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Preeclampsia 1

Pathophysiology Case Study: Preeclampsia

Lori Ley

Jacksonville University

December, 2001

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Pathophysiology Case Study: Preeclampsia

Caring for women in pregnancy presents a unique challenge to the health care team.

Obstetrical nursing requires an in-depth knowledge of the physiological, psychological, and

social processes of the high-risk childbearing woman and her fetus during pregnancy. In a com-

munity hospital setting, care challenges can be further complicated by the possible limitations of

available resources. The following case study will explore the necessary insights and their impli-

cations in caring for the high-risk pregnant client in a community hospital setting.

J.B. is a 24-year-old, gravida 1, para 0, at 25.2 weeks gestation per early ultrasound. She pre-

sented to the Labor and Delivery unit at 09:26 a.m. with complaints of feeling a gush of fluid and

vaginal bleeding. Upon arrival, her blood pressure was elevated at 174/109. Her pulse was 98,

respirations 24, and temperature 97.6 F (36.4 C). Her weight was 230 lbs. (103.5 Kg) with a

reported prepregnant weight of 217 pounds.

The fetal heart rate (FHR) was auscultated at 125-130 beats per minute (bpm) with audible

decreases heard down to 60-90 bpm lasting 30-40 seconds. Uterine activity was palpated and

confirmed J.B.’s complaint of abdominal tightening and cramping. However, due to her obesity

and left lateral positioning, it was difficult to obtain a readable tracing on the electronic fetal mon-

itor (EFM). Additionally, her reflexes were +1, clonus absent, 2+ pedal edema, and +1 urine

albumin. The tocodynamometer and ultrasound transducers of the EFM were readjusted, but the

FHR could not be verified despite several attempts. Labs were drawn for CBC, type and screen,

drugs of abuse, and Chem 20 analysis. An intravenous infusion (IV) of lactated ringers was

started, oxygen 10L/snug facemask was administered, and the obstetrician was notified to report

to the bedside.

Other assessment data revealed her abdomen to be tender but soft per palpation, but again

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due to obesity, it was very difficult to assess timing, duration, and intensity of uterine contrac-

tions. The frequency was documented as every three to five minutes. She was leaking small

amounts of pink fluid from her vagina and ferning was noted to be positive.

Key indicators of the admission assessment data, such as the elevated blood pressure, pro-

teinuria, and edema, pointed to the cardinal symptoms of preeclampsia. Preeclampsia is one of

the classifications that falls under the umbrella term of pregnancy induced hypertension (Creasy

& Resnik, 1999; Mattson & Smith, 2000). J.B.’s risk for preeclampsia was also heightened due to

her obesity (Morin, 1998). Preeclampsia is a condition unique to pregnancy and is characterized

by poor perfusion to vital organs, including the fetoplacental unit. Creasy and Resnik (1999) clar-

ify that, “the successful management of preeclampsia requires an understanding of the pathophys-

iologic changes in this condition and the recognition that the signs of preeclampsia – increased

blood pressure, proteinuria, and edema – are only signs and not causal abnormalities” (p. 835).

Vasospasm, with its associated endothelial damage, is the underlying pathophysiologic

event that occurs in pregnancy-induced hypertension (PIH) (Leicht & Harvey, 1999). The vasos-

pasm causes an increase in arterial blood pressure and resulting resistance to blood flow. The

restriction of blood flow is associated with the endothelial damage, which then initiates stimula-

tion of platelet aggregation and fibrinogen utilization. These vascular changes alter blood flow

and can result in hypoxic damage to vulnerable organ systems such as the liver, kidneys, heart,

and brain.

In addition to the systemic vasospasm and resulting endothelial damage, women with PIH

have exaggerated responses to angiotensin II. Blunting of the responses to angiotensin II is

present in normal pregnancies but, for unknown reasons, it does not take place in women with

PIH. Angiotensin II is made by the renin-aldosterone pathway in the kidney when enzymes are

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released to convert angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor

thereby producing the subsequent rise in blood pressure (Mattson & Smith, 2000).

Patients with PIH also have been noted to have an imbalance of prostacyclin and throm-

boxane A2 but the exact mechanism for this imbalance is unclear. The endothelial cells and the

placenta produce prostacyclin, a prostaglandin dilator. It causes vasodilation, inhibits platelet

aggregation, and encourages uterine relaxation. Prostacyclin is normally increased in pregnancy

but in preeclampsia conditions it’s decreased.

Thromboxane A2 is produced by platelets, renal cells, and placenta and has the opposite

effects of prostacyclin. It causes vasoconstriction, platelet aggregation, and uterine contractions.

Thromboxane levels are increased in both normal pregnancy and preeclamptic states but with the

decrease in prostacyclin it allows for a dominance of thromboxane A2 in preeclampsia (Leicht &

Harvey, 1999). All of these factors contribute to the massive vasoconstriction seen in PIH that

ultimately lead to decreased blood flow, increased microvascular obstruction, and cellular

hypoxia. Let’s now explore some of the risks and potential complications, to both the mother and

her fetus, associated with this condition.

In the preeclamptic patient, due to the vasoconstriction and increased vascular permeabil-

ity, there is a significant decrease in plasma volume, again resulting in decreased end organ perfu-

sion. Maternal preferential blood flow patterns that are usually demonstrated in chronic and acute

crisis states, likely secondary to increased sympathetic activity or catecholamine production,

cause a significant decrease in blood flow to the uteroplacental system. The pathophysiologic

effects of preeclampsia predispose the fetus to intrauterine growth restriction (IUGR), fetal

hypoxia, and death. The risk of chronic hypoxia and acute placental abruption are the most com-

mon factors associated with fetal demise (Leicht & Harvey, 1999). The fetus is at an increased

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risk for uteroplacental insufficiency with a resulting decrease in fetal reserves. With the added

insult of uterine contractions, compromise is inevitable unless interventions occur in an expedi-

tious manner.

Fetal reserve is the term used to describe the concept that the normal fetus is provided with

oxygen and nutrition resources in excess of it’s baseline needs (Parer, 1983). It refers to the

degree of hypoxemia the fetus can tolerate before tissue hypoxia and subsequent acidosis occurs.

In situations of decreased uterine blood flow (as in uteroplacental insufficiency), fetal compensa-

tory mechanisms are activated.

As blood flow is shunted away from the uterus, the vital oxygen and nutritive substances

necessary to sustain the fetus via the placenta are compromised. Fetal gas exchange occurs in the

placental villi contained within the cotyledons and depends on the structural integrity of the pla-

centa and the related placental blood flow. Damage to the cotyledons (infarcts) due to ischemic

changes associated with poor uterine perfusion, further challenge fetal reserves (Feinstein &

McCartney, 1997).

Fetal responses to decreased oxygen and increased carbon dioxide levels are demonstrated

by intrinsic factors that include the fetal mechanisms of FHR control and related fetal cardiovas-

cular anatomy and physiology. Interpreting these intrinsic responses and the adaptive capabilities

in the fetus is done by focusing on the fetal heart rate, rhythm, and it’s variability in conjunction

with various factors such as fetal activity and uterine contractions (Murray, 1997).

The fetal heart, like the adult heart, has an intrinsic rate that is controlled predominately by

the sinoatrial (SA) node of the heart. However, the heart rate in the healthy fetus is seldom static.

The normal baseline rate of a fetus fluctuates nearly continuously as it adapts to the constant

changes in the uterine environment. This “variability” in the baseline rate of the fetus is predic-

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tive of an intact central nervous system and is considered a “reassuring” sign of fetal well being

(Feinstein & McCartney, 1997). Fetal sympathetic and parasympathetic systems exert their con-

trols over the FHR and it’s variability in response to varying blood pressure and/or oxygen (O2)

and carbon dioxide (CO2) levels.

The chemoreceptors, located in the aortic arch, carotid bodies, and the medulla oblongata,

are sensitive to changes in O2, CO2, and pH levels. The baroreceptors, located in the aortic arch

and carotid sinuses, are sensitive to changes in fetal blood pressure. In tandem with other influ-

ences such as the catecholamines, epinephrine, norepinephrine, vasopressin, and the renin-angio-

tensin system, FHR changes help maintain homeostasis within the tiny body of the fetus.

If a stressor, such as decreased uteroplacental blood flow or umbilical cord compression

occurs, the fetal compensatory mechanisms are activated and the resulting change in FHR pat-

terns or variability can be observed on the EFM. Distinct differences in the identified patterns of

FHR signify the mechanism of insult (Feinstein & McCartney, 1997). A variable deceleration is

defined as an abrupt decrease in FHR in response to cord compression. A late deceleration is

described as having two characteristics that distinguish it from the others, “timing and shape”.

The late deceleration occurs late or after the peak of a contraction (timing) and has a smooth tran-

sition (shape). The late deceleration pattern is indicative of a uterine and/or placental blood flow

problem. In the case of PIH, the late deceleration types will most likely be the pattern that is seen

due to the compromised uteroplacental blood flow.

Another risk associated with preeclampsia points to the propensity for decreased maternal

renal blood flow due to vasoconstriction. Vasospasm, with the resulting decrease in blood flow,

leads to a decrease in glomerular filtration rate (GFR), decreased clearance of uric acid and creat-

inine, and sodium retention. Plasma creatinine levels may be elevated. Glomerular damage,

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which causes increased membrane permeability, results in the diffusion of large protein molecules

and the diagnostic finding of proteinuria.

Hematological changes can also carry a significant risk to the patient with preeclampsia.

As described earlier, vasospastic activity causes endothelial damage. In response to this damage,

platelets aggregate to the site of injury. With the narrowing of the lumen of the vessels, red blood

cells (RBCs) and platelets can become damaged as they attempt to traverse through the system.

The resulting damage to the RBCs can reduce the oxygen carrying capacity of the attached hemo-

globin molecule as well as causing hemolysis. Damaged and decreased platelet numbers (throm-

bocytopenia) can have a devastating effect on clotting mechanisms. PIH can result in

disseminated intravascular coagulation (DIC) in the most severe of cases.

Risks to hepatic function are also associated with vasospasm. Continued and profound

vasospasm can lead to life-threatening complications such as hepatic hemorrhage, rupture, and

necrosis. Clinical signs and symptoms of epigastric or right-upper-quadrant pain are considered

highly suspicious for hepatic involvement and warrant further investigation (Leicht & Harvey,

1999). Elevated serum liver function tests [bilirubin, serum glutamic-oxaloacetic transaminase/

aspartate transaminase (SGOT/AST), lactic acid dehydrogenase (LDH), alkaline phosphatase (alk

phos), and blood urea nitrogen (BUN)] will assist in evaluating the severity and hepatic progres-

sion of this disease (Creasy & Resnik, 1999).

The neurological sequelae of preeclampsia can also present challenges and risks to the

PIH patient. Again, vasospasm is the culprit in the visual disturbances sometimes noted in the

severe preeclampsia patient. Retinal detachment caused by vasospasm of the retinal artery has

been documented in 1-3% of the PIH cases. The progression of preeclampsia to eclampsia (the

presence of seizure activity) is associated with the same cascading mechanisms of vasospasm.

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Seizure activity is caused by cortical brain spasms that occur in response to the other vasospastic

precipitators. Pharmacological prevention is key to diverting these types of episodes (Creasy &

Resnik, 1999).

J.B. and her fetus, the case study subjects, carry other risks besides those of preeclampsia.

Her gestation of 25+ weeks as well as her premature ruptured membranes complicated the sce-

nario further. Her abdominal tenderness was suspicious for possible abruption. This was an

emergency situation requiring collaborative medical and nursing action to prevent the potential

for further maternal and fetal compromise.

The obstetrician responded to the bedside within four minutes (0930), was given report,

and performed an ultrasound to rule out placenta previa (bleeding), confirm the FHR, assess cer-

vical dilatation, and verify amniotic fluid volume. Results revealed no previa, decreased amniotic

fluid volume, positive fetal cardiac activity, and a closed thick cervix. The perinatologist was

consulted and the patient and family discussed options for transfer and treatment. The decision

was made to initiate intravenous Magnesium Sulfate (MgSO4) therapy and transport via helicop-

ter to a tertiary Level III facility.

Nursing diagnoses for the case at this time were possible alteration in uteroplacental per-

fusion related to the PIH, preterm gestation, and uterine contractions. Also, possible alteration in

umbilical blood flow related to the decreased amniotic fluid volume, and again PIH and uterine

contractions.

Interventions were directed toward the goals to enhance uteroplacental and umbilical

blood flow by maintaining left lateral positioning, hydrating the patient, improving oxygenation,

reducing uterine activity, reducing maternal anxiety, providing safety measures for seizure pre-

cautions, continuous monitoring of the maternal and fetal status, maintaining strict I&O, adminis-

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tering medications as prescribed, and planning for possible emergency surgical intervention.

The first readable EFM tracing occurred at 0940. Contractions were palpated every 2

minutes. The contractions were mild to moderate intensity, and marked on the fetal tracing as

“UC” by the nurse, as the monitor still would not trace contractions. At 0945, MgSO4 therapy

was initiated per protocol. The FHR was 125-130 bpm with decreased long-term variability and

late decelerations. At 0950 the obstetrician and perinatologist were again called to the bedside to

review the FHR tracing. At this time the decision to abort transfer and prepare the patient for an

emergency cesarean was made. The anesthesia and neonatology crews were notified.

J.B. delivered a viable male at 1009 via primary cesarean section under general anesthesia.

Upon exam of the placenta a 40% abruption was noted. Apgars of the male infant were 3 and 7 at

1 and 5 minutes respectively. Cord gases were drawn. The infant was resuscitated with intuba-

tion and positive pressure ventilation and was transported to the NICU. Further stabilization

occurred in the Level II NICU and the infant was transferred to a Level III tertiary facility for

long-term ventilator therapy. The cord gas results were arterial pH 6.902, pCO2 83.8, pO2 17.6,

BE -19.3, venous pH 6.968, pCO2 68.5, pO2 22.1, BE –17.3. These values revealed a mixed res-

piratory and metabolic acidosis.

Postoperatively, J.B. was taken to the Labor and Delivery recovery area where she was

intensively monitored for 12 hours. She continued on MgSO4 therapy for 24 hours. After

becoming hemodynamically stable (labs, BP, and output WNL), the medication was discontin-

ued. Due to the ruptured membranes and surgical intervention, J.B. was also treated with IV

Ancef 1 gram every 6 hours for three doses. As per protocol, to facilitate uterine involution, she

was treated with IV oxytocin. She was discharged stable on her third day post-op to join her

infant at the Level III NICU. Later, the infant progressed and was discharged home at 3 months

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of age with to date, no known neurologic sequelae.

Due to the emergent nature of this scenario, the diagnostic lab values were reviewed retro-

spectively after delivery. They did serve the purpose of providing a baseline for future compari-

sons in measuring the resolution of the preeclampsia in J.B., as delivery is the only “cure” for this

disease of pregnancy. She was negative for all drugs of abuse. Her CBC values were normal with

the exception of the MPV and neutrophil counts. These were slightly elevated but the extent of

this elevation was normal for the pregnant client, especially in labor (having uterine contrac-

tions)(Creasy & Resnik, 1999). Most liver function markers such as BUN, uric acid, SGOT/AST,

and alkaline phosphatase levels were normal, with only LDH demonstrating a slight elevation,

ruling out the progression of liver involvement at this time. The LDH returned to normal on the

first day post-op. Serum total protein and albumin levels were low as expected due to the GFR

and membrane permeability allowing for diffusion of protein into the urine (+1 urine protein on

admission). Urine was negative for protein 13 hours post-op and remained so until discharge.

In summary, the expedient and goal directed actions of all health care providers in this

case study scenario, contributed significantly to the positive outcomes of this client and her fetus.

Despite the high-risk nature of this situation, the circumstances of this client coming to a commu-

nity hospital instead of a Level III tertiary care center, did not affect care. Even more possible, the

delay that would have ensued in seeking care at such a facility could have had grave conse-

quences in this case. Consistency in the obstetrical nurse’s knowledge regarding the pathophysio-

logic basis for disease and complications of pregnancy should be universal, despite the expected

level of care for any facility.

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References

Creasy, R., & Resnik, R. (1999). Maternal-fetal medicine (4th ed.). Philadelphia, PA: W. B.

Saunders.
Feinstein, N., & McCartney, P. (Eds.). (1997). Fetal heart monitoring principles and practices

(2nd ed.). Dubuque, IA: Kendall Hunt Publishing Company.

Leicht, T., & Harvey, C. (1999). Hypertensive disorders of pregnancy. In L. Mandeville, &
N. Troiano (Eds.), High-risk and critical care intrapartum nursing (2nd ed., pp. 159-170).

Philadelphia, PA: J. B. Lippincott Company.

Mattson, S., & Smith, J. (Eds.). (2000). Core curriculum for maternal-newborn nursing

(2nd ed.). Philadelphia, PA: W. B. Saunders Company.

Morin, K. (1998). Perinatal outcomes of obese women: A review of the literature. Journal

of Obstetric, Gynecologic, and Neonatal Nursing, 27, 434.

Murray, M. (1997). Antepartal and intrapartal fetal monitoring. Albuquerque, NM:

Learning Resources International, Inc.


Parer, J.T. (1983). Fetal cardiorespiratory physiology: Handbook of fetal heart rate monitor-

ing.

Philadelphia, PA: W. B. Saunders Company.

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