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Discuss the pathology, treatment, and nursing care of pregnant women with
anemia.
Antenatal Testing:
Ascertain fetal well-being, growth, and development
Indications:
Performed if there is a reason to believe the fetus has a problem or
may develop one
Maternal risk factors that indicate need antenatal testing:
o Medical conditions (DM, HTN, anemia)
o Demographic factors:
Over age 35 or younger than 17
Family history of genetic disorder
Poverty
Inadequate prenatal care
o Obstetric factors:
Previous delivery of low birth weight infant, or large for
gestational age infant
Multifetal gestation (twins)
Previous unexplained fetal loss
Hydramnios (too much amniotic fluid), oligohydramnios
(deficiency of amniotic fluid)
Preterm labor or prolonged labor
o Maternal Factors
Excessive weight gain
Inadequate or poor pattern of weight gain
Less than/greater than ideal weight at time of
conception
1st Trimester Testing:
Ultrasound (any gestation)
o confirm pregnancy and location of pregnancy
o determine gestational age
o confirm viability (ability to live)
o provide guidance in performing CVS and amniocentesis
Chorionic Villi Sampling (9-12 weeks)
o Sampling the chorionic villi of placenta
o Recommended for those at high risk of delivering infants with
genetic anomalies
Over 35, history of previous fetus w/ anomalies,
carriers of genetic defects
o Transabdominally or transcervically under ultrasound
guidance
o Risks:
Fetal limb reduction if performed prior to 9 weeks
PROM, SAB
Rh sensitization (Rhogam given post-procedure)
infection
o Advantages:
Results available within 24 hrs
Nuchal Translucency Testing (NTT) (11-13 weeks)
o Ultrasound to assess fluid accumulation between spine and
neck of fetus
o If nuchal folds greater than 3 mm, increased risk for
Down’s
o Screening, not Dx
2nd Trimester:
Amniocentesis (15-20 weeks)
o Used for genetic diagnosis
o Used in 3rd (30-39 week) to assess fetal lung maturity
LS ratio 2:1 is good
o Aspirate amniotic fluid
MSAFP and Quadruple screens (14-22 weeks)
o 15-18 most accurate
Doppler Flow Study (2nd trimester)
o Used to detect uteroplacental insufficiency
Percutaneous Umbilical Blood Sampling (PUBS)/Cordocentesis
o Cord punctured close to placental insertion
o used to obtain pure fetal blood from umbilical cord
1-4 ml of blood
3rd Trimester:
Biophysical profile
Non Stress Test
Contraction Stress Test
Fetal movement counts (26-32 weeks)
Dosage Calculation
Complications Prior to Pregnancy 8/24/2015 11:32:00 AM
Iron-Deficiency:
Most common medical complication of pregnancy
Iron needed to synthesize HgB
Defiency of iron will result in less HgB and O2 transportation
Patho:
Expansion of plasma volume without normal expansion of maternal
HgB mass
Pregnant woman needs 1000 mg iron intake during the pregnancy
o Body only retains 200mg through amenorrhea
Complications:
Maternal – may be asymptomatic
o More susceptible to infection
o Increased chance of preeclampsia and postpartal hemorrhage
o Intolerance of minimal blood loss during birth
o Cardiac failure (if HgB < 6)
Fetal
o Low birth weight
o Prematurity
o Stillbirth
o Neonatal death in severe cases
o Not deficient at birth, but may have lower iron stores and are
at increased risk for iron deficiency anemia during infancy
Treatment:
Prevention – 27 mg daily
Treatment – 60-120mg daily (larger dose for twins)
Iron-rich diet
Stool softeners to prevent constipation
Nursing Roles:
Client teaching:
o Take iron with Vit C to increase absorption
o Absorption decreased if taken with meals
But, GI upset is more likely if taken on empty stomach
So eat
o Stool will turn black
o Keep out of reach of children (fatal)
Thalassemia Anemia
Autosomal recessive disorder characterized by defect in alpha or beta chain
of HgB molecule
Patho:
Defect causes shortened RBC life
^ Results in extreme erythropoiesis in liver, spleen, and bones
o hepatosplenomegaly and bony malformations
Heterozygous = Thalassemia minor
Mild anemia only symptom
Homozygous = Thalassemia major
No symptoms present for first few months of life
Once infants start producing adult-type HgB:
o They develop severe anemia
o Dependent on transfusions
Eventually develop iron overload
Must get iron chelation therapy to avoid damage to liver
and heart
Without chelation therapy, they don’t live past 20 or 30
Maternal Complications:
Minor = mild anemia
o Must be distinguished from iron deficiency because they
should not receive iron supplements unless she is iron
deficient
o Iron-deficiency = low serum iron and ferritin levels
o Thalassemia minor = normal iron and ferritin levels
Major = pregnancy is rare
o If pregnant severe anemia, needs transfusion, and at risk
for CHF
Treatment:
Folic Acid supplements (NOT IRON)
Transfusion and chelation therapy
Avoid exposure to infections and seek treatment promptly if
infected
Keep hydrated, oxygenated, and free of infection
Complications Due to Pregnancy 8/24/2015 11:32:00 AM
Hypertensive Disorders:
Account for 17% of maternal deaths in US
Chronic HTN – HTN diagnosed before pregnancy or prior to 20 weeks
gestation
4 types of HTN disorders:
Preeclampsia/Eclampsia
Gestational HTN
Transient Gestational HTN
Chronic HTN with superimposed preeclampsia
Preeclampsia
Proteinuria and HTN that occurs after 20 weeks gestation
Cause is unknown
May be abnormal prostaglandin action, dietary deficiencies (Ca and
Zn), or genetic predisposition
Risk Factors:
Mother over 40 or under 17
Primigravidas (1st child)
DM
Chronic HTN
Close family with history
Complications:
Placental abruption
Premature
IUGR
Fetal hypoxia
CVA
Patho:
KNOW CHART ON 2.7 Page 2
Vasospasms causes endothelial cell damage
Vasospasms and cell damage cause poor organ perfusion
o Affects uteroplacental unit, brain, liver, and kidneys
Goes from mild preeclampsia, to severe preclampsia to either
eclampsia or HELLP syndrome
o Eclampsia
seizure activity (or coma) in woman diagnosed with
preeclampsia with no medical history of seizures
Can be focal, multifocal, or generalized
o HELLP syndrome
Severe preeclampsia with:
Hemolysis (low Hct)
Elevated Liver enzymes
Low Platelets (less than 100,000)
Give birth regardless of fetal age if maternal/fetal
condition worsens
Manifestations:
High BP and proteinuria
Neuro symptoms
o Headache, scotomata (spots in vision), increased blurred
vision, hyperreflexia
Edema (periorbital)
Epigastric or right upper quadrant pain (liver distention)
Abnormal labs (elevated BUN, creatinine, liver enzymes, and clots)
If liver fails:
o Jaundice,
o Increased AST, ALT
If Kidneys fail:
o Elevated BUN/creatinine
o Extreme proteinuria
Worsening Preeclampsia:
o Increasing edema in hands/face – gain of 3 lbs (1.4 kg) in 24
hrs or 4 lbs (1.8 kg) in 3 days
o Worsening headache, visual disturbances, disorientation
o Epigastric pain
o Decreased urinary output - <500 ml/day
o N/V
o Bleeding gums
Diagnosis:
Mild Preeclampsia
o Two BP readings between 140/90 – 159/109 six hours apart
o Proteinuria of 300mg/per day or +1 urine dip
Severe preeclampsia
o Two BP readings at or above 160/110 six hours apart
o Proteinuria of 500mg/per day or +3 urine dip
o Can also have pulmonary edema, cyanosis, epigastric pain,
impaired liver function, thrombocytopenia, and IUGR
Management:
Traditionally delivery regardless of gestational age
o Disease process reverses after birth
o Getting the baby in the NICU is better than the unhealthy
environment of severe preeclampsia
Those at high risk aspirin
Mild:
o At home monitoring of BP and daily weights
o Maintain high protein diet (prevents high edema)
o Fetal movement counts
o Bed rest may be recommended
o Periodic lab testing (platelet counts, uric acid and BUN, liver
enzymes, and 24hr urine for creatinine clearance and total
protein)
o Testing for fetal well-being
Severe:
o Inpatient
o After 34 weeks, may be at home management depending on
maternal and fetal status
o Complete bed rest and dietary restrictions
Left lateral recumbent position
High-protein, moderate sodium (<6g/day)
o Usually have catheter – strict I&O
o BP medicines – hydralazine or labetalol (avoid in asthma &
CHF)
o Seizure prevention meds – mg sulfate
o Meds to promote fetal lung maturity in those mothers who
must deliver preterm – corticosteroids
o Fetal surveillance (non-stress tests and biophysical profile)
o Low stimulation environment
Nursing Process for Preeclampsia:
Antepartum/Intrapartum
o Assessment:
Assess symptoms and VS (differentiate btw mild and
severe)
deep tendon reflexes
lab values
Neuro status (headaches, visual disturbances, seizure
activity)
I/O, edema, and daily weights
Continuous fetal monitoring
o Nursing Dx:
FVE; Risk for injury; Impaired Tissue Perfusion; Anxiety
o Implementation:
Client education
Provide guidance for potential need for and method of
delivery
Emotional support
Administer antihypertensives for acute hypertensive
crisis
Mag Sulfate to prevent eclampsia or seizures
Therapeutic range is 4-8mg
At 4mg – DTR decreases back to normal
levels, 1st indication that it’s working
Have Ca gluconate at bedside
Monitor for toxicity:
Over 9 mg
Check for extreme decreased reflexes
Loss of patellar reflex is right before loss of
respiratory reflex and pulm. paralysis
May occur with decreased urinary output
Corticosteriods to promote fetal lung maturity
Calm, quiet environment
Postpartum:
o Vigilant monitoring of VS, deep tendon reflexes, and neuro
status
o Mag sulfate infusion for 24 hours
Calcium gluconate at bedside
Seizures can occur during 1st 48hrs postpartum
o Monitor I/O, weight, and edema
Diuresis should return
o Monitor lab values
o Client teaching:
Recognized S/S of worsening condition (neuro, visual)
Follow-up appointments
o Promote mother/infant bonding
Nursing Process for Eclampsia:
Assess for signs of impending seizure:
o Change in mental status
o Hyperreflexia (reflexes greater than 2+) and/or clonus
(hyperactive nerves)
o Right upper quadrant or epigastric pain
o Signs of cerebral irritability (severe headache, scotomata)
Nursing Dx:
o Risk for maternal and fetal injury
Implementation (if seizure occurs):
o Maintain airway
o Maintain safety – stay at bedside and call for help
o Monitor duration of seizure and body movement
o Administer Mag Sulfate per protocol
o Once seizure is over:
Put pt on her side
Assess fetal status
Prepare for delivery (C-section)
Support family
Spontaneous Abortion
Pregnancy loss prior to fetal viability (under 20 weeks or under 500g)
No action taken by mother
“miscarriage”
most common cause of bleeding
Caused By:
Result of chromosomal abnormalities (most often)
Teratogen exposure
Chronic medical conditions (DM, SLE)
6 Subsets:
1 GRAM IS ONE ML OF BLOOD LOSS
o peripad
Backache and cramping with bleeding are main indicators of
abortion
o Other less harmful things can cause bleeding
Threatened:
o Manifestations:
Vaginal spotting, light bleeding, uterine cramping,
backache, NO cervical dilation or rupture of membranes
o Treatment:
More symptoms persist more likely the pregnancy
will be lost
Bed rest, pelvic rest
Client education (signs of infection and passage of
tissue)
Inevitable:
o Manifestations:
Vaginal bleeding, uterine cramping, cervical dilation,
rupture of membranes
o Treatment:
Delivery is imminent
Allow natural expulsion
Dilatation and curettage
Incomplete:
o Manifestations:
Heavy vaginal bleeding, severe cramping, cervical
dilation, rupture of membranes, passage of some tissue
o Treatment:
Avoid hypovolemia and shock
Can lead to DIC – disseminated intravascular
coagulation
Overactive clotting
Blood transfusion if necessary
D&C or suction evacuation
Complete:
o Manifestations:
All products are expelled
Cervix is beginning to close
Bleeding starts to subside
o Treatment:
Teach client to watch for excessive bleeding and S/S of
infection
Pelvic rest
Follow-up care
Missed:
o Manifestations:
Fetus dies but is retained in uterus
Uterus stops growing and early symptoms of pregnancy
disappear
o Treatment:
Ultrasound to confirm fetal death
D&C, suction evacuation if less than 12 weeks gestation
Administration of prostaglandins or oxytocin to induce
labor if older than 12 weeks gestation
Can have DIC
Recurrent:
o Manifestations:
Three or more consecutive SABs
o Treatment:
Genetic counseling and thorough exam of reproductive
system
Treat infections or other medical conditions
A cerclage for incompetent cervix
Septic:
o Presence of infection due to not fully passing particles
o May occur after prolonged, unrecognized rupture of
membranes
o May occur if pregnant with IUD in utero
o Common in self-abortion or botched abortion
Ectopic Pregnancy
Implantation of fertilized ovum in any area other than the uterine
endometrium
Responsible for 6% of maternal death due to hemorrhage
Can decrease the chance of subsequent pregnancy due to damage
or destruction of fallopian tubes
Risk Factors:
History of previous ectopic pregnancy
o (increases risk by 10%, 25% in those with multiple previous
ectopic pregnancy)
History of STIs (Chlymidia is common cause)
Pelvic Inflammatory Disease (PID)
Failed tubal ligation or previous tubal surgery (tubes tied)
Presence of IUD
In utero exposure to diethylstilbestrol (DES)
Advanced maternal age
Smoking
Ovulation-inducing medications
Endometriosis
Manifestations:
Missed period
Unusually slow rising hCG levels (n/v)
Lower Abdominal or pelvic pain
o One-sided or diffuse
Vaginal spotting or bleeding
PE reveals adnexal tenderness
Dizziness
Internal hemorrhage
o More commonly slow bleeding and abd becomes rigid and
tender
If rupture occurs:
o Sudden severe lower quadrant abdominal pain
o Profuse hemorrhage
o Hypovolemic shock (even without external bleeding)
Management:
If not ruptured – administer Methotrexate IM
o Folic acid antagonist
o Inhibits embryo cell division and causes regression of tissue
o Decreases hCG levels
Surgical management
o Linear salpigostomy (not ruptured) – incision in tube,
removal of conceptus, leave tube to heal without suturing
o Salpingectomy (ruptured) – removal of tube to control
bleeding and prevent shock
o If woman is in shock, they will make abdominal incision
instead of a laproscopy
Hyperemesis Gravidarum
Persistent, uncontrollable vomiting that begins in the 1st weeks and may
continue throughout pregnancy
Can Result In:
Weight loss, dehydration
Electrolyte imbalance (low K due to dehydration)
Starvation
Caused By:
Unknown
Elevated estrogen or hCG levels
Hyperthyroidism
Vit. B deficiency
Psychological issues (family stressors or ambivalence)
Diagnosis:
Through client report of intractable vomiting
Health care provider findings of dehydration, ketonuria, and five
percent weight loss of pre-pregnancy weight
o Ketonuria – using protein as a fuel source because they are
throwing up all their carbs that can be used for energy
Body starts breaking down fat and glucose in cells
Ultrasound to rule out trophoblastic pregnancy
Management:
Ruling out other causes (ultrasound to rule out molar)
Methods of controlling morning sickness
o Crackers by bedside, avoid triggers
Antiemetics and Pyridoxine (Vit. B6) for 1st line pharm therapy for
n/v
Hospitilize if treatment isn’t working and pt shows signs of
dehydration, electrolyte imbalance, and hemoconcentration
Inpatient:
o Initially: NPO, IVF for dehydration
KCl added to prevent hypokalemia
Replacement of thiamine (vit. B1) and pyridoxine (vit.
B6) important to correct deficiencies to prevent
peripheral neuropathy
Desired urine output is a minimum of 1000 ml/day
o TPN or tube feeding (if non-responsive to IV fluids)
o Stabilize weight loss
Nursing Process:
Assessment:
o Maternal VS
o I/O, daily weights
o Skin turgor, mucous membranes
o Fetal growth/development
Implementation:
o Avoid smells that trigger N/V and heat/humidity
o 5-6 smaller high-carb, low-fat meals instead of three larger
meals
carbonated beverages between meals in small amounts
high-protein snacks
After stabilization progressive diet
low fat soft diet and complex carbs with limited
liquids
o administer antiemetics
o client education
o emotional support
o avoid fatty foods and temperature extremes
o rest with feet up and head elevated
High Risk Pregnancies 8/24/2015 11:32:00 AM
Rh Incompatibility:
Rh blood group present on surface of erythrocytes
If Rh- person is exposed to Rh+ blood:
o Antibody-antigen response – sensitized
Maternal IgG antibodies produced
hemolysis/destruction of fetal RBCs
Patho
Small amount of fetal blood crosses placenta
Rh- mother, Rh+ fetus
Maternal IgG antibodies produced
o Results in positive Coombs tests
Hemolysis of fetal red blood cells
Rapid production of erythroblasts
Hyperbilirubinemia
RhD alloimmunization
o Rh incompatibility
Screening:
First prenatal visit
o Maternal blood type; Rh factor antibody screen
Sensitization may occur antepartally
Rh immune globulin (Rhogam given @28 weeks and within 72
hours of birth - if positive fetus/newborn)
Treatment:
Administration of Rh immune globulin RhoGam
o When there is any chance of maternal and fetal blood
exposure/mixing
o At 28 weeks if father is Rh+ (if mother is not already
sensitized)
If she already has antibodies, there is no point
If mother is positive for antibodies:
o Early birth
Ideally, wait until fully developed
If severe, may deliver earlier
o Intrauterine transfusion