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

PRIMIGRAVIDA
UNDER 17 AND OVER 35

HYDATIFORM MOLE

FAMILY HISTORY

MULTIPLE PREGNANCY

PREDISPOSING FACTORS

VASCULAR DISEASE
Diabetes, renal
LOWER SOCIOECONOMIC STATUS
Severe malnutrition, decrease Protein intake
Inadequate or late prenatal care

PATHOLOGICAL CHANGES
PIH is due to:
GENERALIZED
ARTERIOLAR
CYCLIC
VASOSPASMS
(decrease in diameter
of blood vessel)

INCREASED PERIPHERAL
RESISTANCE;
IMPEDED BLOOD FLOW
(
in blood pressure)

Endothelial
CELL DAMAGE
Intravascular
Fluid Redistribution
Decreased Organ
Perfusion

Multi-system failure Disease

Clinical Manifestations
Clinical Manifestation
HYPERTENSION

Earliest and The Most

Dependable Indicator
of PIH

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

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;
b. 110 / 70;
c. 130 / 80;
d. 125 / 70;

MAP 96
MAP 83
MAP 98
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 (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.)

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 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.

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

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
Protein
Edema
Weight

140/90
1+ 2+
1+, lower legs
<1 lb. / week

Reflexes

1+ 2+ brisk

160/110
3+ 4+
3+ 4+
>2lb. / week
3+ 4+ ( Hyperreflexia)
Clonus present

Retina

GI, Hepatic

CNS

Fetus

Blurred vision, Scotoma

Retinal detachment
N & V, Epigastric pain,
changes in liver enzymes
Headache, LOC changes
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 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

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, DDimer

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
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

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
**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

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

FETAL MONITORING-- assessing for late
decelerations.
NST -- Non-stress test
OCT --oxytocin challenge test
If 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 <100,000mm
(thrombocytopenia)

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.

Assessment:
1.
2.
3.
4.
5.

HELLP

Right upper quadrant pain and tenderness

Nausea and vomiting
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/

HELLP
Intervention:
1. Bedrest any trauma or increase in intraabdominal 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

Every Pregnancy affects the cardiovascu

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

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

 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

Key Point to Remember

Signs 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

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. *Betablockers 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
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

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

The End

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