Preeclampsia

92 Preeclampsia




Overview/pathophysiology


Hypertensive disorders of pregnancy are the most frequently reported medical complications of pregnancy. Classification terminology has been confusing and nonuniform. American College of Obstetrics and Gynecology (ACOG) lists four categories, grouping mild preeclampsia, severe preeclampsia, and eclampsia together.




Preeclampsia/eclampsia:


Occurs after 20 wk gestation. Blood pressure (BP) is elevated and accompanied by significant proteinuria (see Assessment, below). Preeclampsia often develops mildly, becomes severe without intervention, and may result in eclampsia.


• HELLP syndrome is a laboratory diagnosis for a severe variant of preeclampsia associated with high maternal and fetal morbidity. “H” stands for hemolysis of red blood cells; “EL” stands for elevated liver enzymes; and “LP” stands for low platelets.

• Eclampsia: When severe preeclampsia has progressed to generalized seizures, it is called eclampsia. Seizures may occur antepartum, intrapartum, or postpartum. Coma often follows a seizure.


Gestational hypertension:


BP elevation after 20 wk gestation occurs without proteinuria. It may be transient or chronic in nature. Despite the hypertension, good pregnancy outcomes are expected.



Chronic hypertension:


BP elevation was known prior to pregnancy. Chronic hypertension is more prevalent with late childbearing and rising rates of obesity.



Chronic hypertension with superimposed preeclampsia:


The most common hazard for a chronic hypertensive woman.


Although the cause of preeclampsia remains unknown, the resulting generalized vasoconstriction, vasospasms, and endothelial cell damage are known to result in decreased circulation and oxygenation for all organ systems and redistribution of intravascular fluid. Serious and life-long complications can develop in any affected organ system, including the brain, kidney, liver, and uteroplacental unit. Often the presenting signs are the classic signs of hypertension accompanied by proteinuria. As this multisystem disorder progresses from mild to severe preeclampsia, varied clinical manifestations demonstrate the more severe effects on each organ system. The only known cure is delivery of the newborn and removal of the placenta.



Health care setting


Primary care and acute care antepartum and intrapartum hospital units. Home care is possible for mild preeclampsia.



Assessment




Signs and symptoms:


The focus of this nursing care plan is preeclampsia.













Mild Preeclampsia Severe Preeclampsia

• BP elevated × 2, 6 hr apart on bedrest: systolic blood pressure (SBP) 140-160 mm Hg or ↑30 over baseline; diastolic blood pressure (DBP) 90-110 mm Hg or ↑15 over baseline

• Mean arterial pressure (MAP) 105 mm Hg or higher or increased by 20 mm Hg from baseline (90 mm Hg or higher in second trimester)

• Proteinuria: 0.3-4.0 g in 24-hr collection; 2+ or 3+ on random dipstick (without urinary tract infection)

• Reflexia: 2+ or less (normal response)

• Headache: Absent or transient

• No vision changes

• No epigastric pain

• Normal urine output

• Laboratory studies: Platelets normal, ↑ hematocrit (Hct), liver enzymes begin to rise
• BP elevated × 2, 6 hr apart on bedrest: SBP greater than 160 mm Hg; DBP greater than 110 mm Hg

• MAP higher than 105 mm Hg

• Proteinuria: More than 5 g/L in 24-hr collection; 2+, 3+ or more by dipstick

• Increased sodium retention

• Hyperreflexia: 3+ or more; clonus

• Headache: Continuous or severe, affective changes, nausea/vomiting

• Vision: Blurred, scotoma, diplopia, photophobia, retinal detachment (spontaneously reattaches later)

• Epigastric pain: present (impending convulsion)

• Oliguria: Urine output less than 20 mL/hr

• Weight gain: more than 1.5 kg (3.3 lb)/ month or more than 0.5 kg (1.1 lb/ week) in third trimester. Edema is not considered diagnostic but should not remain after 8-12 hr bedrest.

• Placenta: Decreased placental perfusion

• Risk of oligohydramnios

• Early placental aging not apparent yet
• Laboratory studies: ↑ alanine aminotransferase (ALT), ↑ aspartate aminotransferase (AST), ↑ lactate dehydrogenase (LDH), and ↑ serum creatinine (renal compromise), thrombocytopenia

• Edema: generalized, dyspnea, rales/crackles (pulmonary edema)

• Placenta: Markedly reduced perfusion → intrauterine growth restriction (IUGR)

• Risk of abruptio placenta

• Labor: Late decelerations

• Placental evaluation after birth: Intervillous thrombosis, ischemic necrosis (white spots), smaller than expected for gestational age

Additional reportable signs include decreased fetal movement (fetal compromise), spontaneous bruising, prolonged bleeding and epistaxis (thrombocytopenia).



Risk factors:


Nulliparity (status of a woman who has not carried the pregnancy and given birth after 20 wk gestation), African American race, history of preeclampsia, renal disease, diabetes mellitus, hypothyroidism, age younger than 20 yr or older than 40 yr, family history of preeclampsia (mother/sister), chronic hypertension, thrombophilias (antiphospholipid syndrome, proteins C and S, antithrombin deficiency, factor V Leiden), multifetal pregnancy, oocyte donation or donor insemination, urinary tract infections, obesity, gestational trophoblastic disease (molar pregnancy) (Levine et al., 2009; Rath & Fischer, 2009), and male partner whose previous partner had preeclampsia (www.acog.org).



Diagnostic tests




Complete blood count (CBC):


May be within normal limits. Changes reflect hemodynamic changes. Hct rises with hemoconcentration. Platelets drop (thrombocytopenia) with hemoconcentration and with HELLP syndrome. Hemoglobin (Hb) falls with hemolysis.



Renal function studies:


Proteinuria 0.3 g or more in a 24-hr urine specimen is diagnostic for preeclampsia. With kidney involvement, blood tests may show rising serum creatinine, uric acid, and blood urea nitrogen (BUN). Elevated creatinine clearance in a 24-hr urine collection indicates reduced renal function.



Liver function tests:


ALT, AST, and LDH rise with severe preeclampsia and rise even further with HELLP syndrome.



Coagulation studies:


Platelet count decreases in severe preeclampsia and HELLP syndrome. Intrinsic or extrinsic factors may induce clot formation.



Obstetric ultrasound:


Serial ultrasounds are commonly used to estimate fetal growth and amniotic fluid index (AFI).



Daily fetal activity monitoring, nonstress testing (NST), and biophysical profile (BPP):


These tests assess uteroplacental perfusion.





Nursing diagnoses:


Decreased cardiac output


Risk for ineffective renal tissue perfusion

related to hypertension, generalized vasospasms, vascular wall damage, and hypovolemia with decreasing venous return


Desired Outcome: Within 24 hr after interventions, patient begins to return to normotensive BP and pulse for pregnancy and participates in her health care regimen.






















ASSESSMENT/INTERVENTIONS RATIONALES
Assess and document BP and pulse q1-4h as indicated. Hypertension results from biochemical changes that cause vasoconstriction and vasospasm. Rising BP values indicate progression of preeclampsia.
Measure urine volume and proteinuria qh. Maintain strict intake and output. As preeclampsia becomes severe, glomerular endothelial damage allows protein molecules to pass into the urine. Hypovolemia and damage to blood vessel walls decrease circulation to the kidneys.
For patients with worsening preeclampsia, explain importance of bedrest with bathroom privileges and frequent use of left lateral position. Bedrest and left lateral positioning facilitate venous return to the heart, which lowers BP and increases perfusion of the kidneys and uteroplacental unit.
Administer prescribed antihypertensive medication (i.e., hydralazine [Apresoline], labetalol HCl [Normodyne], or methyldopa [Aldomet]). Antihypertensives lower BP via vasodilation and decreasing systemic vascular resistance.
Prepare for cesarean delivery if indicated by the severity of preeclampsia and as determined by the health care provider. Delivery (of placenta) is the definitive way to halt the progression of preeclampsia. Cesarean is selected when induction and vaginal delivery are ruled out.




Nursing diagnosis:


Risk for imbalanced fluid volume

related to vasospasm, endothelial cell damage, and fluid shifts from intravascular to extravascular spaces


Desired Outcome: Signs and symptoms of imbalanced fluid volume diminish within 8-12 hr, as evidenced by decreased BP, normal rate and quality of pulse, unlabored respirations, urine output greater than 30 mL/hr without proteinuria, normal pregnancy weight gain, absence of pitting edema, and Hct within normal limits.






























ASSESSMENT/INTERVENTIONS RATIONALES
Assess BP; heart rate, rhythm, and quality; respiratory rate (RR); and lung sounds q1-4h. Increasing hypertension occurs with worsening vasoconstriction and increasing peripheral vascular resistance. Pulse increases and quality changes occur to compensate for hypovolemia. Pulmonary edema causes dyspnea.
Assess presence, degree, and location of edema q1-8h. Weigh patient daily. Edema develops as fluid shifts from the vascular to the extravascular spaces. Weight gain is an indicator of fluid retention.
Assess deep tendon reflexes (DTRs) and for presence of clonus q1-4h. Increasing hyperreflexia signals a worsening condition. DTRs correspond to the peripheral neurologic condition. Clonus relates to central neurologic irritability. For more details about DTRs and clonus, see Risk for Injury: Maternal, later.
Assess for headaches: presence, location, and severity q1-4h. Headaches increase in intensity and frequency with advancing brain edema.
Assess for mental changes, irritability, and level of consciousness q1-4h. Changes in mentation indicate worsening condition with increased central nervous system (CNS) edema.
Monitor fluid intake and urine output q1-4h. If indicated, limit fluid intake to 2000-3000 mL/day (PO and IV). Fluid retention could lead to pulmonary edema when severe. Oliguria signals renal system compromise.
Collect a 24-hr urine specimen to measure proteinuria and creatinine if prescribed by health care provider. Measure proteinuria with dipstick every void. As preeclampsia becomes severe, glomerular endothelial damage allows protein molecules and creatinine to pass into the urine.
Monitor for hemodynamic changes via the following laboratory values:
– Hct
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Preeclampsia

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