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Structural Disorders Fetal Demise / Intrauterine Fetal Death

Structural Disorders Fetal Demise / Intrauterine Fetal Death. DEFINITION: Death of a fetus after the age of viability. Interventions and Nursing Care Allow patient to decide when she wants to deliver

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Structural Disorders Fetal Demise / Intrauterine Fetal Death

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  1. Structural DisordersFetal Demise / Intrauterine Fetal Death DEFINITION: Death of a fetus afterthe age of viability

  2. Interventions and Nursing Care • Allow patient to decide when she wants to deliver • Most women go into labor on their own in 2 weeks, so may wait for labor to begin spontaneously • Induce labor • Prostaglandin (Prostin E) causes smooth muscles to contract: Side effects - nausea, vomiting, diarrhea • Cytogel • Provide with Emotional Support, allow to hold baby

  3. Assessment: 1. First indication is usually NO fetal movement 2. NO fetal heart tones Confirmed by ultrasound 3. Decrease in the signs and symptoms of pregnancy

  4. PREGNANCY INDUCED HYPERTENSION A hypertensive disease of pregnancy. Known as pre-eclampsia and eclampsia. Pre-eclampsia = hypertension, proteinuria, edema Eclampsia = other signs plus convulsions It develops between the 20th and 24th week of gestation and disappears after the tenth day postpartum

  5. MULTIPLE PREGNANCY PRIMIGRAVIDA UNDER 17 AND OVER 35 HYDATIFORM MOLE PREDISPOSING FACTORS FAMILY HISTORY VASCULAR DISEASE Diabetes, renal LOWER SOCIOECONOMIC STATUS Severe malnutrition, decrease Protein intake Inadequate or late prenatal care

  6. PATHOLOGICAL CHANGES PIH is due to: INCREASED PERIPHERAL RESISTANCE; IMPEDED BLOOD FLOW ( in blood pressure) GENERALIZED ARTERIOLAR CYCLIC VASOSPASMS Endothelial CELL DAMAGE (decrease in diameter of blood vessel) Intravascular Fluid Redistribution Decreased Organ Perfusion Multi-system failure Disease

  7. Clinical ManifestationsClinical Manifestation HYPERTENSION Earliest and The Most Dependable Indicator of PIH

  8. Hypertension B/P = 140 / 90 if have no baseline. 1. 30 mm. Hg. systolic increase or a 15 mm. Hg. diastolic increase (two occasions four to six hours apart) 2. Increase in MAP > 20 mm.Hg over baseline or >105 mm. Hg. with no baseline Positive Roll Over Test

  9. Rationale for HYPERTENSION The blood pressure rises due to: ARTERIOLAR VASOSPASMS AND VASOCONSTRICTION causing (Narrowing of the blood vessels) an increase in peripheral resistance fluid forced out of vessels HEMOCONCENTRATION Increase blood viscosity = Increased hematocrit

  10. Key Point to Remember ! HEMOCONCENTRATION develops because: Vessels became narrowed forcing fluid to shift Fluid leaves the intracellular spaces and moves to extracellular spaces Now the blood viscosity is increased (Hemocrit is increased) **Very difficult to circulate thick blood

  11. Test Yourself ! Which of these readings indicates hypertension in the patient whose blood pressure normally is 100 / 60 and MAP of 77? a. 120 / 76; MAP 96 b. 110 / 70; MAP 83 c. 130 / 80; MAP 98 d. 125 / 70; MAP 88

  12. Proteinuria With Renal vasospasms, narrowing of glomular capillaries which leads to decreased renal perfusion and decreased glomerular filtration rate (damage to glomeruli) PROTEINURIA Protein leaks across the membrane, tubules cannot reabsorb The degree of PROTEINURIA reflects the severity of the disease Spilling of 1+ of protein is significant to begin treatment Oliguria and tubular necrosis may precipitate acute renal failure

  13. Significant Lab WorkChanges in Serum Chemistry • Decreased urine creatinine clearance (80-130 mL/ min) • Increased BUN (12-30 mg./dl.) • Increased serum creatinine (0.5 - 1.5 mg./dl) • Increased serum uric acid (3.5 - 6 mg./dl.)

  14. Weight Gain and Edema • Clinical Manifestation: • Edema may appear rapidly • Begins in lower extremities and moves upward • Pitting edema and facial edema are late signs • Weight gain is directly related to accumulation of fluid

  15. WEIGHT GAIN AND EDEMA Rationale: • Decreased blood flow to the kidneys causes a loss of plasma proteins and albumin • This leads to a decreased colloid osmotic pressure. • A  in COP allows fluid to shift from from intravascular to extravascular. • Now there is an accumulation of fluid in the tissues. • Increased angiotensin and aldostersone triggers retention of sodium and water.

  16. The Nurse Must Know The difference between dependent edema and generalized edema is important. The patient with PIH has generalized edema because fluid is in all tissues.

  17. Placenta With Vasospasms and Vasoconstriction of the the vessels in the placenta. Decreased Placental Perfusion and Placental Aging Positive OCT / Late Decelerations With Prolonged decreased Placental Perfusion: Fetal Growth is retarded - IUGR, SGA

  18. Condition is Worsening

  19. Oliguria – 100ml./4 hrs or less than 30 cc. / hour • Edema moves upward and becomes generalized (face, periorbital, sacral) • Excessive weight gain – greater than 2 pounds per week

  20. Central Nervous System Changes • Cerebral edema -- forcing of fluids to extracellular • Headaches -- severe, continuous • Hyperreflexia • Level of Consciousness changes – changes in affect • Convulsions / seizures

  21. Visual Changes Retinal Edema and spasms leads to: • Blurred vision • Double vision • Retinal detachment • Scotoma (areas of absent or depressed vision)

  22. Nausea and Vomiting • Epigastric pain –often sign of impending coma

  23. Pre-Eclampsia Mild Severe B/P 140/90 160/110 Protein 1+ 2+ 3+ 4+ Edema 1+, lower legs 3+ 4+ Weight <1 lb. / week >2lb. / week Reflexes 1+ 2+ brisk 3+ 4+ (Hyperreflexia) Clonus present Retina 0 Blurred vision, Scotoma Retinal detachment GI, Hepatic 0 N & V, Epigastric pain, changes in liver enzymes CNS 0 Headache, LOC changes Fetus 0 Premature aging of placenta IUGR; late decelerations

  24. Interventions and Nursing Care • Home Management • Decrease activities and promote bed rest • Sedative drugs • Lie in left lateral position • Remain quiet and calm – restrict visitors and phone calls • Dietary modifications • increase protein intake to 70 - 80 g/day • maintain sodium intake • Caffeine avoidance • Weigh daily at the same time • Keep record of fetal movement - kick counts • Check urine for Protein

  25. Hospitalization • If symptoms do not get better then the patient needs to be hospitalized in order to further evaluate her condition. • Common lab studies: • CBC, platelets; type and cross match • Renal blood studies -- BUN, creatitine, uric acid • Liver studies -- AST, LDH, Bilirubin • DIC profile -- platelets, fibrinogen, FSP, D-Dimer

  26. Hospital ManagementNursing Care Goal 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant

  27. Decrease CNS Irritability • Provide for a Quiet Environment and Rest • 1. MONITOR EXTERNAL STIMULI • Explain plans and provide Emotional Support • Administer Medications • 1. Anticonvulsant -- Magnesium Sulfate • 2. Sedative -- Diazepam (Valium) • 3. Apresoline • Assess Reflexes • Assess Subjective Symptoms • Keep Emergency Supplies Available

  28. Magnesium Sulfate • ACTION CNS Depressant, reduces CNS irritability Calcium channel blocker- inhibits cerebral neurotransmitter release • ROUTE IV effect is immediate and lasts 30 min. IM onset in 1 hour and lasts 3-4 hours • Prior to administration: • Insert a foley catheter with urimeter for assessment of hourly output

  29. Magnesium Sulfate • NURSING IMPLICATIONS 1. Monitor respirations > 14-16; < 12 is critical 2. Assess reflexes for hyporeflexia -- D/C for hyporeflexia 3. Measure Urinary Output >100cc in 4 hrs. 4. Measure Magnesium levels – normal is 1.5-2.5 mg/dl Therapeutic is 4-8mg/dl. Toxicity - >9mg/dl; Absence of reflexes is >10 mg/dl; Respiratory arrest is 12-15 mg/dl; cardiac arrest is > 15 mg/dl. • Have Calcium Gluconate available as antagonist

  30. Test Yourself ! A Woman taking Magnesium Sulfate has a respiratory rate of 10. In addition to discontinuing the medication, the nurse should: a. Vigorously stimulate the woman b. Administer Calcium gluconate c. Instruct her to take deep breaths d. Increase her IV fluids

  31. Nursing CareHospital Management 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant

  32. Control Blood Pressure • Check B / P frequently. • Give Antihypertensive Drugs • Hydralzine ( apresoline) • Labetalol • Aldomet • Procardia • Check Hemocrit * Do NOT want to decrease the B/P too low or too rapidly. Best to keep diastolic ~90. Need to maintain uteroplacental perfusion!

  33. Nursing CareHospital Management 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant

  34. Promote Diuresis **Don’t give Diuretic, masks the symptoms of PIH • Bed rest in left or right lateral position • Check hourly output -- foley cath with urimeter • Dipstick for Protein • Weigh daily -- same time, same scale

  35. Nursing CareHospital Management 1. Decrease CNS Irritability 2. Control Blood Pressure 3. Promote Diuresis 4. Monitor Fetal Well-Being 5. Deliver the Infant

  36. Monitor Fetal Well-Being • FETAL MONITORING-- assessing for late decelerations. • NST -- Non-stress test • OCT --oxytocin challenge test • If all else fails ---- Deliver the baby

  37. Key Point to Remember ! SEVERE COMPLICATIONS OF PIH: • PLACENTAL SEPARATION - ABRUPTIO PLACENTA; DIC • PULMONARY EDEMA • RENAL FAILURE • CARDIOVASCULAR ACCIDENT • IUGR; FETAL DEATH • HELLP SYNDROME

  38. HELLP Syndrome • A multisystem condition that is a form of severe preeclampsia - eclampsia • H = hemolysis of RBC • EL = elevated liver enzymes • LP = low platelets <100,000mm (thrombocytopenia)

  39. Etiology of HELLP Hemolysis occurs from destruction of RBC’s Release of bilirubin Elevated liver enzymes occur from blood flow that is obstructed in the liver due to fibrin deposits Vascular vasoconstriction  endothelial damage  platelet aggregation at the sites of damage  low platelets.

  40. HELLP Assessment: 1. Right upper quadrant pain and tenderness 2. Nausea and vomiting 3. Edema • Flu like symptoms • Lab work reveals – a.anemia – low Hemoglobin b.thrombocytopenia – low platelets. < 100,000. c.elevated liver enzymes:    -AST asparatate aminotransferase (formerly SGOT) exists within the liver cells and with damage to liver cells, the AST levels rise > 20 u/L.   - LDH – when cells of the liver are lysed, they spill into the bloodstream and there is an increase in serum. > 90 u/L/

  41. HELLP • Intervention: • 1. Bedrest – any trauma or increase in intra- abdominal pressure could lead to rupture of the liver capsule hematoma. • 2. Volume expanders • 3. Antithrombic medications

  42. Heart Disease in Pregnancy

  43. Cardiac Response in All Pregnancies Every Pregnancy affects the cardiovascular system • Increase in Cardiac Output 30% - 50% • Expanded Plasma Volume • Increase in Blood (Intravascular) Volume A woman with a healthy heart can tolerate the stress of pregnancy, but a woman with a compromised heart is challenged Hemodynamically and will have complications

  44. Effects of Heart Disease on Pregnancy • Growth Retarded Fetus • Spontaneous Abortion • Premature Labor and Delivery

  45. Effects of Pregnancy onHeart Disease The Stress of Pregnancy on an already weakened heart may lead to cardiac decompensation (failure). The effect may be varied depending upon the classification of the disease

  46. Classification of Heart Disease • Class 1 • Uncompromised • No alteration in activity • No anginal pain, no symptoms with activity • Class 2 • Slight limitation of physical activity • Dyspnea, fatigue, palpitations on ordinary exertion • comfortable at rest p. 669

  47. Class 3 • Marked limitation of physical activity • Excessive fatigue and dyspnea on minimal exertion • Anginal pain with less than ordinary exertion • Class 4 • Symptoms of cardiac insufficiency even at rest • Inability to perform any activity without discomfort • Anginal pain • Maternal and fetal risks are high p. 669

  48. Nursing Care - Antepartum • Decrease Stress • Teach the importance of REST! • watch weight • assess for infections - stay away from crowds • assess for anemia • assess home responsibilities • Teach signs of cardiac decompenstion

  49. Key Point to RememberSigns of Congestive Heart Failure • Cough (frequent, productive, hemoptysis) • Dyspnea, Shortness of breath, orthopnea • Palpitations of the heart • Generalized edema, pitting edema of legs and feet • Moist rales in lower lobes, indicating pulmonary edema

  50. Teach about diet high in iron, protein low in sodium and calories ( fat ) Watch weight gain Teach how to take their medicine • Supplemental iron • Heparin, not coumarin – monitor lab work • Diuretics – very careful monitoring • Antiarrhythmics –Digoxin, quinidine, procainamide. *Beta-blockers are associated with fetal defects. Reinforce physicians care

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