MIDWIFERY 102 MODULE 2

PREGNANCY COMPLICATIONS IN THE 2ND and 3rd TRIMESTER &

POST-PARTUM HEMORRHAGE

OBJECTIVES
1. To identify and discuss causes of antepartum bleeding during the
2. To develop skills in assessing patients with danger signs of pregnancy
3. To discuss the management and postpartum hemorrhage

Vaginal bleeding during the second trimester can be due to the following:
 Cervical/ vaginal causes
 Cervicitis/vaginitis
 Cervical polyp
 Cervical or vaginal laceration
 Cervical carcinoma
 Intrauterine causes
 Molar pregnancies
 Placenta previa
 Abruptio placenta
 Incompetent cervix
 Uterine leiomyoma

INCOMPETENT CERVIX
This is also known as cervical insufficiency. It is characterized by painless cervical
dilatation in the second trimester. It can be followed by prolapse and ballooning of
membranes into the vagina and ultimately expulsion of an immature fetus. Unless
effectively treated, this can be repeated in future pregnancies.

Risk Factors: Previous cervical trauma such as dilatation and curettage, conization,
cauterization or amputation has been implicated.

Evaluation and treatment: Sonography is performed to confirm a living fetus

with no major abnormalities. Cervical secretions are tested for gonorrhea and
chlamydia infection. Cervical incompetence is treated by purse-string suture
(cerclage). Contraindications to cerclage usually include bleeding, uterine
contractions, or ruptured membranes. Elective cerclage is usually done between 12
and 14 weeks gestation. Ultrasonography is performed in a high risk woman to
document cervical shortening <25mm, then cerclage is done at that time.
Sonographic findings of incompetent cervix include cervical shortening and
funneling.
 ANTEPARTUM HEMORRHAGE

Definition: Antepartum hemorrhage is defined as vaginal bleeding from the genital

tract during the 24th week of pregnancy and prior to childbirth. It is caused by the
following conditions: abruptio placenta, placenta previa, rarely vasa previa, and
local causes of bleeding such as bleeding from vulva, vagina and the cervix.

ABRUPTIO PLACENTA/ PLACENTAL ABRUPTION

Definition: Separation of a normally implanted placenta either partially or totally-

from its implantation site before delivery

Pathogenesis: Placental abruption is initiated by hemorrhage into the decidua

basalis. The decidua then splits, leaving a thin layer adhered to the myometrium.
The process begins as a decidual hematoma and expands to cause separation and
compression of the adjacent placenta. Bleeding typically insinuates itself between
the membranes and uterus, ultimately escaping through the cervix to cause external
hemorrhage. Less often, the blood is retained between the detached placenta and
the uterus, leading to concealed hemorrhage and delayed diagnosis. The delay
causes greater maternal and fetal hazards. Concealed hemorrhage also increases
the likelihood of consumptive coagulopathy.

Incidence: About 0.5 – 1 in 200 deliveries

Predisposing factors:
1. Demographic factors: The incidence of abruption increases with maternal
age. Women older than 40 years old are 2.3 times more likely to experience
abruption compared with those 35 years or younger. Race or ethnicity also
appears to be important with incidence seen more common in African-
American and white women and less so in Asian women.
2. Hypertension and Preeclampsia
3. Trauma
4. Heavy maternal alcohol use
5. Smoking
6. Cocaine abuse
7. Advanced age and multiparity
8. Premature rupture of membranes
9. History of previous abruption
10. Multifetal gestation
11. polyhydramnios
12. Uterine leiomyoma

Clinical findings and diagnosis:

Most women with a placental abruption have sudden-onset abdominal pain, vaginal
bleeding, and uterine tenderness characterized as persistent uterine hypertonus or
tetanic uterine contraction.
 Signs and symptoms
 Vaginal bleeding: 78%
 Uterine tenderness or back pain: 66%
 Fetal distress: 60%
 High frequency contraction: 17%
 Hypertonus: 17%
 Idiopathic preterm labor: 22%
 Dead fetus : 15%

Differential Diagnosis: With severe placental abruption, the diagnosis generally is

obvious. More common forma of abruption however cannot always be recognized
with certainty. Unfortunately, there are no laboratory tests or other diagnostic
methods to accurately confirm lesser degrees of placental abruption. Sonography
has limited use because the placenta and fresh blood clots may have similar imaging
characteristics. Importantly, negative findings on ultrasound does not exclude
placental abruption. Magnetic resonance Imaging (MRI) is highly sensitive for
placental abruption. In a woman with history of bleeding and live fetus, placenta
previa should be excluded.

Complications:
1. Hemorrhage – Placental abruption may be complicated by massive
hemorrhage causing hypovolemic shock due to maternal blood loss. Massive
blood loss and shock can develop with a concealed abruption. Prompt
treatment of hypotension should be done to avoid acute kidney injury.
2. Consumptive coagulopathy – Abruption is the most common cause of
clinically significant consumptive coagulopathy in obstetrics. The major
mechanism causing procoagulant consumption in intravascular activation of
clotting. There are significant amount of procoagulants in the retroplacental
clots. The pathologically activated cycle of coagulation and fibrinolysis
becomes clinically important when coagulation factors and platelets are
sufficiently depleted to cause bleeding, hence, consumptive coagulopathy.
Consumptive coagulopathy increases the risk for maternal and perinatal
morbidity and mortality.
3. Fetal hypoxia and perinatal death
4. Prematurity
5. Maternal death

Management: Management depends on severity of situation

 Vaginal delivery-Fetus and mother stable
 Urgent/Emergent CS- For compromised fetus, cesarean delivery is
necessary. The speed of the response is important factor in perinatal
outcomes. Living and viable fetus and with vaginal delivery not
imminent, cesarean delivery is indicated.
  Be prepared for massive blood loss with CS
 Couvelaire uterus - when there is widespread axtravasation of blood into the
uterine musculature and beneath the serosa . This can cause uterine atony
(uterus may not contract after delivery)
 On rare occasions, internal iliac ligation/hysterectomy may be necessary

PLACENTA PREVIA
Placenta that is implanted somewhere in the lower uterine segment, either over or
very near the internal cervical os.

Classification:
• Total placenta previa – the internal os is covered completely by placenta
• Partial placenta previa—the internal os is partially covered by placenta
• Marginal placenta previa—the edge of the placenta is at the margin of the
internal os
• Low-lying placenta—the placenta is implanted in the lower uterine segment
such that the placental edge does not reach the internal os, but is in close
proximity to it
• Vasa previa—the fetal vessels course through membranes and present at the
cervical os

Incidence and associated factors:

The reported incidence for placenta previa average 0.3% or 1 case per 300 to 400
deliveries. The following are the risk factors for placenta previa:
 Previous uterine surgery/scar ex prior CS
 Multiple gestation
 Previous abnormal placental implantation
  Advanced maternal age
 Increased parity
 Smoking

Clinical features: Painless bleeding is the most characteristic event with placenta
previa. Bleeding usually does not appear until the end of the second trimester or
later, but it can begin even before mid-pregnancy. Bleeding from a previa usually
begins without warning and without pain or contraction in a woman who has had
uneventful prenatal course. Vaginal bleeding in the 3rd trimester should be
considered previa until proven otherwise. A frequent and serious complication
associated with placenta previa arises from its abnormally firm placenta
attachment. Placenta accrete syndrome arise from abnormal placental
implantation and adherence and are classified according to the depth of placental
ingrowth into the uterine wall.

Diagnosis: whenever there is uterine bleeding after midpregnancy, placenta previa

or abruption should always be considered. Previa should not be excluded until
sonographic evaluation has clearly proved its absence. Diagnosis by clinical
examination is done using double set-up technique. Digital examination (Internal
examination) should not be performed unless delivery is planned. A cervical digital
examination is done with the woman in an operating room and with preparations
for immediate cesarean delivery.
1. Sonographic placental localization – Standard sonographic techniques can
quickly and accurately localize the placenta. Transvaginal sonography is safe
and results are superior compared to transabdominal ultrasound. Women
with suspected diagnosis of placenta previa at 20 weeks of gestation by
abdominal ultrasound should be confirmed by transvaginal ultrasound.
2. Magnetic resonance Imaging

Management: Women with previa are managed depending on their individual

clinical circumstances. The three factors that are considered include fetal age, labor
and bleeding and its severity. If the fetus is preterm and there is no persistent active
bleeding, management favors close observation in an obstetric unit. For women
who are near term and who are not bleeding, plans are made for scheduled cesarean
delivery. Tocolysis for women presenting with symptomatic placenta previa or low-
lying placenta should be considered for 48 hours to facilitate administration of
antenatal corticosteroids. Women with previa are best served by elective delivery
at 36 to 37 weeks. With suspected placenta accrete syndrome, delivery was
recommended at 34-35 completed weeks. Urgent cesarean delivery is warranted in
active ore persistent bleeding or when there is fetal compromise. Placenta previa –
especially with abnormally adherent placenta is currently the most frequent
indication for peripartum hysterectomy.

Maternal and perinatal outcomes: Placenta previa and placenta accrete

syndrome both contribute to maternal mortality and morbidity. In one review,
there was a threefold increased maternal mortality ratio of 30 per 100,000 for
women with previa. Placenta previa also increases the risk for perinatal mortality
and morbidity. Preterm delivery is the primary cause of neonatal mortality. Fetal
anomalies are increased 2-3x in pregnancies with previa.

PLACENTA ACCRETA
The Placenta accreta syndromes describe the abnormally implanted, invasive, or
adhered placenta to the myometrium because of partial or total absence of the
decidua basalis and imperfect development of the fibrinoid or the Nitabuch’s
layer. All affected placenta can potentially cause significant hemorrhage.

Ethiopathogenesis: Accreta syndrome tissue specimens have shown evidence for

“hyperinvasiveness” compared with otherwise uncomplicated previa specimen.
Microscopically, placental villi are anchored to muscle fibers rather than to decidual
cells. This anatomical layer deficiency (Decidual deficiency) then prevents normal
placental separation after delivery. Previous uterine trauma like cesarean section –
increase the vulnerability of the decidua to trophoblastic invasion following incision
into the decidua. Decidual formation may be defective over a previous hysterotomy
scar, and it also may follow any type of myometrial trauma like curettage.
Conditions causing decidual damage and deficiency are antecedent to placenta
accrete. This includes previous cesarean section, placenta previa, Asherman’s
syndrome, previous uterine surgery, maternal age >40 years, and parity >5.
Cesarean section is a well established risk factor for abnormal placentation, both for
placenta previa and placenta acreta. The exact mechanism is unknown but it is
hypothesized that the early embryo implants preferentially into areas of uterine
scarring and deficient decidua because of relative deficiency of blood flow and
oxygen tension in this area with the trophoblasts invading deeply into the
myometrium resulting to placenta accreta.

Classification:
 Accreta:
 Abnormally firm adherence to the uterine wall
 Increta:
 Villi invade the myometrium
 Percreta
 Villi penetrate though the myometrium
Incidence and associated conditions:
The incidence of accrete syndromes has increased remarkably due to increased
rates of cesarean section. In addition to their significant contribution to maternal
morbidity and mortality, accrete syndromes are a leading cause of intractable post
partum hemorrhage and emergency peripartum hysterectomy.

Risk factors:
The two most important risk factors are an associated previa, a prior cesarean
delivery and more likely a combination of the two. A classical hysterotomy incision
has a higher risk for a subsequent accrete placenta.

Clinical presentation and diagnosis:

All pregnant women with placenta previa and a previous uterine surgery should be
screened for placenta accreta. All women with risk factors that predispose them to
placenta accrete, such as advanced maternal age multiparity, prior cesarean section,
prior myomectomy or reconstructive surgery, Asherman’s syndrome and uterine
anomalies, should also be screened for placenta accrete. In cases of first and 2 nd
trimester accrete syndromes, there is usually hemorrhage that is the consequence of
coexisting placenta previa. Such bleeding will usually prompt evaluation and
management. In some women who do not have an associated previa, accrete may
not be identified until third-stage labor when an adhered placenta is encountered.
Gray scale ultrasonography can detect placenta accrete in 77-87%. The addition of
Doppler flow mapping is highly predictive of myometrial invasion. MRI can be used
as an adjunct to sonography to define anatomy, degree of invasion and possible
ureteral or bladder involvement.

Management
When diagnosed antepartum or prior to delivery, the woman is advised delivery in a
tertiary hospital where there are available surgical (obstetric surgeon, gynecologic
oncologist, surgical, urological and interventional radiological consultants)
anesthesia and blood banking capabilities. With regard to timing of delivery, the
American College of Obstetric and gynecologist recommends individualization.
Generally, these women are scheduled at 36 weeks AOG. Confirmation of a percreta
or increta almost always mandates hysterectomy. In a few cases, after the fetus has
been delivered, it may be possible to trim the umbilical cord and repair the
hysterectomy incision but leave the placenta in situ. This may be wise for women in
whom abnormal placentation was not suspected before cesarean delivery and in
whom uterine closure stops bleeding. After this, she can be transferred to a higher
level facility for definitive management.

VASA PREVIA
DEFINITION:
 Vasa previa is a condition where fetal vessels travel within the membranes
and overlie the cervical os. There they can be torn with cervical dilatation or
membrane rupture, and laceration can lead to rapid fetal exanguination.
Over the cervix, vessels can also be compressed by a presenting fetal part.
 This is an uncommon condition with incidence of 2-6 per 10,000
pregnancies.
 Classified as type 1, in which vessels are part of a velamentous cord insertion
and type 2, in which involved vessels span between portions of a bilobate or
a succenturiate placenta
 OBSTETRICAL HEMORRHAGE
Obstetrical hemorrhage, hypertension and infection comprise the “triad” of causes
of maternal deaths worldwide.

Mechanisms of normal hemostasis:

A major concept in understanding the pathophysiology and management of
obstetrical hemorrhage is the mechanism by which hemostasis is achieved after
normal delivery. Near term, about 600ml of blood flows through the intervillous
space. With placental separation, these vessels at the implantation site are avulsed
and hemostasis is achieved by myometrial contraction which compresses the spiral
arteries. Contraction is followed by clotting and obliteration of vessel lumen. If
after delivery, the myometrium within and adjacent to the denuded implantation
site contracts vigorously, fatal hemorrhage from the placental implantation is
unlikely. However, fatal postpartum hemorrhage can result from uterine atony
despite normal coagulation. Adhered placental pieces or large blood clots that
prevent effective myometrial contraction will serve to impair hemostatis at the
implantation site.

Definition
POSTPARTUM HEMORRHAGE is defined as the loss of 500 ml of blood or more
after completion of the third stage of labor.

Predisposing condition:
1. Abnormal placentation –
a. placenta previa,
b. placental abruption
c. placenta accrete/increta/percreta
d. ectopic pregnancy
e. hydatidiform mole
2. Injuries to the birth canal
a. Episiotomy and laceration
b. Forceps or vacuum delivery
c. Cesarean delivery or hysterectomy
d. Uterine rupture
i. Previously scarred uterus
ii. High parity
iii. Hyperstimulation
iv. Obstructed labor
v. Intrauterine manipulation
vi. Midforceps rotation
vii. Breech extraction
3. Obstetrical factors
a. Obesity
b. Previous postpartum hemorrhage
c. Early preterm pregnancy
d. Sepsis syndrome
 4. Vulnerable patients
a. Preeclampsia/eclampsia
b. Chronic renal insufficiency
c. Constitutionally small size
5. Uterine atony
a. Uterine overdistention
i. Large fetus
ii. Multiple fetuses
iii. Hydrmanios
iv. Retained clots
b. Labor induction
c. Anesthesia or analgesia – halogenated agents is general anesthesia
d. Labor abnormalities
i. Rapid labor
ii. Prolonged labor
iii. Augmented labor
iv. Chorioamnionitis
e. Previous uterine atony
6. Coagulation defects

Timing of hemorrhage
1. Antepartum hemorrhage : bleeding during various times in gestation give a
clue as to its cause. Bleeding during the first half of pregnancy can be due to
abortion, hydatidiform mole or ectopic pregnancy
2. Post-partum hemorrhage(PPH): Frequent cause of PPH are uterine atony
and genital tract trauma. Persistent bleeding despite a firm, well contracted
uterus suggests that helorrhage is most likely due to genital tract laceration.
This can be confirmed by careful inspection of the vagina, cervix and uterus
to identify laceration. If there are no lower genital tract laceration and the
uterus is contracted, yet supracervical bleeding persists, then manual
exploration of the uterus is done to exclude a uterine tear.
3. Late post partum hemorrhage: Bleeding after the first 24 hours of delivery.
Women with severe preeclampsia or eclampsia are more vulnerable to
hemorrhage because they frequently do not have a normally expanded blood
volume

Active management of the third stage of labor (AMTSL)

 This is the most effective strategy to prevent PPH. It also reduces risk of
postpartum maternal hemoglobin level lower than 9g/dl and the need for
manual removal of the placenta.
 Components of AMTSL:
o 1. Administering oxytocin soon after the delivery of the infant
o 2. Clamping and dividing the cord when pulsation has stopped
 o 3. Controlled cord traction to deliver the placenta while applying
suprapubic counter-pressure on the uterus with the other hand
o 4. Uterine massage after delivery of the placenta

Causes of obstetrical hemorrhage

A. TONE: uterine atony
 The most frequent cause of obstetrical hemorrhage is failure of the uterus to
contract sufficiently after delivery and to arrest bleeding from vessels at the
placental implantation site. The fundus should always be palpated
following placental delivery to confirm that the uterus is well contracted.
Vigorous post-partum uterine massage and administration of uteronotic
usually prevents PPH from atony. In many women, uterine atony can at least
be anticipated well prior to delivery. However, in one study, up to half of
women who had atony after cesarean delivery were found to have no risk
factors.

 Risk factors of uterine atony:

1. Uterine overdistension
- multiple pregnancy
- polyhydramnios
- fetal macrosomia
2. related to labor and delivery
- induction of labor
- prolonged labor
- precipitate labor
- augmentation with oxytocin
- manual removal of placenta
3. administration of uterine relaxants
- deep anesthesia
- magnesium sulfate
4. Intrinsic factors
- previous postpartum hemorrhage
- antepartum hemorrhage (such as abruption or previa)
- obesity
- age more than 35

 Management:
 With immediate PPH, careful inspection is done to exclude birth canal
laceration. Because bleeding can be due to retained placental fragments,
inspection of the placenta after delivery should be routine. If a defect is
seen, the uterus should be manually explored, and the fragments removed.
Uterotonics are given prophylactically after delivery of the fetus to prevent
most case of uterine atony. The first line uterotonic given is Oxytocin.
 When bleeding persists despite uterine massage and continued uterotonin
administration, the following management steps are performed immediately
and simultaneously:
1. Begin bimanual uterine compression – this is easily done and controls most
cases of continuing bleeding. The posterior uterine wall is massaged by one
hand on the abdomen, while the other hand is made into a fist and placed
into the vagina. This fist kneads the anterior uterine wall. Concurrently, the
uterus is also compressed between the two hands.

2. Immediately mobilize the emergent-care obstetrical team to the delivery

room and call for whole blood or packed red blood cell.
3. Request urgent help from anesthesia team.
4. Secure at least 2 large-bore intravenous catheters so that crystalloid with
oxytocin is continued simultaneously with blood products. Insert indwelling
foley catheter for continuous output monitoring.
5. Begin volume resuscitation with rapid intravenous infusion of crystalloid.
6. Manually explore the uterine cavity for retained placental fragments and for
uterine abnormalities including laceration or rupture.
7. Thoroughly inspect the cervix and vagina again for lacerations that may have
escaped attention.
UTERINE INVERSION
 Definition: Passage of the uterine fundus through the endometrial cavity
and cervix, turning the uterus inside out. It is a rare and serious complication
of the third stage of labor.
 Reported Incidence ranges from 1 in 20,312 to 1 in 1739 deliveries
 Cases are classified using a variety of criteria:
o According to the time from delivery to diagnosis:
 Acute – within 24 hours of the birth of the baby ( most
common type)
 Subacute – after the first 24 hours and within 4 weeks after
delivery
 Chronic – after more than 4 weeks after delivery
o According to the pregnancy state:
 Puerperal – when associated with labor or within 6 weeks of
this event
 Non-puerperal – those involving a non-gravid uterus
o According to the anatomical extent of extrusion
 Incomplete/partial – fundus of uterus not extending beyond
internal os
 Complete – when the fundus protrudes through the external os
 Prolapse – when the fundus protrudes out through the vagina
 Total – usually non-puerperal and tumor related, results in
inversion of the uterus and vaginal wall as well.
  The causes of uterine inversion remain undefined, but it is generally
associated with excessive cord traction in the third stage of labor. Other
associated risk factors are: fetal macrosomia, excessive fundal pressure,
placenta accrete, short umbilical cord, ligaments laxity and congenital
abnormalities of the uterus.
 The use of magnesium sulfate may be a risk factor, although there is no
evidence to support this association.
 The clinical presentation is an obviously displaced uterus while delivering
the placenta, usually in association with postpartum hemorrhage (PPH) and
hypovolemic shock and abdominal pain. The shock is usually out of
proportion to the degree of blood loss, although if the placenta remains
attached following inversion shock is less likely to occur.
 Physical examination findings are key in diagnosing uterine inversion. When
suspecting uterine inversion, bimanual examination is the most useful.
Abdominally, the fundus will not be palpable in the correct anatomic
position, and may be appreciated as a cuplike depression indicating the
collapsed fundus. A soft, congested mass in the vagina is virtually diagnostic,
and if the placenta is still attached, an error in the diagnosis is impossible.

B. TISSUE – Retained products of conception

RETAINED PLACENTA
 Definition: Failure to deliver the placenta within 30 minutes after the
delivery of the infant.
 Thirty (30) minutes is considered as the cut-off point as common
complications such as hemorrhage and infection (postpartum endometritis)
can arise when this limit is exceeded.
 Risk factors: previous history of retained placenta, preterm gestational age,
use of ergometrine, uterine anomalies, preeclampsia, stillbirth, small for
gestational age infant, velamentous cord insertion and maternal age >30
years old).
 Diagnosis: diagnosis is made based on the definition and can either be due to
a detached but trapped placenta or nondetached placenta such as placenta
accrete.
 Manual extraction of the placenta is usually performed if controlled cord
traction and drug therapy are unsuccessful. This should be done with
adequate analgesia and in a set-up that can deal with any complications that
may arise.

Manual removal of placenta. A. one hand grasps the fundus and the other hand is
inserted into the uterine cavity and the fingers are swept from side to side as they
are advanced. B. When the placenta detaches, it is grasped and removed.
C. TRAUMA – Injuries to the birth canal
 Genital tract trauma has been reported to cause about 20% of postpartum
hemorrhage (PPH). This should be suspected among women who underwent
vaginal delivery is bleeding persists despite a well contracted uterus and
administration of multiple uterotonic particularly if with one or more risk
factors.
 The major cause of morbidity and mortality that may arise from genital
injury is bleeding. Early detection and appropriate management of genital
trauma is essential.
 Genital tract lacerations: these can occur in the perineum, cervix, and the
uterus spontaneously or can be iatrogenic arising from episiotomy during
vaginal delivery.

 Lacerations in the perineum can be classified based on location:

o 1. Anterior perineal trauma - usually described as an injury that
involves the labia, anterior vagina, urethra or clitoris.
o 2. Posterior perineal trauma - involves injury to the posterior

 The laceration can be further classified according to the degree or depth:

o 1. First degree laceration – involves the fourchette, perineal skin,
and vaginal mucosa but not the underlying fascia and muscle.
o 2. Second degree laceration – involves the skin and mucous
membranes, the fascia and muscles of the perineal body.
o 3. Third degree laceration – extends through the skin, mucous
membrane, perineal body, and anal sphincter
o 4. Fourth degree laceration - involves all layers of the perineum
from the skin and vaginal mucosa up to anal epithelium and/or rectal
mucosa
UTERINE RUPTURE
 Uterine rupture is a rare but frequently is catastrophic obstetric complication
accompanied by fetal or maternal morbidity and mortality. It may be primary,
defined as occurring in a previously intact or unscarred uterus, or may be
secondary and associated with a preexisting incision, injury, or anomaly of the
myometrium.
 Classification:
o Complete uterine rupture - full thickness defect of the uterine wall, with
rupture of membranes, with or without expulsion of the fetus and/or
placenta; poses a threat to the life of both the mother and her baby.
o Incomplete uterine rupture or uterine dehiscence: partial thickness defect
of the uterine wall with intact visceral peritoneum; usually asymptomatic
and an incidental at the time of abdominal delivery; uncommon adverse
outcomes for mother and baby.
 Risk factors:
o prior uterine surgery
o induction of labor
o high-dose oxytocin induction
o prostaglandin induction
o grand multiparity (>5)
o morbidly adherent placenta
o congenital uterine anomaly (ex. Bicornuate uterus)
o connective tissue disorder
o forceps application
o internal podalic version
o Excessive fundal pressure
o Blunt or penetrating trauma
 Management
o Surgical intervention is the cornerstone of treatment of uterine rupture once
the diagnosis is suspected. The choice of surgical procedure depend upon
the type, extent, and location of the rupture, as well as the woman’s
condition and her desire to preserve her childbearing capability. Treatment
options for uterine rupture include repair of the uterus, arterial ligation and
hysterectomy.

D. THROMBIN – COAGULOPATHY
 Review patient history & coagulation test results
 Blood product replacement to reverse coagulation defects
 Direct pressure at bleeding site until specific therapy takes effect
