over the body. The most famous affected organs and systems include the central nervous system, cardiovascular system, liver, and kidney.

5.1. Central Nervous System (CNS)

The brain is a vital organ that requires approximately 20% of available oxygen to maintain normal function. In most physiological conditions, cerebral blood flow (CBF) has sufficient capability to autoregulate and remains rather stable to cope with its high metabolic demand. However, once brain injury to a certain extent occurs, sequelae including acute severe hypertension, the loss of myogenic tone of the vascular smooth muscle, and uncontrolled vasoconstriction may lead to the failure of autoregulation. As they key to the delicate homeostasis of the brain environment, both hypoperfusion and hyperperfusion may break the balance and bring great harm. Insufficient CBF could lead to ischemic brain injury and ischemic stroke. Hyperperfusion, on the other hand, may disrupt the blood–brain barrier (BBB) and cause edema formation, which is one of the classic findings in preeclamptic and eclamptic patients [ 49 , 50 ].

CBF could be assessed in patients with preeclampsia via transcranial Doppler imaging. The middle cerebral artery is often chosen to be the target of examinations. Perhaps somewhat surprisingly, the cerebral flow index (CFI) appears to be normal in most women with preeclampsia. However, cerebral perfusion pressure (CPP) exhibits greater elevation in preeclamptic women and may serve as the key to brain injury among these women [ 51 ]. Brain damage has been demonstrated in autopsies and image studies [ 52 ]. It has been proven in some studies that elevated CPP corresponds to hypertension, and antihypertensive treatment that decreases CPP lowers the rate of cerebral complications in these patients [ 53 ].

CNS manifestations that are suggestive of severe disease status are headaches, visual disturbances, changes in consciousness, and seizures. The spectrum is coined “preeclamptic encephalopathy” [ 53 ]. Once a seizure takes place, the impression of eclampsia is almost certain after the exclusion of other previously known neurological conditions that may also lead to convulsion events. Eclampsia is one of the most serious forms of preeclampsia and is highly related to obstetric morbidities and mortalities. Management for eclampsia is similar to those for any form of severe preeclampsia, and most patients recover well without neurological sequelae [ 54 ].

Another frequent neurological finding is posterior reversible encephalopathy syndrome (PRES). PRES is a result of hypoxia and vasogenic edema of the brain that is often related to acute uncontrolled hypertension or systemic endothelial dysfunction. The syndrome progresses in a rather rapid manner but also resolves rapidly with a good prognosis once the trigger is withdrawn [ 55 ]. PRES is high among pregnant women with severe preeclampsia or eclampsia, and usually indicates a better prognosis than PRES in non-pregnant women or is associated with other causes [ 56 ].

Stroke—or a cerebrovascular accident—refers to a brain attack when impairment of part of the CBF or a burst in a brain blood vessel occurs. Strongly related to hypertensive disorders, cerebrovascular events are yet another complication that is significantly linked to preeclampsia. Although uncommon in pregnancy, it shares similar disease pathways and risk factors with strokes that take place in non-pregnant patients, and thus is indicative of an increased long-term risk for stroke events [ 57 ].

5.2. Cardiovascular Systems

Preeclampsia has been classified as one independent gender-specific risk factor for cardiovascular events by the American Heart Association (AHA). Studies have proven that women with gestational hypertensive disorders carry a 2- to 4-fold risk for cardiovascular diseases [ 58 ]. In fact, preeclampsia and cardiovascular diseases share many predisposing factors such as elevated blood pressure and increased BMI. The disease spectrum includes coronary heart disease, heart failure, and cardiovascular disease death, and the influences may be life-long [ 59 ].

The long-term cardiovascular sequelae not only affect the mother but have also proven to bring hazards to her children at the same time. Although the establishment of a dependency relationship is difficult, many studies have shown an increased rate of congenital heart disease and future cardiovascular morbidities for offspring. Some scholars believe, however, that the influences of cardiovascular risks on offspring are limited to term infants or cases with early preeclampsia [ 60 ].

The complex multifactorial nature of preeclampsia and cardiovascular diseases makes it hard to make a straightforward ascription of the latter to the former. There is also a lack of a standardized protocol for cardiovascular prevention. Nevertheless, medical staff and preeclamptic patients should keep in mind the importance of continuous screening and early intervention of cardiovascular diseases. Monitoring of the body weight, blood pressure, lipid level, and lifestyle should be performed every five years until the age of 50 when women would qualify for most other international regular cardiovascular risk assessment guidelines [ 61 ].

Preeclampsia-related liver disease is frequently seen in the third trimester. Liver involvement is rare but indicative of severe disease extent. The most notorious example is H(Hemolysis)EL(Elevated Liver Enzymes)LP(Low Platelet Count) syndrome, which is a variant of severe preeclampsia. According to the diagnostic criteria of Tennessee Classification and Mississippi Classification, an elevated liver enzyme is usually defined by an elevated AST or ALT ≥ 70 U/L, although blood tests often reveal a level ≥ 500 U/L. Thrombotic microangiopathy serves as one of the possible explanations, while periportal hemorrhage and necrosis have been observed in histopathology studies. As rare as it may be, the condition could lead to hepatic rupture [ 62 ]. Women treated with corticosteroids exhibit overall improved laboratory results including liver function tests. Administration after delivery helps to avoid a rebound and further complications. Nevertheless, the natural course of HELLP could not be altered by corticosteroids [ 63 ].

Other liver diseases associated with preeclampsia include acute fatty liver of pregnancy (AFLP), hepatic infarction, and rupture. In cases of AFLP, laboratory abnormalities include elevated liver enzymes, prolonged prothrombin time and partial thromboplastin time, and increased bilirubin levels. Other typical clinical symptoms comprise central nervous system involvements such as headache and consciousness disturbances, jaundice, and gastrointestinal symptoms including anorexia, abdominal discomfort, nausea, and vomiting. If the expression of long-chain 3-hydroxyacyl-CoA dehydrogenase is not evident, the prognosis is usually good [ 64 ].

Hepatic complications in pregnancy are rare but could be fatal. They are more likely to be found in preeclamptic or eclamptic cases and indicate severe disease status. Hence, prompt termination of pregnancy or delivery is often indicated. Liver transplantation may be considered in patients with a grave prognosis [ 63 ].

5.4. Kidney

The imbalance of the renin-angiotensin aldosterone system (RAAS) along with the imbalance between proangiogenic and anti-angiogenic factors may explain the relationship between preeclampsia and renal impairment. Similar to cardiovascular risks, preeclampsia shares common predisposing factors with renal risks and confers a higher risk of chronic kidney diseases later in life [ 65 ].

The activation of RAAS is normal during pregnancy, which results in a volume increase. However, excessive activation possibly related to sFlt-1 and AT1-AAs—as may be seen in preeclamptic subjects—could lead to preeclampsia or preeclampsia-like syndrome. Once the delicate balance is disrupted, hypertension and renal involvements may be seen [ 66 ]. Thrombotic microangiopathies in renal cells have been observed in histopathology studies, suggesting glomerular injury in preeclamptic patients [ 67 ].

When acute kidney injury occurs, an abrupt increase in serum creatinine and a decrease in urine output could be detected. However, both the glomerular filtration rate and serum creatinine level are not perfectly reliable markers during pregnancy, as physiological changes allow an increase in the former and a reduction in the latter. The diagnosis may rely on other clinical manifestations such as oliguria, proteinuria, and edema, and is thereby delayed in some cases [ 68 ].

The condition may be life threatening, but also tends to regress rapidly in the postpartum period. Nonetheless, it still warrants concern for screening for later renal diseases. There is a significant association between preeclampsia—the early-onset subgroup in particular—and future chronic kidney diseases, hypertensive diseases, and glomerular or proteinuric diseases. For preeclamptic women, a 10- to 12-fold increase in end-stage renal disease has been proposed in existing statistical analyses. Hence, further screening for kidney diseases years after pregnancy should be implemented [ 69 ].

5.5. Other Targets

Preeclampsia is a global disorder that may present with symptoms and pathologic findings all over the body. Aside from the vital organs, for example, the hematologic system is another commonly affected target. In a study conducted by Neelam Jhajharia et al., lower hemoglobin and platelets were found in these patients, while higher WBC and hematocrit were observed [ 70 ]. Similar findings could also be found in other studies [ 71 , 72 ]. Some parameters may vary from study to study, but a trend of decreased hemoglobin and platelet levels is almost always observed in data analyses. Marked thrombocytopenia signifies a severe disease form, as manifested in HELLP syndrome.

Gastrointestinal involvements are common in preeclamptic patients. Symptoms of nausea and vomiting are frequently experienced by them, and some women complain of indigestion. The more devastating complications include hepatic involvement as described earlier, and pancreatic involvement, namely referring to the increased risk of pancreatitis and necrosis of the pancreas [ 73 ].

Another classic clinical manifestation of preeclampsia is edema. It is worth noting that edema is not essential to the diagnosis of preeclampsia and is often observed in normal pregnancies as a result of the increase in body fluids. General swelling due to water and salt retention is especially prominent in preeclampsia due to elevated blood pressure and endothelial injury causing extravasation from the vessels. As rare as it may be, one of the most severe presentations of fluid overload is pulmonary edema, which has been reported in cases of severe preeclampsia [ 74 ].

6. Prediction and Prevention of Preeclampsia

The potential consequences of preeclampsia pose great threat and harm to mothers and their children, the medical system, and society worldwide. To prevent adverse outcomes, various strategies have been invented and studied, including diet control, exercise, and medication. Among them, the administration of low-dose aspirin has been proven to be one of the most effective ways to prevent the development and progression of preeclampsia.

In order to apply preventive methods in a cost-effective manner, a precise prediction model and timing would be required. According to the two-stage theory of its pathophysiology, the first stage of preeclampsia typically takes place in the first trimester, when inadequate trophoblast invasion leads to abnormal placentation and subsequent uteroplacental insufficiency. During this process, the patient is usually in her subclinical phase, which allows a window for screening and prevention.

6.1. Prediction Models

Apparently, a good prediction tool would provide many benefits to the early prevention and intervention of preeclampsia. Different professional organizations have thus far proposed their own prediction models based on the currently acknowledged risk factors.

An expert review written by Piya Chaemsaithong et al. made a detailed comparison between some of the most widely accepted prediction models ( Table 5 ). Risk factors such as a history of preeclampsia in previous pregnancies, chronic hypertension, autoimmune diseases, renal diseases, diabetes mellitus, and multifetal gestation are included in almost all the prediction models and are primarily considered to be “high” risk factors if the models made a segmentation between “high” risk and “moderate” risk factors. Other risk factors that are taken into consideration include nulliparity, advanced maternal age, maternal obesity, and family history, among others. Some are classified as “moderate” risk factors. A previous medical record and chronic hypertension are considered to be the two most important contributory risk factors [ 5 ].

A comparison between different prediction models of preeclampsia.

Most prediction models have either low detection rates or high false-positive rates, however, and are insufficient for precise prediction. An alternative is to use the Bayes theorem and take the individual maternal history and characteristics into consideration. This competing model allows a more patient-specific and dynamic approach and is used by the Fetal Medicine Foundation (FMF) and is the only one that has undergone extensive internal and external validations. In addition to the checklist for risk factors, other maternal factors including the mean arterial pressure (MAP), uterine artery pulsatility index (UtA-PI), and serum pregnancy-associated plasma protein A (PAPP-A) are also taken into account [ 5 , 75 ]. The best timing of preeclampsia risk screening is around GA 11 to 13 weeks. As soon as the result is revealed, early prevention could be initiated if a high risk for preeclampsia is suspected [ 76 ].

A systematic review examined the performance of soluble fms-like tyrosine kinase-1 (sFlt-1), the placental growth factor (PlGF), and the sFlt-1/PlGF ratio in predicting adverse outcomes in women with preeclampsia. The literature search identified 33 eligible studies (n = 9426). Due to significant heterogeneity between studies, few studies (n = 4–8) were included in the final meta-analysis component. Nonetheless, both PlGF and the sFlt-1/PlGF ratio demonstrated areas ROC values between 0.68 and 0.87 for the prediction of composite adverse maternal and perinatal outcomes, preterm birth, and fetal growth restriction. Conclusively, PlGF and the sFlt-1/PlGF ratio show prognostic promise for adverse outcomes in preeclampsia, but study heterogeneity limits their clinical utility [ 77 ].

Currently, prediction models for gestational hypertension and preeclampsia have been developed with data and assumptions from developed countries. A review aimed to identify and assess the methodological quality of prediction models for gestational hypertension and pre-eclampsia with reference to their application in low-resource settings. The review retrieved 40 eligible articles and revealed 77% of all the prediction models’ combined biomarkers with maternal clinical characteristics. The biomarkers used as predictors in most models were PAPP-A and PlGF. Only five studies were conducted in low- and middle-income countries. Therefore, the review concluded that prediction models using maternal characteristics, with good discrimination and calibration, should be externally validated for use in low- and middle-income countries where biomarker assays are not routinely available [ 78 ].

6.2. Possible Preventative Measures

An article written by Sammya Bezerra Maia and Holanda Moura et al. offered a perspective on the potential preventative measures by classifying them as primary, secondary, or tertiary preventions. Primary prevention is unlikely to be successful since the concept is centered around the avoidance of pregnancy in high-risk populations and lifestyle modification in the whole population in order to decrease the incidence of preeclampsia. Secondary prevention focuses on the interruption of the pathogenic process before its development and is the main target of investigations. Tertiary prevention does not aim to prevent preeclampsia itself, but rather prevent its further complications. Aside from the aforementioned section on aspirin prevention, lifestyle management, nutritional supplementation, and antenatal surveillance may aid primary and secondary prevention. Accordingly, rest, exercise, diet modification such as a low-salt diet, and antioxidant use have all been suggested. Unfortunately, none of them have been proven to be effective [ 79 ]. In contrast, another systematic review solicited 28 RCTs studying the effects of various factors such as anticoagulants (heparin, enoxaparin, dalteparin, and nadroparin), aspirin, paravastatin, nitric oxide, yoga, micronutrients such as L-arginine, folic acid, vitamin E and C, phytonutrients, lycopene, and vitamin D alone or in combination with calcium. The results of this review showed that low-molecular-weight heparin, enoxaparin, yoga, L-arginine, folic acid, and vitamin D prevented preeclampsia alone or combined with calcium [ 80 ].

6.3. Low-Dose Aspirin

In fact, for women perceived as high-risk individuals for developing preeclampsia, the administration of low-dose aspirin on a daily basis since early pregnancy has proven to be the most effective way to prevent preeclampsia.

Aspirin is one of the oldest medications still in use to date. It is widely applied as an antithrombotic drug due to its effect on platelet inactivation. The mechanism of platelet inactivation relies on COX-1 inhibition, which blocks TXA2 synthesis. It is usually administered in a low dose (75–81 mg/day), which is sufficient for TXA2 but not PGI2 inhibition. The application of aspirin is primarily related to secondary prevention for cardiovascular diseases, while its use in primary prevention remains somewhat controversial. Another common use of aspirin is anticoagulant treatment in neurological diseases such as transient ischemic attack (TIA) or stroke. A recent history or increased risk for gastrointestinal bleeding, intracerebral bleeding, and other adverse events is worth noting, and aspirin should only be administered when the benefits outweigh the risks—primarily related to the increased bleeding tendency [ 76 ].

Ever since the first publication of a case report suggesting the role of aspirin in preeclampsia prevention in 1978, numerous studies have aimed to quantify the effects of aspirin on preventing preeclampsia but without a consensus owing to the heterogeneity of the study groups. Meanwhile, meta-analyses have suggested prophylactic aspirin use, which is best started before GA 16 weeks and ahead of the completion of placentation. Later, the ASPRE trial confirmed the effect of aspirin on early-onset preeclampsia. With good compliance, aspirin prophylaxis could reach 76–90% effect size [ 79 ].

A meta-analysis including a total of 18,907 participants in eight trials reported that the administration of aspirin was associated with a reduction in the risk of preterm preeclampsia (relative risk: 0.62; 95% confidence interval: 0.45–0.87), but there was no significant effect on term preeclampsia (relative risk: 0.92; 95% confidence interval: 0.70–1.21). The reduction in preterm preeclampsia was confined to the subgroup in which aspirin was initiated at ≤16 weeks of gestation and at a daily dose of ≥100 mg (relative risk: 0.33; 95% confidence interval: 0.19–0.57). Thus, aspirin can reduce the risk of preterm preeclampsia rather than term preeclampsia, and only when it is initiated at ≤16 weeks of gestation and at a daily dose of ≥100 mg [ 81 ].

Many organizations have proposed their own guidelines regarding the dosage and timing of aspirin use. Table 6 presents the current recommendations for the administration of low-dose aspirin in women at risk of future preeclampsia. While some differences exist, most agree on a daily dosage between 60 and 150 mg per day, and some have a precise dosage of 81 mg per day for low-dose aspirin tablets in the U.S. Administration is recommended late in the first trimester and could be initiated as early as GA 12 weeks and before GA 16 weeks. Low-dose aspirin is usually prescribed until the late preterm period. Bleeding disorders are uncommon, while some women might experience a certain degree of gastrointestinal discomfort [ 79 , 82 ].

Recommendations for administration of low-dose aspirin in women at risk of future preeclampsia.

Low-dose aspirin use for preeclampsia prevention has been proven to be cost-effective and safe in pregnancy. Therefore, when the prediction model suggests a high risk of preeclampsia or when a mother carries some risk factors, low-dose aspirin should be initiated if no contraindications are identified.

7. Management of Preeclampsia

Table 7 is a summary of the current management practices of preeclampsia.

A summary of current management practices of preeclampsia.

7.1. Antihypertensive Treatment

Elevated blood pressure is essential to the diagnosis of preeclampsia and is associated with increased cardiac, vascular, and neurological risks. Therefore, antihypertensive medication should be administered for the control of blood pressure.

Some studies divide gestational hypertension into “severe” and “non-severe” groups, typically setting 160 mmHg as the cutoff point for systemic blood pressure (SBP). While the choice of antihypertensive regimen may be designed in an individualized manner, most clinicians agree with the initiation of antihypertensive therapy when the SBP exceeds 140 or 160 mmHg or when the diastolic blood pressure (DBP) reaches above 100 mmHg. The treatment target also differs between different guidelines; some set no specific treatment target, while some target an SBP below 110 mmHg or a DBP less than 80 to 90 mmHg [ 83 ].

The majority of common antihypertensive medications are contraindicated during pregnancy, so the choice of drugs is rather limited. Currently, almost all the approved medications belong to class C, including labetalol, hydralazine, nifedipine, methyldopa (class B), diazoxide, and the relatively contraindicated nitroprusside. The former three are used more frequently even though the FDA has not approved the usage of nifedipine in hypertension management [ 83 ].

7.1.1. Labetalol

Labetalol could be administered in the intravenous or oral form, while the intravenous form is more often used in hypertensive emergencies or grave conditions. It is a combined alpha- and beta-adrenoceptor-blocking agent with more potency on the beta receptor. It is widely used as an antihypertensive agent and has the advantage of exerting a minimal effect on heart rate and cardiac output. Side effects and adverse events are primarily related to the influence on the RAAS and respiratory system. Therefore, other alternatives should be contemplated for patients with asthma [ 84 ].

When given in preeclamptic pregnancies, labetalol also decreases proteinuria and perinatal deaths. No other antihypertensive medications have proven to produce similar effects [ 85 ]. In non-severe cases, the oral dosage of 200 to 1200 mg per day can be divided into two to three doses, depending on the individual condition [ 83 ]. On the other hand, an intravenous bolus of 20 mg labetalol is indicated in severe cases and could be followed by a double dose in ten minutes [ 86 ].

7.1.2. Hydralazine

Hydralazine is another popular medication of choice, which also comes in intravenous and oral forms similar to labetalol. It lowers blood pressure by acting as a direct arteriole vasodilator. Headache, flushing, chest discomfort, and gastrointestinal upset have been reported with hydralazine use. It is also known to be associated with drug-induced lupus syndrome [ 87 ]. However, drug toxicity is uncommon. The drug is fairly safe except for contraindication in women with coronary artery disease since the increased cardiac output and oxygen demand may be hazardous [ 87 ]. Its effects have been proven, but it may be less efficacious than other antihypertensive drugs such as labetalol and nifedipine and is perceived by some as a second-line choice instead of a first-line option [ 85 ]. In regular oral use for blood pressure control, the recommended regimen is to start with 10 mg four times per day with gradual adjustment. The maintenance dosage could be as much as 50 mg four times per day and still has room for titration as long as it does not exceed the daily maximum dosage of 300 mg [ 87 ].

7.1.3. Nifedipine

Nifedipine is a safe and effective oral drug for lowering blood pressure in preeclamptic patients. The advantages include its relatively low cost and wider accessibility [ 88 ]. This medication functions as a calcium channel blocker with a rapid vasodilating effect but is associated with few adverse events and a low risk of hypotension [ 89 ]. Headache, flushing, and palpitations are the most frequent complaints encountered [ 90 ]. Its simultaneous relaxing effect on the myometrium also makes it a tocolytic drug commonly used to avoid preterm delivery [ 90 ]. It is usually initiated with a 10 mg dose and could be repeated later [ 86 ].

7.2. Magnesium Sulfate

Magnesium sulfate is used extensively for the prevention of seizures in preeclampsia and recurrent seizures in eclampsia for a lengthy period of time. Compared to placebo and other anticonvulsants such as phenytoin and diazepam, magnesium sulfate has proven to be more effective with fewer side effects. Although the mechanism is not fully understood, several possible explanations have been proposed [ 91 ].

Since the twentieth century, the action of magnesium sulfate used in preeclampsia has been studied. It is less likely related to antihypertensive effects as eclampsia does not necessarily take place in a hypertensive condition. Instead, magnesium sulfate may function as a calcium antagonist and inhibit acetylcholine-calcium-dependent release. While calcium may induce vasospasm and activate smooth muscle constriction, magnesium works in the opposite fashion. Since cerebral vasospasm is a common finding in preeclamptic seizures, this may serve as a plausible explanation to justify the use of magnesium sulfate. Another hypothesis suggests magnesium functions as a blocker of NMDA receptors, and thus prevents calcium influx [ 92 , 93 ].

In women with severe preeclampsia or eclampsia, magnesium could be given with an initial loading dose via the intravenous or intramuscular route, followed by a maintenance infusion. To reach the therapeutic serum concentration of 3.5 to 7 mEq/L (4.2 to 8.4 mg/dL), the recommended loading dose is 6 g intramuscularly, 2 to 4 g intravenously with a rate of 1 g/min, or a combination of both. Different guidelines and studies may suggest a slight modification. Some minor side effects such as a warm sensation, flushing, nausea, and vomiting may be encountered within the therapeutic window. However, serious adverse events may occur if marked hypermagnesemia is noted. The loss of the normal patellar reflex may be seen when the serum concentration of magnesium reaches 8 to 10 mEq/L, and more devastating respiratory depression could result when the serum concentration of magnesium reaches or exceeds 13 mEq/L. Therefore, persistent monitoring of the neurological performance such as the presence of the patellar reflex, respiratory pattern, and urine output should be implemented to avoid magnesium toxicity and severe adverse events. If a dosing error or toxicity is noted, calcium gluconate could be administered as an antidote [ 94 ].

Overall, magnesium sulfate use in pregnant women is still considered to be safe as long as close surveillance is performed. Its effects on seizure prevention have been assuring, and associated morbidity and mortality rates are low.

7.3. Delivery and Termination of Pregnancy

Preeclampsia is a pregnancy-specific condition, which would require delivery or termination of pregnancy under certain circumstances. A dilemma between expectant management and delivery is sometimes faced, especially when the patient has not reached term pregnancy. Hence, the timing of delivery in preeclamptic patients has raised keen discussions.

Lucy C Chappell et al. conducted a randomized clinical trial on late-preterm preeclamptic patients to survey this issue. A total of 901 gravidas with preeclampsia from GA 34 weeks to less than GA 37 weeks were included and randomly allocated to expectant management or planned delivery evenly. Planned delivery was initiated within 48 h of randomization to allow corticosteroid use if needed, and labor induction was prioritized unless an indication for cesarean delivery existed. The maternal outcomes included severe hypertension, deficits, impairments of different organs, placenta abruption, and maternal death. The perinatal outcomes were a composite of NICU stays, neonatal deaths, and further neurological developments. The statistical findings suggested a significantly lower rate of maternal morbidities and mortalities but more adverse perinatal outcomes in the planned delivery group. The higher rate of adverse perinatal outcomes, however, was primarily related to NICU admissions due to preterm birth, and other neonatal outcomes were similar to those in the expectant group otherwise. The total maternal and neonatal medical costs were lower in the planned delivery group. Collectively, the results suggested planned delivery in women with late-preterm preeclampsia, but the risk of increased NICU admission, although not associated with further morbidities, should be informed and discussed with the patient [ 95 ].

A systematic review in 2017 solicited six articles regarding preterm preeclampsia and the timing of delivery. The subjects of discussion included both early-preterm and late-preterm women. The statistics suggested postponing delivery until GA 37 weeks for better fetal outcomes, and no severe maternal complications or fetal distress existed. However, delivery should be considered even with early preterm patients once severe maternal complications or impaired fetal well-being was noted. It is important to note that suggested delivery is not equivalent to an emergency delivery and should still allow a 24-h interval for preparation (e.g., corticosteroid use to promote fetal lung maturity) since an immediate delivery is often associated with greater risks. On the other hand, women who chose expectant management should receive close monitoring and medication if needed. For example, magnesium sulfate could be used to reduce the risk of eclampsia, and more recently, has been suggested as a neuroprotective medication for the fetus before GA 32 weeks in particular [ 96 ].

According to the most updated ACOG guidelines in 2018, the choice between expectant management and prompt delivery should be made based on gestational age, maternal condition, and fetal well-being. Those with reassuring antenatal testing, no signs of preterm labor, and no severe disease features make good candidates for expectant management until GA 37 weeks. There are no benefits to delaying delivery afterward. Conversely, those with potentially severe features and a worrisome fetal condition should be advised for immediate delivery. For patients with severe preeclampsia, early delivery indicates a trade-off between fetal benefits and maternal risks, and a thorough discussion between the medical team and the patient should be performed. Delivery should be considered at any time when the maternal or fetal condition deteriorates or becomes unstable regardless of the gestational age. A complete course of corticosteroid administration is not always necessary, especially when the woman has reached late preterm (GA ≥ 34 weeks) [ 97 ].

7.4. Fluid Management

Fluid management is important in women with preeclampsia because they are more prone to fluid overload, which could lead to pulmonary edema. However, research on an ideal fluid strategy has been limited to date. Present data fail to suggest an optimal regimen, in turn provoking future research [ 98 ]. Nevertheless, intravenous medication with fluids is almost inevitable for hospitalized patients and should therefore be administered with caution. For instance, some clinicians have recently suggested avoiding intravenous fluid preloads before epidural or spinal anesthesia [ 98 ].

7.5. Diet Management

Fl Diet and nutrient intake may impact the risks of preeclampsia, and some studies have aimed to seek the best policy for diet management. In 2022, BMJ published a review based on data from 2000 to 2021 regarding the effects of dietary factors, nutritional supplements, and maternal weight on preeclampsia. Some of the findings may be contradictory to public belief; for instance, a low-salt diet to prevent hypertension and antioxidant (e.g., Vit. C and E) supplements to relieve oxidative stress seem to be plausible ways to prevent preeclampsia, but the review fails to show enough evidence in reality. However, it is important to note that a low amount or lack of evidence does not imply that they are not helpful and should not be recommended. In fact, the dietary factors that have proven to reduce the risk of preeclampsia include maternal weight control, high fiber intake, probiotics use, calcium and vitamin D supplements, multivitamin and multimineral supplements, and the avoidance of a high-salt diet and raw food [ 99 ].

A cohort study conducted by Anum S. Minhas et al. suggested that a self-reported Mediterranean-style diet is associated with lower preeclampsia risks. A Mediterranean-style diet is rich in vegetables, fruits, and healthy fats, of which the coherence could be assessed with a food-frequency questionnaire, in which individuals answer the questions by recalling their eating habits regarding meat, seafood, vegetables, beans, fruits, oil, wine, sweetened beverages, and commercially baked foods. It has been previously proven to lower cardiovascular risks in the non-pregnant population, and this study further suggested that greater adherence is associated with >20% lower odds of developing preeclampsia in the pregnant population compared to women with less adherence [ 100 ].

7.6. Exercise

Many clinical and animal studies have identified significant or non-significant effects of exercise during pregnancy on the reduction of gestational hypertensive disorders including preeclampsia.

There are a few possible explanations in so for the results observed. To begin with, maternal exercise creates a transient hypoxic environment, which in turn promotes the compensatory proliferation of the trophoblastic, endothelial, and stromal cells of the placenta, and consequently leads to improved placentation. Secondly, exercise stimulates antioxidant pathways and increases the number of mitochondria, relieving much of the oxidative stress that is linked to preeclampsia. Thirdly, exercise has an anti-inflammatory effect, which allows the body to maintain a healthy immune reaction, thus reducing the abnormal immune response to the fetus that is witnessed in preeclamptic patients [ 101 ].

A review study in 2017 suggested that aerobic exercise is beneficial in pregnancy and should be encouraged. Whether or not aerobic exercise could reduce preeclampsia remained controversial in some studies, but overall, the review concluded that 30 to 60 min aerobic exercise two to seven times per week during pregnancy reduced the incidence of gestational hypertensive disorders and the rate of cesarean deliveries [ 102 ]. However, this may not be the perfect regimen for every pregnant woman. The pre-pregnancy physical activity levels and maternal condition should always be taken into consideration for physicians to offer the best advice on the frequency, intensity, type, and time of exercise [ 103 ].

7.7. Long-Term Follow Up

Last but not least, preeclampsia is a syndrome that develops before delivery, yet also demands extra healthcare in the long run. Long-term follow-up for potential complications is indicated since sequelae of the cardiovascular system, liver, and kidney could take place. Close surveillance for years is suggested, which requires alertness from a good medical team and good medical compliance from the patient herself.

8. Discussion

The true cellular and molecular mechanisms underlying preeclampsia remain largely unexplained, which are assumed to be a two-stage process of impaired uteroplacental perfusion with or without prior defective trophoblast invasion (stage 1), followed by general endothelial dysfunction and vascular inflammation that lead to systemic organ damages (stage 2). Although the causes of preeclampsia are multi-factorial and cannot be described in a simple way, the aforementioned theories may provide a reasonable explanation for the results observed in past studies. Nevertheless, the detailed etiology, pathophysiology, and effect of preeclampsia seem complicated and remain to be clarified.

As mentioned above, overweight including pre-pregnancy obesity and excessive weight gain during pregnancy predisposes women to the progression of preeclampsia. As a state of chronic inflammation, overweight will increase the risk of preeclampsia by means of activating macrophages, NK cells, and peripheral helper T cells within the placenta to produce inflammatory cytokines such as IL-6, IL-7, and TNF-α. Established on these findings and reasons, avoiding excessive weight gain before and during pregnancy, rather than merely using overweight as a predictor, may be the best strategy to prevent the occurrence of preeclampsia. Therefore, proper weight control for pregnant females can not only decrease the physical burden on the body but also reduce the risk of preeclampsia.

Well-recognized risk factors for preeclampsia include race, advanced maternal age, obesity, nulliparity, multi-fetal pregnancy, and co-existing medical disorders. These factors can serve as warnings or markers to label pregnant women who need enhanced surveillance of maternal and fetal well-being. For at-risk females, appropriate information, counseling, and suggestions should be provided to facilitate a timely intervention or specialty referral. For pregnancies complicated with preeclampsia, closer monitoring and antepartum surveillance including a Doppler ultrasound blood flow study, biophysical profile, non-stress test, and oxytocin challenge test can be arranged. If the results are unfavorable, early intervention and aggressive therapy should be considered. Moreover, affected females should have access to higher levels of obstetric units and neonatal institutes. Before, during, and after delivery, monitoring and preparation should be intensified for affected gravidas to avoid serious complications of preeclampsia. In response to the potential physiological effect and psychological impact, consultation and discussion are usually beneficial for females diagnosed with preeclampsia. For severe cases, delivery of the fetus and placenta is the ultimate solution to treat preeclampsia. However, the determination of the appropriate timing for delivery depends on the severity of maternal preeclampsia and the maturity of the fetus.

It remains not fully understood with regard to the molecular level and pathologic mechanism of preeclampsia and its associated treatment. More studies are still required to investigate the role of anticoagulant therapy (such as aspirin, as described above) in preeclampsia. To minimize the heterogeneity of research in the future, the standardization of several critical factors in preeclampsia and the related treatment should be carefully considered. Two of the important factors are the timing and intensity of screening and intervention, which have a remarkable impact on the therapeutic effects. Furthermore, the severity and outcome in the individuals diagnosed with preeclampsia need standardization. Moreover, a larger sample size is also required to draw a reliable conclusion and to improve the reproducibility of the study result.

9. Conclusions

Preeclampsia accounts for one of the most common documented gestational complications, with a prevalence of approximately 2 to 15% of all pregnancies. It is life-threatening for both the mother and the fetus, in turn, increasing the rate of mortality and morbidity.

Preeclamptic pregnancies are strongly associated with significantly higher medical costs. The maternal costs are related to the extra utility of the healthcare system, more resources used during hospitalization, and likely more surgical spending due to an elevated rate of cesarean deliveries. The infant costs also contribute to a large percentage of the expenses as the babies are prone to preterm deliveries and relevant or causative adverse events. Preeclampsia imposes a considerable financial burden on our societies. It is important for healthcare providers and policy-makers to recognize this phenomenon and allocate enough economic budgets and medical and social resources accordingly.

The true cellular and molecular mechanisms underlying preeclampsia remain largely unexplained, which are assumed to be a two-stage process of impaired uteroplacental perfusion with or without prior defective trophoblast invasion (stage 1), followed by general endothelial dysfunction and vascular inflammation that lead to systemic organ damages (stage 2).

Risk factors for preeclampsia, including race, advanced maternal age, obesity, nulliparity, multi-fetal pregnancy, and co-existing medical disorders, can serve as warnings or markers that call for enhanced surveillance of maternal and fetal well-being. Doppler ultrasonography and biomarkers including the mean arterial pressure (MAP), uterine artery pulsatility index (UtA-PI), and serum pregnancy-associated plasma protein A (PAPP-A) can be used for the prediction of preeclampsia. For women perceived as high-risk individuals for developing preeclampsia, the administration of low-dose aspirin on a daily basis since early pregnancy has proven to be the most effective way to prevent preeclampsia. For preeclamptic females, relevant information, counseling, and suggestions should be provided to facilitate timely intervention or specialty referral. In pregnancies complicated with preeclampsia, closer monitoring and antepartum surveillance including a Doppler ultrasound blood flow study, biophysical profile, non-stress test, and oxytocin challenge test can be arranged. If the results are unfavorable, early intervention and aggressive therapy should be considered. Affected females should have access to higher levels of obstetric units and neonatal institutes. Before, during, and after delivery, monitoring and preparation should be intensified for affected gravidas to avoid serious complications of preeclampsia. In severe cases, delivery of the fetus and placenta is the ultimate solution to treat preeclampsia.

Although the aforementioned theories may provide a reasonable explanation for the results observed in the past studies, the detailed etiology, pathophysiology, and effect of preeclampsia seem complicated, and further research to address the primary etiology and pathophysiology underlying the clinical manifestations and outcomes is warranted.

Funding Statement

This review and APC were funded by a grant from Taipei Tzu-Chi Hospital, Taiwan (TCRD-TPE-111-10) for K.-H.C. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in writing the manuscript, or in deciding to publish the results.

Author Contributions

K.-J.C., K.-M.S. and K.-H.C. conceived the review and designed the search methods for the literature; K.-J.C. and K.-H.C. collected the data in the literature; K.-J.C., K.-M.S. and K.-H.C. performed data analyses; K.-J.C. and K.-H.C. wrote the review. All authors have read and agreed to the published version of the manuscript.

Institutional Review Board Statement

Informed consent statement, data availability statement, conflicts of interest.

The authors declare no conflict of interest.

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Pregnancy Induced Hypertension Essay Example

• Pages: 6 (1487 words)
• Published: August 6, 2018
• Type: Research Paper

As of a day prior, the patient's medical history indicated no serious concerns. But during her standard prenatal appointment at Klinik Kesihatan Jalan Raja Abdullah, unusually elevated blood pressure was detected. Before this occurrence, her blood pressure measurements had consistently been within the normal spectrum. Despite this, the most recent check-up revealed a steady rise in blood pressure levels to 170/100 mmHg. The patient denies having any past episodes of primary hypertension and there are no instances of hypertension documented in her familial lineage.

Further inquiries revealed that the woman had experienced a headache without any other immediate symptoms of potential eclampsia such as blurred vision, nausea, upper belly pain or passing out preceding her admission. She mentioned that she first suffered from a headache during her most recent antena

tal consultation where they detected high blood pressure in her system. In relation to her latest pregnancy history, suspicion arose when she did not have her menstruation for a month. A urine test (UPT) at a private clinic confirmed the pregnancy and there were no initial ultrasound scans conducted at this stage.

She experienced early pregnancy symptoms such as nausea, vomiting, and headaches up until the 20th week. Her medical registration was completed at Klinik Kesihatan Jalan Raja Abdullah in her 13th gestational week, during which she underwent blood and urine tests. The recorded blood pressure was 112/70 mmHg. She has an O positive blood type and a non-reactive VDRL test result. Her urine test results were also normal. She made it a point to attend all scheduled prenatal appointments without any complications. During these visits, the measurements of symphyseal-fundal height consistentl

aligned with the expected values.

During her regular medical examinations, she consistently exhibited normal blood pressure levels. Unexpectedly, a surge was observed in her most recent visit. The movements of the fetus commenced at 20/52 weeks into the pregnancy and have been progressively amplifying in both frequency and power. Considering her past obstetric track record, she tied the knot in 2011 when she was just 21 years old and is currently experiencing her maiden pregnancy. Discussing her earlier gynaecological history, she began menstruating at the age of 13 with cycles regularly lasting between five to six days every four to five weeks interval. Her heaviest menstrual flow occurs on day two but without any symptoms of menorrhagia or dysmenorrhea. She has not encountered inter-menstrual bleeding or bleeding after intercourse.

The patient has not previously used any form of birth control and lacks past pap smear results. A comprehensive check-up did not uncover any considerable health issues, with no signs such as headache, nausea, vomiting or vision disturbances that might be associated with hypertensive heart disease present. This is the initial hospital admission for the patient. Their medical history does not document instances of conditions like asthma, primary hypertension, diabetes mellitus or cardiac diseases. Moreover, they have never undergone any surgical operations before. It's reported that all their siblings are in good health condition.

In her family, there's no record of twins or inborn disorders. Both her parents are alive and enjoy good health. As for her personal and social background, she lives with her student husband in Taman Jalan Abdullah. She herself is a student too and affirms not to smoke or

drink alcohol. Like his wife, the husband also refrains from smoking and drinking alcohol. When it comes to allergies related to food or drugs, none are known presently in relation to her diet and drug history. To conclude, my patient being a 23-year-old primigravida at 37/52 POA was brought into admission due to high blood pressure observed during an ante-natal check-up that had symptoms.

PHYSICAL EXAMINATION

The woman being examined was comfortably reclined on her back, with a single pillow providing support. She revealed no signs of discomfort or breathing problems. The patient's body mass was average, and she displayed good hydration and nutritional status clinically. There were no apparent abnormalities or unusual skin pigmentation in her physical appearance. Additionally, there was no intravenous line attached to any part of her body. Vital Signs: Blood Pressure: 140/88 mmHg Heart Rate: Regular rhythm and robust volume at 96 beats per minute. Body Temperature: Measures 37 degrees Celsius Respiration Rate: Recorded as 20 breaths each minute In-depth Physical Examination: Hand: Her hand was warm and slightly damp upon contact while the creases on her palm appeared more pink than pale.

No palmar erythema or peripheral cyanosis and clubbing were present. The conjunctiva was pink and there was no jaundice. Oral hygiene was good and there was no central cyanosis or injected tonsils. There was no ankle edema in the lower limbs. The abdomen was distended due to the gravid uterus, evidenced by the presence of linea nigra and striae gravidarum. The umbilicus was centrally located and flat, with no dilated veins or surgical scars. The abdomen was soft and non-tender. Clinical fundus corresponded to 38 weeks of gestation and the symphyseal-fundal

height measured 36 cm, which was consistent with the date.

The baby was a singleton with a longitudinal lie and cephalic presentation. The fetal back was positioned on the mother's left side and the fetal head was not engaged. The amount of amniotic fluid was clinically adequate and the fetal heart sound was detected. The examination of other systems found the following: i. Cardiovascular System - The apex beat was located at the left 4th intercostal space, lateral to the mid-clavicular line. Both heart sounds were present with no additional sounds. ii. Respiratory System - Air entry was normal and equal on both sides with no additional sounds. iii. Central Nervous System - All motor and sensory functions were grossly intact.

DISCUSSION PREGNANCY-INDUCED HYPERTENSION

Pregnancy Induced Hypertension (PIH) is defined as a rise in blood pressure after the 20th week of pregnancy. The condition becomes noticeable when systolic blood pressure reaches or surpasses 140/90 mmHg, with an increase of at least 30 mmHg from the original systolic BP and a similar elevation of no less than 15 mmHg in diastolic BP from its initial level. To ensure accurate readings, there needs to be at least a six-hour gap between each BP measurement while the patient is resting. PIH can further be broken down into sub-categories such as mild or severe pre-eclampsia, gestational hypertension, and eclampsia.

When high blood pressure is identified in pregnant women during prenatal examinations, it's crucial to consider PIH as a potential cause. A thorough medical evaluation including obstetric history and indications of heart disease, liver dysfunction, and renal diseases should be carried out to exclude

essential hypertension and upcoming eclampsia. In this particular case study, the patient had no previous record or familial history of essential hypertension. Her elevated blood pressure was discovered during her third trimester check-up at week 37. She was diagnosed with mild Pregnancy Induced Hypertension because her recorded BP continually fluctuated around 170/100 mmHg during subsequent prenatal appointments. Due to the absence of proteinuria, pre-eclampsia could not be confirmed.

The patient was meticulously examined for any possible issues stemming from pregnancy-induced hypertension, which could affect both the pregnant woman and her unborn baby. However, no irregularities were detected in all performed tests. This might be attributed to the fact that the elevated blood pressure was relatively mild and only presented itself late in the pregnancy, thereby reducing potential complications. Hypertension triggered by pregnancy can lead to an array of complications.

• Cerebral hemorrhage
• Heart failure

Hepatic necrosis and acute tubular necrosis of the kidney occur in the placenta.

• Placental insufficiency
• Abruptio placenta

The fetus is experiencing oligohydramnios.

• Intrauterine growth retardation Drugs that can be used in pregnancy

Methyldopa, also known as Aldomet, is a medication used for various medical conditions.

• It is a central adrenergic inhibitor
• Action: v sympathetic activity, v total peripheral resistance
• Adverse effect: lethargy, drowsiness
• It is the safest drug in pregnancy

2. The medication Labetalol is also known as Trandate.

• adrenergic blocker
• Action : v total peripheral resistance, v cardiac output
• Adverse effect: fetal bradycardia, IUGR Contra-indication: 1st-degree heart block, severe asthma

Nifedipine, also known as Adalet, is a calcium channel blocker.

• Action: inhibit calcium influx in vascular smooth muscle
• Adverse effect: headache, reflex tachycardia, flushing

Hydralazine

is number 4.

• Peripheral vasodilator
• Action: direct action on vascular smooth muscle, v TPR
• Adverse effect : headache, sweating, nausea, palpitation
• Indication of use : in hypertension crisis In the ward, the blood pressure of the patient was controlled by given her good bed rest and daily monitoring of blood pressure.

In addition to various methods, the health of the fetus is monitored using cardiotocography (CTG). The potential for labor induction is also being explored. Reasons for this induction are full-term pregnancy and a necessity to reduce high blood pressure that can be caused by pregnancy. However, it's important to recognize that there can be risks linked with inducing labor.

• Failed induction - indicates that the attempt to induce labour has failed to result in full dilatation of the cervix.
• Uterine hyperstimulation - which can cause fetal distress and uterine rupture
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