Structural Disorders Fetal Demise / Intrauterine Fetal Death

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Structural DisordersFetal Demise
/ Intrauterine Fetal Death

• DEFINITION
• Death of a fetus after the age of
  viability

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• 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

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• 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

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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

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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
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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
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Clinical ManifestationsClinical Manifestation


HYPERTENSION
Earliest and The Most Dependable Indicator
of PIH
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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 gt 20 mm.Hg over baseline or gt105
mm. Hg. with no baseline
Positive Roll Over Test
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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

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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

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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

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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
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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.)

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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

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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.

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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.

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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
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• Condition
• is
• Worsening

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• 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

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Central Nervous System Changes

• Cerebral edema -- forcing of fluids to
  extracellular
• Headaches -- severe, continuous
• Hyperreflexia
• Level of Consciousness changes changes in
  affect
• Convulsions / seizures

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Visual Changes

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

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• Nausea and Vomiting
• Epigastric pain often sign of impending coma

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Pre-Eclampsia Mild Severe

• B/P 140/90
  160/110
• Protein 1 2
  3 4
• Edema 1, lower legs
  3 4
• Weight lt1 lb. / week
  gt2lb. / 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
• 
  

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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

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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

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Hospital ManagementNursing Care Goal

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

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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

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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

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Magnesium Sulfate

• NURSING IMPLICATIONS
• 1. Monitor respirations gt 14-16 lt 12 is
  critical
• 2. Assess reflexes for hyporeflexia -- D/C
  for
• 
  hyporeflexia
• 3. Measure Urinary Output gt100cc in 4 hrs.
• 4. Measure Magnesium levels normal is
  1.5-2.5 mg/dl
• Therapeutic is 4-8mg/dl. Toxicity -
  gt9mg/dl Absence of reflexes
• is gt10 mg/dl Respiratory arrest is
  12-15 mg/dl cardiac arrest is
  
• gt 15 mg/dl.
• Have Calcium Gluconate available as antagonist

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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

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Nursing CareHospital Management

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

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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!
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Nursing CareHospital Management

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

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Promote Diuresis

• Dont 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

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Nursing CareHospital Management

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

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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

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Key Point to Remember !

• SEVERE COMPLICATIONS OF PIH
• PLACENTAL SEPARATION - ABRUPTIO PLACENTA DIC
• PULMONARY EDEMA
• RENAL FAILURE
• CARDIOVASCULAR ACCIDENT
• IUGR FETAL DEATH
• HELLP SYNDROME

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HELLP Syndrome

• A multisystem condition that is a form of severe
  preeclampsia - eclampsia
• H hemolysis of RBC
• EL elevated liver enzymes
• LP low platelets lt100,000mm
  (thrombocytopenia)

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Etiology of HELLP

• Hemolysis occurs from destruction of RBCs
• 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.

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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. lt
  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 gt 20
  u/L.
•   - LDH when cells of the liver
  are lysed, they spill into
• the bloodstream and there is an
  increase in serum.
• gt 90 u/L/

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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

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• ?Heart Disease in
• Pregnancy

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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
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Effects of Heart Disease on Pregnancy

• Growth Retarded Fetus
• Spontaneous Abortion
• Premature Labor and Delivery

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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

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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

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• 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

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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

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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
• 
  

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

• Labor in an upright or side lying position
• Restrict fluids
• On O2 per mask throughout labor and cardiac
  monitoring.
• Sedation / epidural given early
• Report fetal distress or cardiac failure
• Stage 2 - gentle pushing, high forceps delivery

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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

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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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The End

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