Structural Disorders Fetal Demise / Intrauterine Fetal Death Structural Disorders Fetal Demise / Intrauterine Fetal Death DEFINITION: Death of a fetus.

Structural DisordersStructural Disorders

Fetal Demise / Intrauterine Fetal DeathFetal Demise / Intrauterine Fetal Death

Structural DisordersStructural Disorders

Fetal Demise / Intrauterine Fetal DeathFetal 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 FACTORSPREDISPOSING FACTORS

PRIMIGRAVIDA MULTIPLE PREGNANCY

VASCULAR DISEASE

UNDER 17 AND OVER 35

LOWER SOCIOECONOMIC STATUSSevere malnutrition, decrease Protein intake

Inadequate or late prenatal care

FAMILY HISTORY

HYDATIFORM MOLE

Diabetes, renal

PATHOLOGICAL CHANGESPIH is due to:

GENERALIZED ARTERIOLAR CYCLICVASOSPASMS

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 DiseaseMulti-system failure Disease

Clinical Manifestations

Clinical Manifestation

HYPERTENSIONHYPERTENSION

Earliest and The Most Earliest and The Most Dependable IndicatorDependable Indicator of PIHof 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; 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 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.)

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 140/90 160/110Protein 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 detachmentGI, Hepatic 0 N & V, Epigastric pain, changes in liver enzymesCNS 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 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, D-Dimer

Hospital ManagementNursing 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 Medications1. Anticonvulsant -- Magnesium Sulfate2. Sedative -- Diazepam (Valium)3. Apresoline

Assess Reflexes

Assess Subjective Symptoms

Keep Emergency Supplies Available

Magnesium SulfateACTION

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 CareHospital Management



3. Promote Diuresis



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 orDo NOT want to decrease the B/P too low ortoo rapidly. Best to keep diastolic ~90.too rapidly. Best to keep diastolic ~90.Need to maintain uteroplacental perfusion!Need to maintain uteroplacental perfusion!




3. Promote Diuresis



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




3. Promote Diuresis



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 HELLPHemolysis 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.

HELLPAssessment: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 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

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 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

Teach about diethigh in iron, proteinlow 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

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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Structural Disorders Fetal Demise / Intrauterine Fetal Death Structural Disorders Fetal Demise / Intrauterine Fetal Death DEFINITION: Death of a fetus.

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