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Treatment includes:
Any degree of glucose intolerance that has
Restricting dietary intake of calories &
its onset or it is first diagnosed during
pregnancy
carbohydrates
Risk factors: Obesity, women w/ prior GDM, Educating pt on monitoring blood glucose &
glycosuria, strong family history of DM,
diet & exercise management
Educating
pt on s/s of hypoglycemia &
over 30 yrs
Symptoms may disappear a few weeks
hyperglycemia w/ careful monitoring of
following delivery
fetus for macrosomia
50% of women develop DM within 5 yrs
3 meals & 3 snacks (one at bedtime)
Risks to the fetus: spontaneous abortion,
Administering insulin to the client for
infection, hydramnios, ketoacidosis,
glucose control as prescribed if needed
hypoglycemia, hyperglycemia (can cause Client instruction on self-administration of
insulin
macrosomia), hydramnios (can cause
Oral hypoglycemic are contraindicated due
overdistention of uterus, premature
to possible teratogenic effects
rupture of membranes, preterm labor,
Instruct pt to perform daily kick counts to
hemorrhage), preeclampsia/eclampsia,
assure fetal well-being
polycythemia, hyperbilirubinemia,
respiratory distress syndrome, neural tube Keep 2 IV lines, one with 5% dextrose
solution & one with a saline solution
effects (spina bifida)
NANDAs
Altered nutrition < body requirements
Risk for fetal/mother injury
Risk for noncompliance w/ diabetic diet
Risk for infection
Notes:
Maternal insulin requirements decrease
dramatically during labor
Calorie needs increase during lactation to
500-800 kcal above prepregnant
requirements & insulin must be adjusted
accordingly
Women should be reassessed 6 wks
postpartum to determine whether her
glucose levels are normal
Monitor BP frequently
Observe pt for behaviors indicative of shock
(pallor, clammy skin, perspiration,
dyspnea, restlessness)
Count & weigh pads to assess amount of
bleeding over a given time period; save
clots/tissues expelled
Assess fetal heart tones w/ Doppler if > 12
wks
Prepare for IV therapy
Have O2 available
Collect & organize data, including
antepartal history, onset of bleeding
episode, laboratory studies
Notify physician or nurse-midwife
Obtain order to type & crossmatch for blood
Assess coping mechanisms of the woman in
crisis. She may feel quilty
Give emotional support, explain clearly
procedures, and communicate her status
to family. Prepare woman for possible fetal
loss.
Assess familys response to situation
ECTOPIC PREGNANCY
Implantation of fertilized ovum in a site
other than endometrial lining of the uterus
Occurs when the fertilized ovum is
prevented or slowed in its passage
through the tube & thus implants before it
reaches the uterus, usually in the fallopian
tube, which can result in a tubal rupture
causing a fatal hemorrhage
Risk factors: PID, contraceptive IUD,
congenital anomalies of tube,
endometriosis, previous tubal surgery
Initially symptoms of pregnancy
hCG present in blood & urine
Chorionic villi grow into the tube wall or
implantation site
Rupture & bleeding into abdominal wall
occurs
S/S: sharp unilateral pain, syncope, referred
shoulder pain, lower abdominal pain,
vaginal bleeding, adnexal tenderness.
NANDAs
Acute pain
Anticipatory grieving
Nursing Interventions:
Take VS, check skin color & urine output
Determine level of pain
Monitor for signs of shock
Methotrexate injection IM to inhibit cell
division & enlargement of the embryo.
Prevents rupture of fallopian tube in order
to preserve it if future pregnancy is
desired
Replacement of fluid loss & maintenance of
electrolyte imbalances
Provide pt education & psychological
support
Prepare client for surgery & postoperative
nursing care
Salpingostomy: via laparoscope. Incision
made lengthwise & the products of
conception are gently removed. Surgical
incision is left open & allowed to close
naturally. Possible before rupture.
Salpingectomy (removal of the tube): via
laparoscope. If the tube is ruptured or if
future childbearing is not an issue.
Note: Rh- women nonsensitized women are
given Rh- immune globulin to prevent
sensitization
chromosomes
S/S: vaginal bleeding, elevated serum hCG,
Chemotherapy if choriocarcinoma
(Methotrexate)
Nursing Interventions:
Monitor for s/s of trophoblastic disease:
rapid uterine growth, vaginal bleeding
accompanied by discharge, excessive
vomiting (hyperemesis gravidarum) due to
excessive hCG levels, symptoms of
pregnancy-induced hypertension (HTN,
edema, proteinuria)
Measurement of fundal height
Check VS
Type cross & match
Administer oxytocin as ordered to keep
uterus contracted & prevent hemorrhage
Advise pt to avoid pregnancy for 1 year
Give immune globulin (RhoGAM) to any Rhwoman
Give emotional support, explain procedures
NANDAs
Fear r/t possible development of
choriocarcinoma
Anticipatory grieving r/t loss of the
pregnancy
ABRUPTIO PLACENTAE
Premature separation of a normally
implanted placenta from the uterine wall
HTN increases the risk of abruption
placenta although causative factors
are not clear.
Considered catastrophic event because of
the severity of the resulting hemorrhage
Vasospasms of placental vessels occur
because of increased blood pressure,
and the placenta may separate
prematurely
Marginal: placenta separates at its edges,
the blood passes between the fetal
membranes & the uterine wall, blood
Management:
Place client on bed rest
Refrain from vaginal exams (may
exacerbate bleeding)
Assess cardiovascular status of mother
frequently - VS every 15 min, skin color &
pulse quality hourly, measure CVP hourly
as ordered
Monitor fetus & uterine activity
electronically resting tone& fetal status
every 15 min
Develop a plan for the birth of the fetus
(prepare for cesarean as needed) if fetus
is at term, vaginal delivery is preferred.
escapes vaginally
Central: placenta separates centrally,
blood trapped between placenta & uterine
wall. Concealed bleeding
Complete: Total separation of placenta.
Massive vaginal bleeding
It is painful due to concealed
hemorrhage. The blood cannot escape
from behind the placenta; the abdomen
becomes boardlike and painful because of
the entrapment of blood
S/S: sudden sharp localized pain and
dark-red bleeding, (usually small
amounts) board-like abdomen that is
tender, fetal distress. Painful vaginal
bleeding in the third trimester
Complications:
- Disseminated intravascular coagulation
(DIC) CHARACTERIZED BY ABNORMAL
BLEEDING
Maternal Implications: intrapartum
hemorrhage, DIC, hypofibrinogenemia
(coagulation factors decreased), fatal
hemorrhagic shock, renal failure, vascular
spasm, intravascular clotting
Fetal-Neonatal Implications: sequelae of
prematurity, hypoxia, anemia, brain
damage, fetal demise
PLACENTA PREVIA
Placenta is abnormally implanted in the
lower uterine segment rather than the
upper portion of the uterus.
This implantation may be on a portion of
the lower segment or over the internal
cervical os
Total internal os completely covered
Partial internal os is partially covered
Marginal edge of os is covered
Low-lying placenta implanted in lower
Interventions:
Bed rest with bathroom privileges as long
as the woman is not bleeding
Instruct the side-lying position to avoid
putting pressure on the vena cava
ensuring adequate oxygenation of the
fetus
NO VAGINAL EXAMINATIONS
No douching
No vaginal intercourse
segment in proximity to os
Monitor blood loss, pain, uterine
Major complications: maternal hemorrhage,
contractility
Evaluating FHR with an external fetal
fetal prematurity, death
monitor
Monitoring maternal vital signs every 5 min
S/S: painless, bright-red vaginal
during active hemorrhage & every 15 min
bleeding in the third trimester
in the absence of hemorrhage
Give O2 as ordered/needed
NANDAs
Complete laboratory evaluation Hgb, Hct,
Fluid volume deficit
Rh factor, urinalysis
Anxiety
Maintain
large bore IV access for blood
Impaired gas exchange
transfusion
IV fluids (lactated Ringers solution)
2 U of crossmatched blood available for
transfusion
Provide information & emotional support
Verify familys ability to cope with anxiety of
unknown outcome
INCOMPETENT CERVIX
Premature dilatation of the cervix, usually in
abortions
Surgical Procedures:
Shirodkar procedure (cerclage) or a
modification of it by McDonald: reinforces
the weakened cervix by encircling it at the
level of the internal os w/ suture material.
Purse-string suture placed in cervix. Once
suture is placed, a cesarean birth may be
planned (to prevent repeating procedure
in future pregnancies) or the suture may
be cut at term & vaginal birth permitted
Nursing Interventions:
Bed rest, hydration (to promote relaxed
uterus & inhibit uterine contractions),
antibiotics, anti-inflammatory,
progesterone supplement
Monitor/Teach for premature labor &
premature rupture of membranes& to
notify healthcare provider
VS
Measure of s/s of incompetent cervix
Pelvic pressure
Assess vaginal discharge pink stained
bleeding
Uterine contractions, ROM, infection
Educate client to refrain from sex, heavy
lifting & prolonged standing
Administer tocolytics prophylactically to
inhibit uterine contractions
HYPEREMESIS GRAVIDARUM
Excessive nausea & vomiting during
pregnancy
Rare, cause unclear
NANDAS
Interventions:
NPO until dehydration corrected (48 hrs)
IV fluids to correct dehydration & F & E
imbalance (KCl)
Administer antiemetics as prescribed
Improve nutritional status: Vitamin B6 &
B12 & TPN (if no improvement)
Advance to clear liquids when vomiting
stops
Advance diet as tolerated with frequent,
small meals, avoid greasy & highly
seasoned foods, increase intake of K & Mg
Stress-reduction techniques, relaxed
environment
Maintain oral hygiene
Monitoring weight
Interventions:
Assessment of cervicovaginal fibronectin (
protein of amniotic fluid found in vaginal
secretions when fetal membrane is lost)
Assessment of cervical length via
ultrasound (if shorter than expected,
positive signs of PTL)
Assess signs of vaginal infection
Obtain history of previous preterm birth
Assess laboratory studies (CBC, C-reactive
protein, vaginal cultures, urine cultures)
Mother is asked to lie on her side to ^
profusion
IV infusion to promote maternal hydration
Tocolysis: medications used in an attempt
to stop labor (B-adrenergic agonists, Mg
Sulfate, prostaglandin synthetase
Fetal-neonatal implications:
Morbidity & mortality (Respiratory distress
syndrome)
Increased risk of trauma during birth
Maturational deficiencies
gestation
Decreased level of vasodilators & increase
level of vasoconstrictors
Mild Preeclampsia
S/S : Puffiness of the fingers, eyes, face.
A characteristic of preeclampsia is
vasospasms that cause renal injury,
resulting in loss of protein in the urine.
S/S:
-Anasarca (generalized edema)
-Sudden weight gain.
- Increased blood pressure.
Management:
Home care of Mild preeclampsia:
Woman monitors her BP, weight, urine
protein daily. Remote NSTs performed daily
or biweekly. Advise to report any changes.
Hospital care of mild preeclampsia:
Bed rest primarily on left side to decrease
pressure on vena cava, moderate-high
protein diet.
Tests to evaluate fetus status:
- Fetal movement record
- Nonstress test
- Ultrasonography every 3-4 wks for
serial determination of growth
- Biophysical profile
- Serum Creatinine
- Amniocentesis to determine fetal lung
maturity
Severe preeclampsia: Birth may be
treatment of choice for both mother &
fetus, even if fetus is immature. Other
include: bed rest, diet (high protein,
moderate Na+), anticonvulsants (Mg
Sulfate treatment of choice), F & E
replacement, corticosteroids,
antihypertensives
Assessment:
BP every 1-4 hrs, Temperature every 4 hrs,
pulse & respirations
Fetal heart rate
Urinary output: 700 mL or greater in 24 hrs,
or at least 30 mL/hr
Urine protein: 3+ or 4+ indicates loss of 5g
or more of protein in 24 hrs
Urine specific gravity hourly
symptoms))
LP low platelet count platelet count of 3
(thrombocytopenia, abnormal bleeding or
clotting time, bleeding gums, petechiae,
DIC)
Differs slightly from preeclampsia:
-BP may be slightly elevated or even normal
- Proteinuria may be absent.
Management:
BP measurements
Platelet transfusions if <20,000/mm3.
Assess fetus using NST & biophysical profile
Observe for edema
Rh ALLOMMUNIZATION
Fetal-Neonatal risks: anemia, hemolytic
Sensitization
syndrome (erhythroblastosis fetalis), fetal
Most often occurs when an Rh- woman
edema (hydrops fetalis), CHF, marked
carries an Rh+ fetus either to term or to
jaundice
termination by miscarriage or induced
abortion
Screening for Rh Incompatibiliy &
It can also occurs if an Rh- woman receives
Sensitization:
an Rh+ blood transfusion
RBCs from fetus invade the maternal
Take a history of previous sensitization,
circulation, thereby stimulating the
abortions, blood transfusions, or children
production of Rh antibodies.
who developed jaundice or anemia during
Because this transfer occurs at birth, first
the newborn period
child is not affected
Identify Rh- woman by asking if she knows
In subsequent pregnancies, however, Rh
her blood type & Rh factor.
antibodies cross the placenta & enter the Ask if she had ever received Rh immune
fetal circulation, causing severe hemolysis
globulin, if she has any previous
Destruction of fetal RBCs cause anemia in
pregnancies & their outcomes, & if she
the fetus
knows her partners Rh factor
Identify other medical complications such
as diabetes, infections or hypertension
Note: Rh immune globulin (RhoGAM)
Antibody screen (Indirect Coombs test
administration prevents maternal
done on the mothers blood to measure #
sensitization. It provides passive antibody
of Rh+ antibodies & Direct Coombs test
protection against Rh antigens. This tricks
done on the infants blood to detect
the body, which does not then produce
antibody-coated Rh+ RBCs)
Give injection of 300 mcg Rh immune
antibodies of its own.
An Rh- mother who has no antibody titer
globulin to pregnant Rh- women who have
(indirect Coombs test negative,
no antibody titer, at 28wks gestational
nonsensitized) & has given birth to an Rh+
age, to mothers whose babys father is
fetus (Direct Coombs test negative) is
Rh+, after each abortion & within 72 hrs
given an injection of Rh immune globulin
postpartum, amniocentesis & placenta
ABO INCOMPATIBILITY
Management:
Type O mother incompatibility with a
Assess for potential for ABO incompatibility
type A,B, or AB fetus
Anti-A & Anti-B antibodies occurs naturally
type O mother & type A or B father
because women are naturally exposed to Following birth, assess newborn carefully for
the A & B antigens through the foods they
development of hyperbilirubinemia & treat
eat & through exposure to infection.
it with phototherapy
Once they become pregnant, the maternal
serum Anti-A & Anti-B antibodies cross the
placenta & produce hemolysis of the fetal
RBCs
Unlike Rh incompatibility, 1st infant is often
involved
Antepartal treatment is never warranted
DISSEMINATED INTRAVASCULAR COAGULATION
hemorrhage.
Abruptio placentae
Amniotic fluid embolism
Dead fetus syndrome (fetus dies but is
retained in utero for at least 6 weeks)
Severe preeclampsia
Sepsis
Saline abortion
Management:
Primary medical management in all cases of
DIC involves:
Correction of the underlying cause (e.g.,
removal of the dead fetus, treatment of
existing infection or of preeclampsia or
eclampsia, or removal of a placental
abruption)
Volume replacement, blood component
therapy, optimization of oxygenation and
perfusion status, and continued
reassessment of laboratory parameters
Resolution of DIC usually begins with the
birth of the neonate
Nursing interventions include:
Assessing for signs of bleeding,
Administering fluid or blood replacement as
ordered.
Because renal failure is one consequence
of DIC, urinary output is closely monitored,
usually by insertion of an indwelling
urinary catheter. Urinary output must be
maintained at more than 30 mL/hr.