Diagnostic Tests

Part of the initial evaluation involves identification of symptoms of organ dysfunction such as severe headache, visual changes, epigastric pain, and difficulty breathing, and edema. Serial blood pressure checks and urinalysis are of primary importance for differential diagnosis of preeclampsia. Serum laboratory tests include 24h urine protein, CBC, liver enzymes and creatinine to evaluate renal and liver function. Fetal evaluation includes NST and AFI which identify fetal status, growth, gestational age and uterine growth restriction. The AFI in particular, measures amniotic fluid which is indicative of placental perfusion. The NST helps identify fetal stress, fetal bradycardia and decelerations indicative of distress.

References
Cunningham, C., Rivera, J., & Spence, D. (2011). Severe preeclampsia, pulmonary edema, and peripartum cardiomyopathy in primigravida patient. AANA Journal, 79(3), 249-255. Goldman-Wohl, D. S., Ariel, L., Greenfield, C., Hochner-Celnikier, D., Cross, J., Fisher, S., & Yagel, S. (n.d.). Lack of human leukocyte antigen-G expression in extravillous throphoblasts is associated with preeclampsia. Oxford Journals: MHR Basic Science of Reproductive Medicine, 6(1), . Retrieved July 21, 2011, from http://www.oxfordjournals.org Hladunewich, M., Karumanchi, S. A., & Lafayette, R. (2007). Pathophysiology of the clinical manifestations of preeclampsia. Clinical Journal of the American Society of Nephrology, 2(3), 543-549. PREECLAMPSIA Foundation (2010). Preeclampsia: Know the symptoms. Retrieved from http://www.preeclampsia.org Salmon, J. E., Triebwasser, M., Heuser, C., Liszewski, M. K., Kavanagh, D., Roumenina, D.,...Atkinson, J. P. (2011, March). ,mutations in complement regulatory proteins predispose to preeclampsia: a genetic analysis of the PROMISSE cohort. Retrieved July 15, 2011, from http://www.plosmedicine.org Shaker, O. G., & Shehata, H. (2011). Early prediction of preeclampsia in high risk women. Journal of Women's Health, 20(4), 539-543. Steegers, E. A., Dandelszen, P., Duvekot, J. J., & Pijnenborg, R. (2010). Preeclampsia. The Lancet, 376, 631-644. Trowsdale, J., & Betz, A.G., (2006). Mother's little helpers: Mechanisms of maternal fetal tolerance. Goldman-Wohl et al. (n.d.) Nature Immunology, 7, 241-246. Yoshimura, T., Chowdhury, F.A., Yoshimura, M., Okamura, H., (2006). Genetic and environmental contributions to severe preeclampsia: Lack of association with the endothelial nitric oxide synthase Glu298Asp variant in a developing country. Gynecologic & Obstetric Investigation, 56

PREECLAMPSIA

Monica M. Delson

Collaborative Management

After differential diagnosis has been established, a collaborative management approach is important in order to decide whether the patient should be admitted, or managed on an outpatient basis. Outpatient management criteria: Gestational age between 32 and 37 weeks, systolic BP< 150, diastolic <100, normal liver enzymes and platelet count, proteinuria < 1000mg, and no symptoms of severe preeclampsia. Nurses can educate patients on issues of home-rest, fetal movement count. In addition, nurses should schedule daily BP, and urine dip, and any changes should be reported to the physician. Twice a week, preeclampsia labs, as well as AFI and NST monitoring. US and Doppler if indicated. Signs and symptoms of severe preeclampsia: Admit to labor and delivery

Preeclampsia: A Multifactorial Process

Pathophysiology: Placenta poorly perfused; immunologic intolerance; Inflammation; Abnormal placental implantation

Maternal Immunologic Intolerance:

Maternal-fetal immune intolerance of paternal antigens expressed by the fetus is characterized by a defective interaction between maternal natural killer cells and the HLA-C antigen. This in turn leads to antibodies that bind to the vascular endothelial cells and subsequent inflammatory responses similar to those seen in graft rejection (an alloimmune response): Coagulation cascade activation and excess activation of leukocytes, results in endothelial dysfunction and stasis of blood flow to the placenta. The immune response and histologic changes are regulated by T-helper cells that directly attack the endothelial cells

resistance and subsequent hypertension Genetic Factors Evidence of familial inheritance (1st degree maternal relatives) is correlated with development of preeclampsia. Genes that play a role in vascular diseases, regulation of BP, and immunity have been studied and implicated in this familial inheritance. In addition, gene mutations which impair capacity to limit compliment activation predispose women to the disease.

o
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Abnormal Trophoblastic invasion Placental HypoperfusionHypoxia Leads to Vasoactive responses

Maternal Immunologic Intolerance o o o o NK cells; (HLA)-C Activation of Inflammatory response Coagulation cascade Markers of endothelial injury

Abnormal Placental Implantation

Alloimmunity

and release cytokines that activate

Angiogenic Factors Vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) are proangiogenic factors released by the placenta. Studies have shown that both of these are decreased in preeclampsia. This decrease can be explained by increased levels of circulating antiangiogenic proteins (sFlt-1 and sEng) and act as potent antagonists to VEGF and PIGF, leading to the hypertension and proteinuria characteristic of preeclampsia. Metabolic Syndrome: a predisposing factor HPA-axis dysfunction causes high cortisol release, hyperglycemia, hyperinsulinemia and dyslipidemia. Elevated triglycerides which induce visceral fat, ultimately result in insulin

Decreased GFR

Increased filtration in pregnancy results from decreased plasma oncotic pressure in the glomerular capillaries. Normally, Hemodilution resulting from hypervolemia lowers the protein concentration that enters the glomerular circulation while at the same time restricting oncotic pressure along the capillaries during filtration. Renal insufficiency in preeclampsia is marked by a decreased GFR, which perhaps helps explain proteinuria that is characteristic of the disease. It is important to note however that the exact mechanism of proteinuria in preeclampsia is not well understood. What is known however is that proteinuria marks the differentiation between preeclampsia and gestational hypertension. In addition, gestational HTN usually occurs in the 3rd trimester and may progress to preeclampsia.

placental hypoxia, and inflammatory response that result. Eclampsia, a major complication of severe preeclampsia, is marked by seizures that cannot be explained by any other factors in women with diagnosed preeclampsia.

Signs and Symptoms

The hallmarks signs of preeclampsia can be explained by endothelial damage, increased vascular resistance, decreased GFR, and an exagerated inflammatory response: Systolic BP > 140 mmhg; diastolic BP >90 mmhg occurring after 20 weeks gestation; on two occasions 4h apart within 1 week period in women with previously normal readings Proteinuria >300 / 24 hrs. Severe preeclampsia presents as BP>160 or a diastolic BP >110 on two occasions 6 hours apart while on bed rest. In addition, one or more of the following: Oliguria of less than 500ml in a 24 hour period, visual disturbances, pulmonary edema, thrombocytopenia, impaired liver function, and fetal growth restriction. All of the features of severe disease can be explained by the pathogenesis leading to severe HTN,

Risk Factors
Nulliparity, chronic HTN, DM, renal disease and obesity. As can be expected chronic HTN , can lead to superimposed preecampsia characterized by new-onset proteinuria, and a sudden increase in BP that was previously controlled. Renal insufficiency can disturb homeostasis of sodium and volume and an increased vascular sensitivity to the reninangiotensin system (RAS). In normal pregnancy the RAS