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Caring for women in pregnancy presents a unique challenge to the healthcare 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 community 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 implications in caring for the high-risk pregnant client in a community hospital setting. J. B.
is a 24 -year-old, gravity 1, para 0, at 25. 2 weeks gestation per early ultrasound. She presented 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 pre pregnant 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 monitor (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 IV of lactated ringers was started, oxygen 10 L/snug face mask 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 due to obesity, it was very difficult to assess timing, duration, and intensity of uterine contractions. The frequency was documented as every three to five minutes. She was leaking small amounts of pink fluid from her vagina and feeling was noted to be positive.
Key indicators of the admission assessment data, such as the elevated blood pressure, proteinuria, 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 (Creamy & 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.
Creamy and Resnik (1999) clarify that, the successful management of preeclampsia requires an understanding of the patho physiologic 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 patho physiologic event that occurs in pregnancy-induced hypertension (PIH) (Leicht & Harvey, 1999). The vaso spasm 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 stimulation 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 vaso spasm 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, this blunting does not take place in the woman with PIH. Angiotensin II is made by the renin-aldosterone pathway in the kidney when enzymes are 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 thromboxane A 2 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 its decreased. Thromboxane is produced by the platelets, renal cells, and the 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 preeclampsia states but with the decrease in prostacyclin it allows for a dominance of thromboxane A 2 in preeclampsia (Leicht & Harvey, 1999). All of these factors contribute to the massive vasoconstriction seen in PIH that ultimately lead to the decreased blood flow, increased microvascular obstruction, and cellular hypoxia. Lets now explore some of the risks and potential complications, to both the mother and her fetus, associated with this condition.
In the preeclampsia patient, due to the vasoconstriction and increased vascular permeability, there is a significant decrease in plasma volume, again resulting in a decreased end organ perfusion. 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 utero placental system. The patho physiologic 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 common factors associated with fetal demise (Leicht & Harvey, 1999). These fetuses are at an increased risk for utero placental insufficiency with a resulting decrease in fetal reserves. With the added insult of uterine contractions, compromise is inevitable unless interventions occur in an expeditious 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 its baseline needs (Parer, 1983). It refers to the degree of hypoxia the fetus can tolerate before tissue hypoxia and subsequent acidosis will occur. In situations of decreased uterine blood flow (as in utero placental insufficiency), fetal compensatory 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 placenta and the related placental blood flow. Damage to the cotyledons (infarcts) due to the ischemic changes associated with poor uterine perfusion, further challenge fetal reserves (Feinstein & McCartney, 1997).
The 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 cardiovascular 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 its 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 sino atrial (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 predictive 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 controls over the FHR and its variability in response to varying blood pressure and / or oxygen (O 2) and carbon dioxide (CO 2) levels. The chemoreceptors, located in the aortic arch, carotid bodies, and the medulla oblong ata, are sensitive to changes in O 2, CO 2, 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 influences such as the catecholamines, epinephrine, norepinephrine, vasopressin, and the renin-angiotensin system, the FHR changes help maintain homeostasis within the tiny body of the fetus. If a stressor, such as decreased utero placental blood flow or umbilical cord compression occurs, the fetal compensatory mechanisms are activated and the resulting change in FHR patterns 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 transition (shape). The late d...
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