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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
Risk factors: Obesity, women w/ prior GDM, Educating pt on monitoring blood glucose &
glycosuria, strong family history of DM,
diet & exercise management

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
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)

Altered nutrition < body requirements
Risk for fetal/mother injury
Risk for noncompliance w/ diabetic diet
Risk for infection

Maternal insulin requirements decrease
dramatically during labor
Calorie needs increase during lactation to
500-800 kcal above prepregnant
requirements & insulin must be adjusted
Women should be reassessed 6 wks
postpartum to determine whether her
glucose levels are normal


1st & 2nd trimesters major cause of bleeding: Note: Spotting is relatively common during
pregnancy & usually occurs following sexual
Abortion: expulsion of fetus prior to viability intercourse or exercise because of trauma
to the highly vascular cervix. However,
(before 20 weeks gestation, weight <
women are advised to report any spotting
500g)> Can be spontaneous (often called
or bleeding that occurs during pregnancy so
miscarriage) or induced
that it can be evaluated
1 half of pregnancy causes of bleeding:
ectopic pregnancy & gestational
Initial Assessment of bleeding:
trophoblastic disease

2nd half of pregnancy causes of bleeding:

placenta previa & abruption placenta
Spontaneous abortions categories:
- Threatened: Unexplained bleeding,
cramping & backache. Cervix closed.
Bleeding may persist for days. May be
followed by partial or complete expulsion
of embryo or fetus, placenta &
membranes. products of conception.
- Imminent/Inevitable: Bleeding &
cramping increase. Internal cervical os
dilates. Membranes may rupture.
- Complete: All the products of conception
are expelled. Cervix closed.
- Incomplete: Placenta is retained. Internal
cervical os dilated. S/S Abd cramping
- Missed: Fetus dies is uterus but is not
expelled. No bleeding or cramping occurs.
Uterine growth ceases, breast changes
regress, & woman may report brown
vaginal discharge. Cervix closed.
- Recurrent/Habitual: Occurs consecutively
in 3 or more pregnancies
- Septic: Infection is present. Malodorous
Acute pain r/t abdominal cramping
secondary to threatened abortion
Anticipatory grieving r/t expected loss of
unborn child

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
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
Assess familys response to situation

Nursing Interventions for

bleeding/spontaneous abortion:
Perform a pregnancy test
Assist with an ultrasound
Bed rest, abstinence from sex & sedation
Administering analgesics is cramping is
Administering antibiotics is septic abortion
IV therapy or blood transfusions to replace
fluids, & dilation & curettage (D&C) or
suction evacuation (D&E) is performed to
remove remainder of the products of
If woman is Rh- & not sensitized, RhoGAM
is given within 72 hrs
Give oxytocin (Pitocin) as prescribed to
expulse products of conception

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
S/S: sharp unilateral pain, syncope, referred
shoulder pain, lower abdominal pain,
vaginal bleeding, adnexal tenderness.

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
Replacement of fluid loss & maintenance of
electrolyte imbalances
Provide pt education & psychological
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


Pathologic proliferation of the trophoblastic
It includes hydatidiform mole, invasive mole Suction curettage to aspirate & evacuate
(chorioadenmoma destruens) &
the mole
Follow up hCG for 1 year (^hCG may
choriocarcinoma (form of cancer)
indicate choriocarcinoma)

Hydatidiform mole (molar pregnancy) is a

disease in which:
Abnormal developments of the placenta
occurs resulting in hydropic vesicles (fluidfilled, grapelike cluster)

Trophoblastic tissue proliferates

Molar pregnancies are classified in:
Complete: develops from an ovum
containing no maternal genetic material,
an empty egg, which is fertilized by a
normal sperm
Partial: A normal ovum w/ 23 chromosomes

is fertilized by two sperm or by a sperm

that failed to undergo under the first

meiotic division & therefore contains 46

S/S: vaginal bleeding, elevated serum hCG,

anemia, no fetal heart tones & no fetal

movement, gestational HTN before 24

wks, uterine enlargement

Chemotherapy if choriocarcinoma
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

Fear r/t possible development of
Anticipatory grieving r/t loss of the

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
Marginal: placenta separates at its edges,
the blood passes between the fetal
membranes & the uterine wall, blood

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

Monitor for signs of DIC

Maintain 2 large bore IV sites fluids &
blood products as ordered
Monitor I & O & urine Specific Gravity
Measure abdominal girth as ordered
Review & evaluate diagnostic tests Hgb,
Hct, coagulation status
Neonatal resuscitation as ordered
Provide information & emotional support

If RN suspect of Abruptio placenta and


- Disseminated intravascular coagulation
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 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

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
No douching
No vaginal intercourse

segment in proximity to os
Monitor blood loss, pain, uterine
Major complications: maternal hemorrhage,
Evaluating FHR with an external fetal
fetal prematurity, death
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
Complete laboratory evaluation Hgb, Hct,
Fluid volume deficit
Rh factor, urinalysis

large bore IV access for blood
Impaired gas exchange
IV fluids (lactated Ringers solution)
2 U of crossmatched blood available for
Provide information & emotional support
Verify familys ability to cope with anxiety of
unknown outcome

Premature dilatation of the cervix, usually in

the 4th or 5th month

Associated w/ repeated 2 trimester
Causes: cervical trauma, infection,

congenital cervical/uterine anomalies,

^uterine volume (as in multiple gestation)
Diagnosis: based on positive history of
repeated painless/bloodless 2nd trimester


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
Measure of s/s of incompetent cervix
Pelvic pressure
Assess vaginal discharge pink stained
Uterine contractions, ROM, infection
Educate client to refrain from sex, heavy
lifting & prolonged standing
Administer tocolytics prophylactically to
inhibit uterine contractions

Excessive nausea & vomiting during

Rare, cause unclear

^ levels of hCG may play a role

Severe cases cause dehydration, F & E

imbalances, alkalosis, metabolic acidosis if

untreated, severe K+ loss, decreased
urinary output, hypovolemia, hypotension,
tachycardia, ^ Hct & BUN, liver

dysfunction (enzymes elevated)

S/S: excessive vomiting for prolonged
periods, dehydration, weight loss,
decreased BP, increased pulse, poor skin


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
Advance diet as tolerated with frequent,
small meals, avoid greasy & highly
seasoned foods, increase intake of K & Mg
Stress-reduction techniques, relaxed
Maintain oral hygiene
Monitoring weight

Imbalanced nutrition < body requirements



PROM Spontaneous rupture of the
Start antibiotic therapy immediately if
membranes prior to the onset of labor
PPROM (Preterm premature rupture of
maternal signs of infection are evident
membranes: is the rupture of membranes On admission to nursery, newborn is
occurring after 20 wks but before 37 wks
assessed for sepsis & placed on antibiotics
Management of PROM in the absence of
of gestation
infection & gestation < 37 wks is usually
Infection is the major risk of PROM &
conservative: hospitalization, bed rest,
PPROM for both the client & fetus
CBC, C-reactive protein & urinalysis,
because once the amniotic membranes
continuous electronic fetal monitoring,
have ruptured, micro-organisms can
regular NST or biophysical profiles, VS
ascend from the vagina into the
every 4 hrs, regular laboratory
amniotic sac causing Chorioamnionitis
evaluations, vaginal examination avoided,
a condition in pregnant women in

which the membranes that surround

the fetus and the amniotic fluid are
infected by bacteria
Associated with: infection, previous history
of PROM, hydramnios, multiple pregnancy,
UTI, amniocentesis, placenta previa,
abruption placentae, trauma, incompetent
cervix, bleeding during pregnancy,
Risk for abruption placenta

Maternal risk of infection ^

Fetal-Newborn risk: respiratory distress
syndrome, fetal sepsis, malpresentation &
prolapsed of umbilical cord
Sterile speculum to detect amniotic fluid in
Nitrazine paper turns blue
Microscopic examination Ferning Test
DONT DO Digital vaginal examination increases risk of infection


Labor that occurs 20-37 wks gestation
Risk factors: UTI or vaginal infections,
previous preterm birth, multifetal
pregnancy, hydramnios (excessive
amniotic fluid), age <17 or >35, low
socioeconomic status, smoking, substance
abuse, domestic violence, history of
multiple miscarriages/abortions, DM, HTN,
incompetent cervix, placenta previa,
abruption placentae, uterine
abnormalities, etc..
Indications of PTL:
Documented uterine contractions: 4 in 20
min or 8 in 1 hr
Documented cervical change: dilatation >
Cervical effacement of 80% or more

fetal lung maturity studies, administration

of surfactant, administration of maternal
Note: maternal corticosteroid
administration to promote fetal lung
maturity & prevent respiratory distress
syndrome remains controversial
If patient discharged, give instructions: To
continue bed rest w/bathroom privileges,
monitor temperature & pulse every 4 hrs,
keep fetal movement chart, have weekly
NST, abstain from intercourse; & to call
physician & return to hospital if she has
fever/uterine tenderness or contractions/
increased leakage of fluids/decreased fetal
movement/foul-smelling vaginal discharge

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 ^
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
Increased risk of trauma during birth
Maturational deficiencies

inhibitors, Ca channel blockers

Identify woman at risk
Assess progress of labor
Teach mother to recognize onset of labor
(low backache, pressure in pelvis &
cramping; increase/change/or blood
vaginal discharge; regular uterine
contractions with a frequency of every 10
Selfcare Measures to prevent PTL: rest
min lasting 1 hr or longer, GI cramping
2-3 times a day on left side, drink
sometimes w/ diarrhea, premature rupture
water & juice fruit, avoid caffeine
of membranes)
drinks, avoid lifting, contact
Management of a client who is in
healthcare provider if s/s of PTL,
preterm labor includes focusing on
sexual activity may need to be
stopping uterine contractions by
modified/ avoided.
restricting activity, ensuring
hydration, identifying & treating an
infection, administering tocolytic
medications, & assuring fetal wellbeing by accelerating fetal lung
maturity with glucocorticoids


BP begins to rise after 20 weeks of

Decreased level of vasodilators & increase
level of vasoconstrictors
Mild Preeclampsia
S/S : Puffiness of the fingers, eyes, face.

Preeclampsia is the most common

hypertensive disorder in pregnancy. It is
defined as gestational hypertension with a
BP of 140/90 (mild) or 160/110 (severe) or
higher on 2 occasions at least 6 hrs apart
accompanied by proteinuria (5g in a 24 hr
urine collection +2, +3) & edema. Dipstick
urine protein 31-41 in 2 random samples
obtained 4 hrs apart. It most often occurs
in the last 10 wks of gestation, during
labor, or in the first 48 hrs after childbirth.
Most common in women < 17 yrs or > 35.

A characteristic of preeclampsia is
vasospasms that cause renal injury,
resulting in loss of protein in the urine.
-Anasarca (generalized edema)
-Sudden weight gain.
- Increased blood pressure.

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
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,

Blurred vision and epigastric pain indicates

worsening of preeclampsia, which could
lead to seizures.
Eclampsia: An eclamptic seizure requires
immediate, effective treatment. Bolus of
4-6 g Mg Sulfate is given IV over 5 min.
Sedatives (Diazepam), Dilantin (for
prevention), Diuretics (Lasix) for
Eclampsia is the most severe form of
pulmonary edema, Digitalis (for circulatory
preeclampsia, characterized by
failure). I & O monitored hourly. Woman is
generalized seizures or coma. May
observed for signs of labor & vaginal
occur antepartum, intrapartum or
bleeding & abdominal rigidity which may
indicate abruption placentae. While she is
Epigastric pain, blurred vision, and
comatose, she is positioned on her left
headache are prodromal symptoms of
side / the side rails up.
eclampsia in a client with preeclampsia
Intrapartal Management: Labor
Maternal Risks: Hyperreflexia, headache,
seizures, renal failure, abruption placentae, inducement with IV oxytocin if evidence of
fetal maturity & cervical readiness.
DIC, ruptured liver, PE, HELLP syndrome
Epigastric discomfort suggests liver
edema; it is an ominous symptom that
indicates an impending seizure.

Fetal-Neonatal Risks: Small for gestational

age, premature, Hypermagnesemia (Mg
Sulfate administration to mother), increased
morbidity & mortality

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

Weight: weigh the woman daily at the same

time, she should be wearing the same

robe or gown & slippers

Pulmonary edema: observe for coughing,

auscultate lungs for moist respirations

Deep tendon reflexes & clonus: for signs of
Placental separation: for vaginal bleeding &
uterine rigidity
Visual disturbances: blurring or any changes
Epigastric pain
Laboratory blood tests
Level of consciousness, emotional response
& level of understanding
Assess for Mg sulfate toxicity: if suspected,
immediately discontinue infusion &
administer calcium gluconate
H hemolysis AEB burr cells or
bilirrubin(anemia & jaundice)

EL elevated liver enzymes AST & ALT

(epigastric pain, nausea, vomiting, flu-like

LP low platelet count platelet count of 3
(thrombocytopenia, abnormal bleeding or
clotting time, bleeding gums, petechiae,
Differs slightly from preeclampsia:
-BP may be slightly elevated or even normal
- Proteinuria may be absent.

Assessment for signs of worsening

preeclampsia. Analgesics may be used for
discomfort or epidural block. O2 is
Postpartal Management: Woman with
preeclampsia usually improves rapidly after
giving birth, although seizures can still
occur during first 48 hrs postpartum. If
hypertension is severe, woman may
continue to receive antihypertensives or Mg
Extra interventions:
Explain medical therapy & its purpose &
offer honest information
Maintain quiet, low-stimulus environment
Avoid unlimited phone calls
Keep woman on left side as much as
Explain to family the reason of the seizures

BP measurements
Platelet transfusions if <20,000/mm3.
Assess fetus using NST & biophysical profile
Observe for edema

Sometimes associated with severe

Variant of gestational hypertension in which
hematologic conditions coexist with severe
preeclampsia involving hepatic
Increased risk for: placenta abruption, acute
renal failure, pulmonary edema, hepatic
hematoma, ruptured liver, DIC, PE,
fetal/maternal death

Fetal-Neonatal risks: anemia, hemolytic
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
termination by miscarriage or induced
Screening for Rh Incompatibiliy &
It can also occurs if an Rh- woman receives
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

within 72 hrs of childbirth so she does not

have time to produce antibodies to fetal
cells that entered her bloodstream when
the placenta separated

previa, before invasive procedures that

may cause bleeding

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
Unlike Rh incompatibility, 1st infant is often
Antepartal treatment is never warranted

Disseminated intravascular coagulation

(DIC), also known as consumptive

coagulopathy, is an imbalance between

the bodys clotting and fibrinolytic

Wide- spread external bleeding, internal
bleeding, or both can result.
DIC can occur as a result of:
Acute antepartum or postpartum

Abruptio placentae
Amniotic fluid embolism
Dead fetus syndrome (fetus dies but is
retained in utero for at least 6 weeks)
Severe preeclampsia
Saline abortion

Acute fatty liver of pregnancy

Physical examination reveals unusual

bleeding; spontaneous bleeding from the

womans gums or nose can occur.

Petechiae can appear around a blood
pressure cuff placed on the womans arm.
Excessive bleeding can occur from the site
of a slight trauma (e.g., venipuncture
sites, intramuscular or subcutaneous
injection sites, nicks from shaving of
perineum or abdomen, and injury from
insertion of a urinary catheter).
Hypotension is out of proportion to the
observed blood loss. Other symptoms
include tachycardia and diaphoresis.

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
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
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.