Kelsie Gray & Candace Bradshaw

Patient Scenario: Kim Johnson, a 38 yo White female presents to the ER with her husband Ray; chief complaints are headache, tightness in chest, blurred vision and slight abdominal cramping. Patient also states difficulty emptying bladder accompanied by a consistent urge to void. She is a primigravida at 36 week gestation. Past med hx: none; Medications: daily prenatal vitamin; Family hx: both parents have hx of HTN Vitals: BP: 172/118 HR: 102 RR: 26 O2 : 96% - RA T: 98.3 (oral) Pain: 6/10 Ht: 5’3” Wt: 171 lb. Fundal height is appropriate for 36 weeks; there is no dilation to cervix. ER staff Dr. Barrow orders 4 g magnesium sulfate to be given over 10 minutes along with 5 mg IV hydralazine, then 5-10 mg every 20-40 minutes. The following labs: CBC, Serum Creatinine, Uric acid, urinalysis and CT of the pts head Abnormal labs: urinalysis = 3+ protein; 1.4 Creatinine; Primary dx: Preeclampsia Mrs. Johnson is admitted to the OB floor for further monitoring.

1. What are the qualifications for a patient to be diagnosed with preeclampsia: Increase in patients blood pressure, > or equal to 140 systolically and > or equal to 90 diastolically, that occurs 2 times four hours apart after 20 weeks gestation Proteinuria (> or equal to 300 mg of protein in 24 hours) Sudden, severe edema noted should prompt evaluation to R/O preeclampsia or renal disease Rationale: Preeclampsia is a pregnancy-specific syndrome clinically defined as an increase in blood pressure (systolic greater than or equal to 140 and diastolic greater than or equal to 90, that occurs 2 times within 4 hours) that is present after 20 weeks gestation with proteinuria (greater than or equal 300 mg protein/24 hours). Once upon a time edema was included, but now because edema is so common during pregnancy, this has been removed and modified where if sudden severed edema is present, you should monitor closely to rule out preeclampsia.

2. What lab tests would you monitor for a patient with preelampsia: CBC with platelets Coagulation profile to assesses for DIC Metabolic studies ALT AST LDH electrolyte studies to establish renal functioning Rationale: Laboratory tests include a complete blood count with platelets, coagulation profile to assess for disseminated intravascular coagulation (DIC), metabolic studeies for determination of liver ensymes (AST, ALT, and LDH), and electrolyte studies to establish renal functioning.

Rationales for Diagnostic tests: Blood testing is done to evaluate how well liver & kidneys are functioning, as well as platelet count and electrolyte status. LDH & Indirect bilirubin levels are tested if HELLP syndrome is suspected. If HELLP syndrome is suspected, special precautions are considered in order to prevent adverse outcomes if there were to be a cesarean birth. Nurse is responsible for adminstering 5-10 units of platelets on the physician’s order before the birth to prevent thrombocytopenia. Always remember provide patient and family with ongoing information to help decrease any anxiety and fear they may have. When headaches are present, CT scans can detect intracranial hemorrhage. Fetal ultrasound will be done to determine fetal status including heart rate, and amount of amniotic fluid.

3. What are the nursing interventions associated with severe preeclampsia? Maintain bed rest. Administer magnesium sulfate (use a controlled infusion device) as prescribed to prevent seizures; magnesium sulfate may be continued for 24-48 hours postpartum. Monitor for signs of magnesium toxicity, including flushing, sweating, hypotension (sudden onset), depressed deep tendon reflexes (hyporeflexia), urine output (oliguria), central nervous system depression (depressed respirations), and indicators of fetal compromise); keep antidote (calcium gluconate) available for immediate use, if necessary. Administer antihypertensives as prescribed. Prepare for the induction of labor.

Rationale: Pregnancies that are complicated by preeclampsia with severe features have been associated with increased rates of perniatal mortality and significan risks for maternal morbidity and mortality; because of this prompt delivery should occur if diagnosed after 34 weeks gestation if there is fetal or maternal compromise evident. Management includes: seizure prophylaxis with magnesium sulfate and antihypertensive medications in cases where the diastolic blood pressure has reached or exceeded 110 mm Hg. You are wanting to reduce the patient’s risk of cerebral vascular accident while maintaining uteroplacental perfusion. If there is a decrease in the diastolic to less than 90 mm Hg, the placental blood flow will decrease also, resulting in a decreased fetal heart rate (FHR). When managing care, you want to reduce the diastolic blood pressure to less than 110 mm Hg, but greater than 95-100 mm Hg. You also want to do invasive hemodynamic monitoring if there is oliguria that is unresponsive to fluid replacement, pulmonary edema, hypertensive crisis refractor to conventional therapy, cerebral edema, disseminated intravascular coagulation (DIC), or multisystem organ failure.

4. SPASMS is a pneumonic used to remember the care for a client eperiencing preeclampsia. SPASMS stands for: S – Significant blood pressure changes without warning P – Proteinuria is a serious sign of renal involvement A – Arterioles are affected by vasospasms that result in endothelial damage and leakage of intravascular fluid into the interstitial spaces. Edema results. S - Significant laboratory changes (mostly notably, liver function tests {LFTs} and the platelet count) signal worsening of the disease. M - Multiple organ systems can be involved: cardiovascular, hematological, hepatic, renal, and central nervous system. S - Symptoms appear after 20 weeks of gestation.

Rationale: Preeclampsia is a multisystem, vasopressive disease process that targets the cardiovascular, hematological, hepatic, renal, and central nervous systems. It is a disease of the placenta where there is a distinctive termed “acute artherosis,” which is fat accumulation in the placental arteries. The placentas also exhibit a greater degree of infarction (necrosis related to decreased blood supply). Both of these pathological changes lead to decreased placental perfusion and placental hypoxia. Along with the decreased placental perfusion, there is a placental production of endothelin (a toxic substance to the endothelial cells), which then leads to vasospasms and endothelial cell damage. In return, there is increased thromboxane (a compound synthesized in platelets from a prostaglandin) to prostacyclin/increased senstivity to angiotension II, fluid shifts from intravascular to intracellular space (decreased plasma volume and increased hematocrit), which leads to edema, and intravascular coagulation. Changes occur within the uteroplacental arteriole lesions which can cause intrauterine growth restrictino, abruptio placentae, and increased uterine contractility; glumerular damage which causes proteinuria, increased plasma uric acid and creatinine, oliguria, and increased sodium retention; generalized edema leading to visible edema of face, hands, and abdomen, along with pitting edema after 12 hours bedrest; cortical brain spasms leading to headaches, hyperreflexia, and seizure activity; pulmonary edema causing dyspnea; retinal arteriolar spasms causing blurred vision and scotoma; hemolysis of RBCs leading to decreased hemoglobin and maternal hyperbilirubinemia; hepatic microemboli and liver damage which causes elevated liver enzymes (AST and LDH, nausea and vomiting, epigastric pain, right upper quadrant pain, decreased blood glucose, and liver rupture; and platelet aggregation and fibrin deposition causing a low platelet count (thrombocytopenia) and DIC.

5. When administering magnesium sulfate, what should you monitor with the patient? Maternal vital signs along with neurological status RR should be at least 16/min before each dose FHR and pattern urine output deep tendon reflexes (DTRs) IV flow rate serum magnesium levels to assess for magnesium sulfate toxicity Administer calcium gluconate (the antidote for magnesium sulfacte toxicity) whenever the patient’s RR is < 12 and d/c the magnesium sulfate infusion.

Rationale: Be sure to explain the purpose and side effects of the medication to the patient and her companion. Explain she may feel warm and become flused, experience nausea and vomiting, visual blurring, and headaches. Do not ever abbreviate magnesium. Always use an infusion pump for administration and run it as a piggyback. Monitor pulse, BP, RR, and ECG frequently throughout therapy. RR should be 16/min before each dose. Monitor neurological status before and during therapy. Institute seizure precautions. Keep room quiet and darkened to decrease likelihood of triggering seizure activity. Patellar reflexes should be tested before each dose and if they are absent, no additional dose should be administered until a positive response returns. Monitor intake/output. Urine should be maintained at level of at least 100 mL/4 hr. Serum magnesium and renal function should be monitored throughout therapy (normal=1.5-2; therapeutic=4-7; ECG changes=5-10; loss of reflexes=8-12; respiratory distress=15; cardiac arrest=25). Have 10% calcium gluconate available incase toxicity occurs. Administer 10 mL IV over 1-3 minutes until signs/symptoms are reversed. After delivery, monitor the newborn for hypotension, hyporeflexia, and respiratory distress.

6. If a patient is experiencing magnesium toxicity, what would your assessment findings be? Flushing sweating hypotension (sudden onset) depressed DTR (hyporeflexia) decreased urine output (oliguria) CNS depression (respiratory depression) indicators of fetal compromise

Rationale: Magnesium sulfate can cause respiratory depression, depressed reflexes, flushing, sweating, hypotension, bradycardia, extreme muscle weakness, decreased urine output, pulmonary edema, diarrhea, drowsiness, arrhythmias, hypothermia and elevated serum magnesium levels (<7.5). High doses can cause loss of DTR, heart block, respiratory paralysis, and cardiac arrest. Call HCP if respirations are less than 12 breaths/minute and discontinue the magnesium sulfate infusion or if any other adverse effects occur. Fetal heart rate should be monitored and after delivery the newborn should be monitored for hypotension, hyporeflexia, and respiratory depression.

Sources for Information: Preeclampsia. (2016, September 15). Retrieved February 17, 2017, from http://emedicine.medscape.com/article/1476919-overview http://americanpregnancy.org/pregnancy-complications/preeclampsia/ Ward, S. L., & Hisley, S. M. (2009). Maternal-child nursing care: Optimizing outcomes for mothers, children, and families. pps 351-360, 518. Philadelphia: F.A. Davis. pages 351-360; 518 Silvestri, L. A., & Silvestri, A. E. (2017). Saunders comprehensive review for the NCLEX-RN examination (7th ed.). St. Louis, MO: Elsevier. pages 320-322; 393-394