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 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

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

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

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

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

Clinical Manifestations Clinical Manifestation HYPERTENSION Earliest and The Most Dependable Indicator of PIH of PIH

Hypertension B/P = 140 / 90 if have no baseline 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

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

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

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

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

Significant Lab Work Changes in Serum Chemistry Decreased urine creatinine clearance ( mL/ min) Increased BUN (12-30 mg./dl.) Increased serum creatinine ( mg./dl) Increased serum uric acid ( mg./dl.)

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

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.

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

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

Condition is Worsening

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

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

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

Nausea and Vomiting Epigastric pain –often sign of impending coma

Pre-Eclampsia Mild Severe B/P 140/90 160/110 Protein Edema 1+, lower legs Weight 2lb. / week Reflexes brisk ( 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

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 g/day » maintain sodium intake » Caffeine avoidance –Weigh daily at the same time –Keep record of fetal movement - kick counts –Check urine for Protein

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

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

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

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

Magnesium Sulfate DNURSING 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 mg/dl Therapeutic is 4-8mg/dl. Toxicity - >9mg/dl; Absence of reflexes is >10 mg/dl; Respiratory arrest is mg/dl; cardiac arrest is > 15 mg/dl. Have Calcium Gluconate available as antagonist

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

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

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!

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

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

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

Monitor Fetal Well-Being uFETAL MONITORING-- assessing for late decelerations. uNST -- Non-stress test uOCT --oxytocin challenge test uIf all else fails ---- Deliver the baby

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

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

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.

HELLP Assessment: 1. Right upper quadrant pain and tenderness 2. Nausea and vomiting 3. Edema 4.Flu like symptoms 5.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/

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

Heart Disease in Pregnancy

Cardiac Response in All Pregnancies ¤ Increase in Cardiac Output 30% - 50% ¤ Expanded Plasma Volume ¤ Increase in Blood (Intravascular) Volume Every Pregnancy affects the cardiovascular system 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

Effects of Heart Disease on Pregnancy  Growth Retarded Fetus  Spontaneous Abortion  Premature Labor and Delivery

Effects of Pregnancy on Heart 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

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

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

ª Nursing Care - Antepartum ªDecrease Stress –Teach the importance of REST! –watch weight –assess for infections - stay away from crowds –assess for anemia –assess home responsibilities ªTeach signs of cardiac decompenstion

Key Point to Remember Signs of Congestive Heart Failure ªCough (frequent, productive, hemoptysis) ªDyspnea, Shortness of breath, orthopnea ªPalpitations of the heart ªGeneralized edema, pitting edema of legs and feet ªMoist rales in lower lobes, indicating pulmonary edema

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

Key point to remember ! Never eat foods high in Vitamin K while on an anticoagulant! ( raw green leafy vegetables)

Nursing Care Intrapartum ªLabor in an upright or side lying position ªRestrict fluids ªOn O 2 per mask throughout labor and cardiac monitoring. ªSedation / epidural given early Report fetal distress or cardiac failure ªStage 2 - gentle pushing, high forceps delivery

Nursing Care Postpartum  The immediate post delivery period is the MOST significant and dangerous for the mom with cardiac problems  Following delivery, fluid shifts from extravascular spaces into the blood stream for excretion  Cardiac output increases, blood volume increases  Strain on the heart! Watch for cardiac failure

Test Yourself ! Mrs. B. has mitral valve prolapse. During the second trimester of pregnancy, she reports fatigue and palpitations during routine housework. As a cardiac patient, what would her functional classification be at this time? a. Class I b. Class II c. Class III d. Class IV

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