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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 l.jpg
Structural DisordersFetal Demise / Intrauterine Fetal Death

DEFINITION:

Death of a fetus afterthe 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 > 20 mm.Hg

over baseline or >105 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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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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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


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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 > 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


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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

**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


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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 <100,000mm (thrombocytopenia)


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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.


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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. < 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/


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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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