INTRODUCTION Pregnancy-induced hypertension is a condition in which vasospasm occurs during pregnancy. Signs of hypertension, proteinuria, and edema develop. PIH, a condition separate from chronic hypertension tends to occur most frequently in primiparas younger than age 20 years or older than 40 years, women who have had five or more pregnancies, women of color, women with a multiple pregnancy, women with hydramnios and women with underlying disease such as heart disease, diabetes with vessel or renal involvement and essential hypertension. The condition may be associated with poor calcium or magnesium intake. A woman has passed from mild to Severe Preeclampsia when her blood pressure has risen to 160mmHg systolic and 110mmHg diastolic or above on at least two occasions 6 hours apart at bed rest or her diastolic pressure is 30mmHg above the prepregnancy level. Marked proteinuria, 3+ or 4+ on a random urine sample, or more than 5g in a 24 hours sample, and extensive edema are also present. The hypertension, albuminuria and edema of preeclampsia, usually arise 32 weeks into a first pregnancy, and are often accompanied by headache and disruptions of vision. Preeclampsia seems to originate from an implantation abnormality that affects placental blood vessels. The resulting placental ischemia may be severe enough to produce placental infarcts. Complications of hypertension are the third leading cause of pregnancy-related deaths, superseded only by hemorrhage and embolism. Preeclampsia is associated with increased risks of placental abruption, acute renal failure, cerebrovascular and cardiovascular complications, disseminated intravascular coagulation, and maternal death. In the case of Mrs. Geanette Tamargo, 38 years old from Pudoc San Vicente, Ilocos Sur, she was admitted to Gabriela Silang General Hospital ( OB ward ) last August 23, 2006 at 1:27 pm with diagnosis of Post-op and severe preeclampsia.

OBJECTIVES OF THE STUDY 1. 2. 3. 4. Gather factual health assessment of the patient. Perform proper assessment of the patient. To gain new facts and ideas about the disease. To gain better and clearer understanding on the nature, course, physical and emotional changes and signs and symptoms relevant to this disease. 5. To disseminate information to the patient as well as his relative about the illness and how to care for the patient. 6. To be able to formulate related nursing diagnosis from the patients health data and to the current problems the patient experiences and to come out with different nursing interventions effective for the patient to improve and progress on the most possible time. 7. Set realistic objectives of care.

PATIENTS PROFILE NAME: ADDRESS: Geanette Tamargo Pudoc Sur, San Vicente, Ilocos Sur

HOME ADDRESS: Pudoc Sur, San Vicente, Ilocos AGE: 34 years old RELIGION: Iglesia ni Kristo BIRTHDAY: July 14, 1972 SEX: Female NATIONALITY: Filipino August 23, 2006 TIME: 1.27 pm

DATE OF ADMISSION: INSTITUTION: WARD: WBC DATE DISCHARGED: GSGH

September 2, 2006

TIME: 3:00PM

DIAGNOSIS: Post-operative, Preeclampsia

NURSING HISTORY OF PAST AND PRESENT ILLNESS Geanette Agpoon Tamargo, was 8 months pregnant; a resident of Pudoc Sur, San Vicente Ilocos Sur. During my interview with her, last August 28, 2006, she states that in her previous pregnancy, she had a normal delivery with her first baby. It was in the morning of August 23, 2006 when she went to Gabriela hospital for her scheduled check up while she was being check by doctor Trilles the patient instantly suffered a blurred vision. Her blood pressure was 160/90. After being checked, the doctor told her then that she will be delivering her baby through C.S operation in the afternoon. She was then formally admitted and confined at the hospital on that same date. During the operation the doctor was surprised for she found out that the patients have twin babies. Its so good the operation was successful and the babies are both females and they are alive and that they were placed at the incubator for they are premature babies. But then the mother suffered from preeclampsia where in her blood pressure was high.

ANATOMY AND PHYSIOLOGY OF THE ORGAN INVOLVED

PATHOPHYSIOLOGY A. ALGORITHM Pregnant woman with blood pressure higher than 140/90mmHg Before 20 weeks of Gestation No/stable Proteinuria New/ proteinuria, devt of blood pressure/ HELLP syndrome After 20 weeks of Gestation Proteinuria No Proteinuria

Preeclampsia Gestational HPN Preeclampsia Super Imposed On Chronic Hypertension

B.

EXPLANATION The current concepts regarding the pathophysiology of preeclampsia recognize

that preeclampsia is a multisystem disorder characterized by vasoconstriction, metabolic changes, endothelial dysfunction, and activation of the coagulation cascade in conjunction with an inflammatory response. A 2-stage model of preeclampsia has been proposed in which failure of placental vascular remodeling results in reduced placental perfusion and initiates a cascade of events that result in serious maternal illness with the potential for significant perinatal morbidity and death. Women with underlying microvascular disease, such as diabetes, hypertension, and collagen vascular disease, have a higher incidence of preeclampsia. Normal placental development involves progressive loss of the musculoelastic tissue in the spiral arteries that feed the vessels of the intervillous spaces, which results in uterine blood flow increases of nearly 25% during the first trimester. This process of remodeling the maternal spiral arteries that branch from the uterine artery is typically completed by 18-20 weeks' gestation. In women destined to develop preeclampsia (and in infants who are small for gestational age or whose mothers have diabetes mellitus), this physiologic dilatation of the spiral arteries does not occur because the placental trophoblast cells do not invade the spiral arteries, resulting in maintenance of narrow vessels with resultant placental hypoperfusion and ischemia. In severe cases, not only do the spiral arteries maintain their muscular structure, but other pathologic changes also occur. Accumulation of fat-laden macrophages with fibrinoid necrosis (ie, acute atherosis), disruption of the basement membranes, platelet deposition, mural thrombi, and proliferation of intimal and smooth muscle cells all decrease the luminal diameter. The narrowed and damaged spiral arteries become thrombosed, resulting in placental infarction and necrosis. Uteroplacental blood flow is then reduced by 50-75%. The anatomical reduction in blood flow may be complicated by vasospasm of the uteroplacental bed. The primary defect in preeclampsia appears to originate at the maternal-fetal interface (the placenta). Decreased placental perfusion is thought to lead to fetoplacental ischemia. The ischemic placenta may produce circulating antiangiogenic factors that promote generalized maternal vascular endothelium dysfunction, leading to systemic manifestations of preeclampsia. Associated abnormalities in clotting and platelet function

contribute to vasoconstriction and platelet adhesion and aggregation, as well as to the activation of coagulation factors that increase the risk of thromboembolic formation. The primary feature of preeclampsia, development of hypertension, occurs when normally extreme vasodilatation does not occur. Although cardiac output increases 3050%, the decreased peripheral vascular resistance (PVR) results in decreased BP, even in women with chronic hypertension. Women who develop preeclampsia experience an increase in PVR and alterations in vascular sensitivity to endogenous hormones (eg, angiotensin II, catecholamines, vasopressin). This increase in vascular reactivity to pressor hormones may be mediated, at least in part, through damage to vascular endothelial cells, disrupting the normal prostaglandin balance. The normal expansion of blood volume by 50% that occurs with pregnancy is decreased by 15-20% in patients with preeclampsia. This is the result of diminished plasma volume, leading to the relative hemoconcentration observed in preeclampsia. The plasma volume abnormality involves a redistribution of extracellular fluid, such that interstitial fluid volume is increased while the plasma volume is decreased. The hematocrit increases as the severity of preeclampsia increases. Circulating blood volume is maintained by the increased vascular tone. Whether the vasospasm is the cause or effect of the vascular endothelial injury is not known. Regardless, this injury likely results in the microangiopathic hemolysis and disseminated intravascular coagulation that accompanies severe preeclampsia. The increased circulating blood volume and cardiac output of normal pregnancy results in increased renal blood flow and glomerular filtration rates (GFRs). Women with preeclampsia have markedly decreased renal blood flow and GFRs. Renal biopsies of these women show a constellation of lesions, termed glomerular capillary endotheliosis. Some consider glomerular capillary endothelial swelling that is accompanied by deposits of fibrinogen degradation products within and under the endothelial cells as pathognomonic of the disease. These lesions resolve within a month of delivery.

MANAGEMENT MADICAL SURGICAL INTERVENTIONS A. MEDICAL CARE Incomplete understanding of the genesis and underlying pathophysiology in preeclampsia has impeded attempts at prevention. Empiric approaches of dietary manipulations, low-dose aspirin, use of diuretics or antihypertensives, and manipulations of mineral and electrolyte concentrations have not produced consistent results. Resolution of the disease only occurs after delivery of the placenta. Antepartum management is fraught with controversies before 37 weeks' gestation. In mild cases, fetal and maternal surveillance may allow pregnancy to proceed toward maturity, while prevention of CNS effects, control of hypertension, and management of fluid balance is attempted. Timing and mode of delivery are obstetrical decisions generally based on the maternal and fetal condition. Maternal treatment often includes magnesium sulfate infusions. Depending on the duration of infusion and maternal blood levels, this may result in symptomatic neonatal hypermagnesemia. Although the hypotonia and apnea are transient, they may result in the need for respiratory support in the infant. Among infants born to women with preeclampsia who exhibited absent or reverse end-diastolic umbilical artery Doppler flow velocity on fetal monitoring, an increased frequency of hypoglycemia and polycythemia that is independent of the degree of gestational age and fetal growth restriction has been found. B. SURGICAL CARE Preeclampsia is not a surgical disease of the mother or affected newborn. However, cesarean delivery may be required to address increasing maternal disease severity and minimize maternal and fetal-neonatal morbidity and mortality. C. NURSING CARE > Monitor v/s and report to the doctor if there is an abnormal findings. > Give antihypertensive medicines as ordered. Monitor therapeutic effect and side effects. > Implement no added no salt diet. > Provide educational teaching related to hypertension.

> Assess, monitor and document type, duration of seizure activity. > Support head on side to prevent aspiration. > Assess weight daily. > Assess breath sounds, monitor I&O. PREVENTION There currently are no well-established measures for preventing preeclampsia. Both low-dose aspirin therapy and daily calcium supplementation have been studied as preventive measures but have not been shown to be beneficial in the general pregnant population and are not recommended for primary prevention of preeclampsia. Some evidence does support the use of low-dose aspirin therapy and daily calcium supplementation in certain high-risk women. Calcium supplementation has been shown to produce modest blood pressure reductions in pregnant women who are at aboveaverage risk for hypertensive disorders of pregnancy and in pregnant women with low dietary calcium intake. An optimum calcium dosage for these women has not been established. Low-dose aspirin therapy (100 mg per day or less) has been shown to reduce the incidence of preeclampsia in women who were found to have an abnormal uterine artery on Doppler ultrasound examination performed in the second trimester. Research on the use of antioxidants in the prevention of preeclampsia is promising. However, further study is needed, and antioxidant therapy currently is not recommended. Although preeclampsia is not preventable, many deaths from the disorder can be prevented. Women who do not receive prenatal care are seven times more likely to die from complications related to preeclampsia-eclampsia than women who receive some level of prenatal care. Some studies indicate that preeclampsia-related fatalities occur three times more often in black women than in white women. Although the precise reasons for the racial differences remain elusive, the differences may be indicative of disparities in health status, as well as access to, and quality of, prenatal care. To decrease preeclampsia-related mortality, appropriate prenatal care must be available to all women. Early detection, careful monitoring, and treatment of preeclampsia are crucial in preventing mortality related to this disorder.

TREATMENT Delivery remains the ultimate treatment for preeclampsia. Although maternal and fetal risks must be weighed in determining the timing of delivery, clear indications for delivery exist. When possible, vaginal delivery is preferable to avoid the added physiologic stressors of cesarean delivery. If cesarean delivery must be used, regional anesthesia is preferred because it carries less maternal risk. In the presence of coagulopathy, use of regional anesthesia generally is contraindicated. Women with preeclampsia and preterm pregnancy can be observed on an outpatient basis, with frequent assessment of maternal and fetal well-being. Women who are noncompliant, who do not have ready access to medical care, or who have progressive or severe preeclampsia should be hospitalized. Women whose pregnancy is remote from term should be cared for in a tertiary care setting or in consultation with an obstetrician or family physician who is experienced in the management of high-risk pregnancies. During labor, the management goals are to prevent seizures and control hypertension.4 Magnesium sulfate is the medication of choice for the prevention of eclamptic seizures in women with severe preeclampsia and for the treatment of women with eclamptic seizures. One commonly used regimen is a 6-g loading dose of magnesium sulfate followed by a continuous infusion at a rate of 2 g per hour. Magnesium sulfate has been shown to be superior to phenytoin (Dilantin) and diazepam (Valium) for the treatment of eclamptic seizures.1 Although magnesium sulfate commonly is used in women with preeclampsia, studies to date have been inadequate to show that it prevents progression of the disorder. Antihypertensive drug therapy is recommended for pregnant women with systolic blood pressures of 160 to 180 mm Hg or higher24 and diastolic blood pressures of 105 to 110 mm Hg or higher. The treatment goal is to lower systolic pressure to 140 to 155 mm Hg and diastolic pressure to 90 to 105 mm Hg. To avoid hypotension, blood pressure should be lowered gradually. Although evidence about the potential adverse effects of most antihypertensive drugs has been poorly quantified, use of many of these agents is contraindicated during pregnancy. Hydralazine (Apresoline) and labetalol (Normodyne, Trandate) are the antihypertensive drugs most commonly used in women with severe preeclampsia Nifedipine (Procardia) and sodium nitroprusside (Nitropress) are potential alternatives, but significant risks are associated with their use. Note that labetalol therapy should not

be used in women with asthma or congestive heart failure. Use of angiotensin-converting enzyme inhibitors is contraindicated in pregnant women In women with preeclampsia, blood pressure usually normalizes within a few hours after delivery but may remain elevated for two to four weeks. As previously noted, a diagnosis of chronic hypertension is made if blood pressure remains elevated at 12 weeks postpartum. Women with preeclampsia should be counseled about future pregnancies. In nulliparous women with preeclampsia before 30 weeks of gestation, the recurrence rate for the disorder may be as high as 40 percent in future pregnancies. Multiparous women have even higher rates of recurrence.