00:01
objective video about placentation the
00:04
objectives for this video are to
00:07
understand the role of embryonic since
00:09
SEO trophoblastic and Saito
00:10
trophoblastic cells and placental
00:12
development describe the layers of the
00:15
chorion and how the phenyl percentual
00:16
development affects the maternal surface
00:19
appreciate the basic functions of the
00:21
placenta be able to counsel a patient
00:23
regarding her risk factors for a
00:25
suspected placenta previa or accreta and
00:28
the subsequent impact on delivery and
00:30
understand the possible pathophysiology
00:32
related to the development of placenta
00:35
previa or accreta
00:38
alright before you can appreciate
00:40
obstetrics you need to understand the
00:42
development of the placenta the most
00:44
overlooked part of pregnancy during the
00:47
second week of gestation the primary
00:49
villi develop which is the first stage
00:51
of placental formation the trophoblastic
00:54
stem cells the outer sense issue of
00:56
trophoblasts and the inner synote ROFL
00:58
blasts form finger-like extensions into
01:00
the maternal decidua also known as the
01:03
maternal uterine wall at week 3 the
01:06
secondary villi form during this time
01:09
the extraembryonic mesoderm grows into
01:11
the villi and covers the entire surface
01:13
of the chorionic sac during the fourth
01:17
week the tertiary villi form this weak
01:20
mesenchyme differentiates into blood
01:22
vessels and forms an arterial capillary
01:24
network fuses with placental vessels and
01:27
develops connecting stalks the stem or
01:30
anchoring villi are formed as extra
01:32
Billis saito choko plastic cells and
01:35
attached to maternal tissue branched or
01:37
terminal villi grow from the sides of
01:39
the stem villi in the third trimester
01:42
the terminal villi emerge from the
01:44
proliferation of the trophoblastic cells
01:46
they are induced by capillary coiling
01:49
during the growth of fetal capillaries
01:51
within the mature villi at the base of
01:53
the villi the placental arteries and
01:55
veins pass through the chorionic plate
01:57
terminal villi serve as the region of
02:00
Maine gas and nutrients exchange they
02:02
are surrounded by maternal blood in the
02:04
interval of spaces there are four layers
02:07
separating maternal and fetal blood
02:09
since the shield trophoblast Saito
02:11
trophoblast relied connective tissue and
02:14
fetal capillary endothelial vascular
02:18
endothelial growth factor or veg F
02:20
drives two main phases of development in
02:22
pregnancy
02:23
initially the sign of truffle blast is
02:25
the cellular stimulus to vascular
02:27
genesis and angiogenesis later the
02:31
Hofbauer cells placental macrophages of
02:33
the Meza Connell origin and stromal
02:35
cells take over the stimulation of blood
02:37
vessel development the fibrin oeid layer
02:40
existed to forms within the
02:41
extracellular matrix vibrant type fiber
02:45
enoyed is a maternal blood clotting
02:46
product which replaces degenerating
02:48
syncytial trophoblasts matrix type
02:51
fibrin oyd is secreted by invasive extra
02:54
villus trophoblastic cells the fibrin
02:56
oyd layer or knitted book’s layer is
02:58
thought to present excessively deep
03:00
implantation and the loss of this layer
03:02
may lead to ad normal a cetacean
03:04
invasion now let’s pause think and apply
03:07
think fast the trophoblast consists
03:12
primarily of two layers
03:13
what are these layers and how do they
03:15
contribute to the phenol or maternal
03:16
surface of the chorion the outer layer
03:19
of the trophoblast is the synthesis otro
03:22
the blast and after implantation is
03:24
replaced by fiber enoyed extracellular
03:26
matrix to form knit a book’s layer
03:28
between the Quarian and the decidua lies
03:30
and de metrio surfaces the inner side of
03:33
trophoblasts stimulates fetal vascular
03:36
genesis in the chorion
03:38
now that we’ve gone through placental
03:40
development let’s look at some clinical
03:42
implications the placenta has four main
03:45
functions prevent fetal allograft
03:48
rejections metabolism and transport and
03:51
endocrine production there are several
03:54
risk factors for abnormal placental
03:56
development increasing parody increasing
03:59
maternal age infertility treatments
04:01
previous abortion previous uterine
04:05
surgeries such as dilation and curettage
04:07
cesarean section or myomectomy
04:09
maternal smoking maternal cocaine use
04:12
male fetus or non-white race of the
04:15
mother let’s look at two types of
04:17
placental pathology a little closer the
04:20
pathogenesis of placenta previa is
04:22
unknown one hypothesis is that previous
04:25
surgeries or fetal implantation leads to
04:27
areas of sub-optimal vascularized
04:30
decidua this promotes movement of
04:34
trophoblast to the lower uterine cavity
04:35
another theory is that a large placenta
04:38
such as with multiples increases the
04:41
probability that the placenta will
04:42
encroach or cover the internal AHS a
04:44
special type of previa is a vasopressin
04:48
vessels from the placenta or the
04:50
umbilical cord across the internal
04:51
cervical us these åberg vessels result
04:54
from filament discordant searches and by
04:57
lobed or suck Centurion lobed placentas
05:00
placental bleeding can be devastating
05:02
securely a placenta praevia uterine
05:05
contractions are gradual cervical change
05:08
apply shearing forces to the inelastic
05:10
placental sites resulting in a partial
05:12
detachment Digital vaginal exams of
05:16
penetrative intercourse can also cause
05:19
similar disruptions bleeding in a previa
05:22
is mainly maternal while Ave is a
05:24
preview bleeding is mainly fetal another
05:28
major placental pathology is placenta
05:30
accreta
05:30
this results from abnormal placental
05:33
implantation in which anchoring
05:35
placental villi attached to the
05:37
myometrium rather than the decidua
05:39
resulting in a net here
05:41
Ascenta pasetta accreta is a consequence
05:44
of abnormal adherence and absence of the
05:47
decidua base Alice the incidence is
05:50
higher in women with higher cesarean
05:52
section over 80% are associated with a
05:55
disruption in knit a book’s layer
05:57
placenta accreta occurs when the
06:00
placenta grows in to the uterine muscle
06:02
but does not penetrate the serosa this
06:06
accounts for about 15% of all abnormal
06:08
implantation cases finally in a placenta
06:12
percreta the placenta penetrates both
06:14
the myometrium and the serosa this
06:17
accounts for 5% of all cases and is the
06:19
most morbid the causes of placenta
06:23
accreta are unknown but may be related
06:25
to defective decidua lies ation from
06:27
prior surgeries or anatomic factors this
06:30
is supported by observation that 80% of
06:32
these cases occur in women with a
06:34
history of a prior cesarean section
06:37
dilation and curettage or myomectomy Wow
06:43
I have to admit I never really gave the
06:44
placenta much thought especially not the
06:46
clinical impact of the placental
06:48
development
06:48
I wonder if I will get to put this
06:50
didactic to you soon now let’s pause
06:53
think and apply think fast a 30 year old
06:57
grab at a 3 para 2 0 0 2 at 30 weeks
07:00
gestation and a history of two prior
07:03
cesarean deliveries presents with
07:05
hematuria and sonographic evidence of an
07:07
anterior placenta in the lower uterine
07:08
segment she has told she will possibly
07:11
need a bladder resection at the time of
07:12
delivery name the type of abnormal
07:14
presentation described and briefly
07:16
described the histopathology the patient
07:20
likely has placenta percreta which
07:22
occurs when the anchoring villi
07:23
penetrate the myometrium and neuter and
07:25
serosa and possibly adjacent organs in
07:28
this case the bladder wall theoretically
07:30
this may happen due to defected vascular
07:32
remodeling of the uterine scar or
07:34
partial or complete dehiscence of a
07:36
previous history t’me
07:38
I have your ultrasound report the fetal
07:45
Anatomy does not show any signs of
07:46
concerns but we should talk about your
07:48
placenta a little at this point we think
07:51
you have pasetta previa we will repeat
07:54
imaging at the start of the third
07:55
trimester to see if it has resolved Oh
07:58
what are the chances that the placenta
08:00
will move the more the placenta extends
08:03
over the US and the more interior it is
08:06
situated the more likely it will be
08:08
previa at delivery although our models
08:12
are not good if the placenta extends
08:14
over the ausf I 50 to 25 millimeters the
08:17
likelihood of previa at delivery is
08:19
about 20%
08:20
contrast that with someone whose
08:22
placenta is more than 25 millimeters
08:24
across the US their likelihood of a
08:27
previa at delivery is over 40%
08:29
our biggest concern if the premia does
08:32
not resolve is maternal hemorrhage
08:34
however we can start to address that
08:37
further once we get closer oh that
08:40
sounds great for now I’ll let you know
08:42
if I have any vaginal bleeding and we
08:45
can reevaluate as you recommend thanks
08:47
so much
08:48
boy am I glad I reviewed my placental
08:50
physiology with dr. Smith this concludes
08:54
the aapko basic science video on
08:56
abnormal presentation you should now
08:59
understand the role of embryonic since
09:01
Ciccio trophoblastic and Saito
09:02
trophoblastic cells in placental
09:05
development be able to describe the
09:07
layers of the chorion appreciate the
09:09
basic functions of the placenta and
09:11
understand the basic pathophysiology of
09:13
placenta previa or accreta
09:28
[Music]
09:36
[Music]

Bleeding during the second and third trimester has special clinical significance, encompassing problems that are quite serious and those that are normal or expected. It’s important to be able to distinguish between them.

One normal occurrence of bleeding is called Bloody show

As the cervix thins and begins to dilate in preparation for labor, the patient may notice the passage of some bloody mucous. This is a normal event during the days leading up to the onset of labor at term. If this is the only symptom, the patient can be reassured of its normalcy. If the patient is also having significant contractions, she should be evaluated for the possible onset of labor.

If this bloody mucous show appears prior to full term, then it may signal the imminent onset of preterm labor. These patients are evaluated for possible pre-term labor.

Bleeding that is more than bloody mucous (bright red, no mucous, passage of clots) requires further evaluation.

Cervicitis and cervical trauma ARE relatively innocent causes for bleeding.

During pregnancy, the cervix becomes softer, more fragile, and more vulnerable to the effects of trauma and microbes.

Cervical ectropion, in which the soft, mucous- producing endocervical mucosa grows out onto the exocervix is common among pregnant women. This friable endocervical epithelium bleeds easily when touched. This situation can lead to spotting after intercourse, a vaginal examination, or placement of a vaginal speculum.

Cervical ectropion also can lead to cervicitis. The normal squamous cell cervical epithelium is relatively resistant to bacterial attack. The endocervical mucosa is less resistant. If infected, the cervical ectropion is even more likely to bleed if touched.

These changes are usually easily seen during a vaginal speculum exam.

Placental abruption can be a very serious cause for bleeding at this time.

Placental abruption is also known as a premature separation of the placenta. All placentas normally detach from the uterus shortly after delivery of the baby. If any portion of the placenta detaches prior to birth of the baby, this is called a placental abruption. Placental abruption occurs in about 1% of all pregnancies.

A placental abruption may be partial or complete.

• • A complete abruption is a disastrous event. The fetus will die within 15-20 minutes. The mother will die soon afterward, from either blood loss or the coagulation disorder which often Women with complete placental abruptions are generally desperately ill with severe abdominal pain, shock, hemorrhage, a rigid and unrelaxing uterus.

• • Partial placental abruptions may range from insignificant to the striking abnormalities seen in complete abruptions.

Clinically, an abruption presents after 20 weeks gestation with abdominal cramping, uterine tenderness, contractions, and usually some vaginal bleeding. Occasionally, the blood loss is trapped inside the uterus. These cases are called “concealed abruptions.”

A number of factors are associated with an increased risk of placental abruption.

• • Prior placental abruption roughly doubles the risk of abruption in a subsequent pregnancy.

  • Abdominal trauma, including motor vehicle accidents are associated with placental abruption.

  • Many previous babies, Low socio-economic status , and Poor nutrition have an association.

  • Use of cocaine or its derivatives and Cigarette smoking , as well as Maternal hypertension, including pre-eclampsia and eclampsia are all associated with abruption.

  • Abnormalities in amniotic fluid volume, including Polyhydramnios and Oligohydramnios have the association.

  • Finally, Multiple gestations are associated with abruption.

Abruptions are often diagnosed clinically, based on the symptoms of bright red vaginal bleeding, frequent contractions and uterine tenderness.

There are no laboratory findings that are specific for placental abruption. In mild cases, laboratory tests are usually normal. In more advanced cases, the Hgb and Hct go down, as do the platelets and fibrinogen (due to the massive bleeding and consumption of coagulation factors) while fibrin split products go up. Fetal RBCs may be identified in the maternal blood.

In the case of large abruptions, ultrasound may identify a retroplacental blood clot. In milder cases, ultrasound scans are frequently normal.

Mild abruptions may resolve with bedrest and observation, but the moderate to severe abruptions generally result in rapid labor and delivery of the baby. If fetal distress is present (and it sometime is), an emergency cesarean section may be needed.

Because so many coagulation factors are consumed with the internal hemorrhage, coagulopathy is common. This means that even after delivery, the patient may continue to bleed because she can no longer effectively clot. In a hospital setting, this can be treated with infusions of platelets, fresh frozen plasma and cryoprecipitate. If these products are unavailable, fresh whole blood transfusion can give good results.

Placenta previa is another potentially disastrous cause of bleeding during the second and third trimester.

Normally, the placenta is attached to the uterus in an area remote from the cervix. Sometimes, the placenta is located in such a way that it covers the cervix. This is called a placenta previa.

There are degrees of placenta previa:

• • A complete placenta previa means the entire cervix is This positioning makes it impossible for the fetus to pass through the birth canal without causing maternal hemorrhage. This situation can only be resolved through cesarean section.
  • A marginal placenta previa means that only the margin or edge of the placenta is covering the In this condition, it may be possible to achieve a vaginal delivery if the maternal bleeding is not too great and the fetal head exerts enough pressure on the placenta to push it out of the way and tamponade bleeding which may occur.

Clinically, these patients present after 20 weeks with painless vaginal bleeding, usually mild. This is in contrast to patients with placental abruption, who usually experience significant pain and contractions. An old rule of thumb is that the first bleed from a placenta previa is not very heavy. For this reason, the first bleed is sometimes called a “sentinel bleed.”

Later episodes of bleeding can be very substantial and very dangerous. This can lead to hypovolemic shock and maternal death. Because a pelvic exam may provoke further bleeding it is important to avoid a vaginal or rectal examination in pregnant women during the second half of their pregnancy unless you are certain there is no placenta previa.

Factors associated with an increased risk of placenta previa include:

• • High maternal parity, Increased maternal age, previous cesarean section, previous uterine surgery, and uterine malformations.
  • It may also be associated with the use of cocaine or its derivatives, cigarette smoking, Ascherman’s syndrome, and large numbers of D&Cs.

The location of the placenta is best established by ultrasound. If ultrasound is not available, one reliable clinical method of ruling out placenta previa is to check for fetal head engagement just above the pubic symphysis.

Using a thumb and forefinger and pressing into the maternal abdomen, the fetal head can be palpated. If it is deeply engaged in the pelvis, it is basically impossible for a placenta previa to be present because there is not enough room in the birth canal for both the fetal head and a placenta previa. An x-ray of the pelvis (pelvimetry) can likewise rule out a placenta previa, but only if the fetal head is deeply engaged. Otherwise, an x-ray will usually not show the location of the placenta.

Clinical approach to third trimester bleeding

The clinical approach depends on the clinical situation. For example:

• • A 3rd trimester patient who is actively hemorrhaging bright red blood should go directly to the operating room for a cesarean section to deliver her from the placental abruption or placenta previa. While en route to the OR, call for blood transfusions and labs to determine coagulopathy.
  • A patient at term with regular contractions and a small amount of bloody mucous can be examined vaginally after confirming (through ultrasound or clinical exam of the abdomen) that there is no placenta previa.
  • Patients with bright red vaginal bleeding that is less than hemorrhage should be carefully evaluated prior to performing a pelvic Ultrasound can be helpful in locating the placenta and looking for retroplacental blood clot. Laboratory tests for coagulopathy can be helpful. Hgb is useful, not to determine whether to transfuse or not (that is a clinical, not laboratory decision), but to indicate the margin of safety available to the clinician in caring for this patient.
  • Continuous electronic fetal monitoring is important to determine the degree of tolerance the fetus has for this bleeding and the extent to which uteroplacental circulation has been disrupted. After ruling out a placenta previa, examine the patient with a speculum to determine the source of the bleeding (from the cervical os? from the surface of the cervix? from a laceration of the vaginal wall? etc.)

00:01
-My name is Dr. Melody Russell
00:02
and I’m a resident physician
00:03
in the Department of Obstetrics
00:05
and Gynecology.
00:06
This presentation is entitled
00:07
“Placenta Previa.”
00:11
00:12
The learning objectives
00:13
of this presentation
00:14
are to understand
00:15
the definitions, epidemiology,
00:17
and risk factors
00:18
for placenta previa; to review
00:20
clinical manifestations
00:21
of placenta previa
00:22
and associated conditions;
00:24
and to discuss the management
00:26
of asymptomatic and symptomatic
00:28
placenta previa.
00:29
00:32
We will begin by reviewing
00:33
definitions relevant to placenta
00:35
previa followed by a discussion
00:37
of the pathogenesis, risk
00:39
factors, and epidemiology
00:40
of placenta previa.
00:42
Lastly, we will review diagnosis
00:44
and management.
00:45
00:48
Placenta previa describes
00:50
a situation in which
00:51
the placenta is overlying
00:52
or near the internal cervical
00:53
os.
00:54
This occurs in one of 300
00:56
deliveries.
00:57
First, let’s review
00:58
the classification for placenta
01:00
previa.
01:01
Marginal previa is when
01:02
the placenta is immediately
01:04
adjacent to the internal
01:05
cervical os
01:06
but does not cover it.
01:07
In a complete previa,
01:09
the placenta covers
01:09
the entire internal cervical os.
01:12
Of complete previas, 20% to 30%
01:15
are central previas in which
01:17
the os is
01:17
equidistant from the anterior
01:19
and posterior edges
01:20
of the placenta.
01:22
Lastly, a low-lying placenta
01:24
is one in which the placenta is
01:25
within two centimeters
01:26
of the internal cervical os.
01:28
01:31
Next we will review proposed
01:32
pathogenetic mechanisms
01:34
and associated risk factors
01:35
for placenta previa.
01:37
Conditions that cause
01:38
endometrial scarring
01:40
increase the risk of placenta
01:41
previa.
01:43
Endometrial scarring may allow
01:44
for trophoblastic invasion
01:46
into the lower uterine segment.
01:48
Risk factors for scarring
01:49
include prior cesarean delivery,
01:52
increasing parity,
01:54
and prior curettage.
01:56
Increasing demand
01:57
for uteroplacental exchange
01:59
is another proposed mechanism
02:00
for previa, as this may result
02:03
in the need for increasing
02:04
placental surface area.
02:06
Associated risk factors include
02:08
maternal smoking, high altitude,
02:10
and multiple gestation.
02:11
02:14
The incidence of placenta previa
02:16
is one in 300 deliveries.
02:19
The incidence of previa
02:20
in early gestational age
02:22
is 5% to 15% of all deliveries.
02:25
And prior cesarean section
02:27
incidence is 1% to 4%.
02:29
Other risk factors for placenta
02:31
previa include advancing
02:33
maternal age,
02:35
early gestational age,
02:36
male fetus, maternal race,
02:39
and elevated maternal serum
02:40
alpha-fetoprotein.
02:41
02:45
The classic clinical
02:46
presentation for placenta previa
02:48
is painless vaginal bleeding.
02:50
A significant minority
02:52
of patients
02:52
present
02:53
with uterine contractions
02:54
accompanied by vaginal bleeding.
02:57
Symptoms occur
02:58
in the third trimester
02:59
as the lower uterine segment
03:00
develops
03:01
and uterine contractions start
03:03
to cause cervical change.
03:04
As the cervix dilates
03:06
and effaces, the lower uterine
03:08
segment develops.
03:09
This produces shearing forces
03:11
that cause the placenta to shear
03:13
and bleed.
03:14
Placenta previa is associated
03:16
with
03:16
other abnormal placentation,
03:18
which we will review
03:20
momentarily,
03:21
as well as
03:21
fetal malpresentation, preterm
03:24
premature rupture of membranes,
03:26
fetal growth restriction, vasa
03:28
previa, which is vessels
03:30
presenting at the cervical os,
03:32
velamentous cord insertion,
03:34
congenital anomalies,
03:36
and amniotic fluid embolism.
03:38
03:41
Placenta accreta occurs with 5%
03:43
to 10% of all placenta previa.
03:46
Placenta accreta occurs
03:48
due
03:48
to abnormal placental
03:50
implantation when placental
03:52
villi attach to the myometrium,
03:54
resulting
03:54
in an abnormally adherent
03:56
placenta.
03:58
Increta occurs when
03:59
chorionic villi invade
04:00
the myometrium.
04:02
And placental percreta occurs
04:04
when chorionic villi penetrate
04:06
the uterine serosa,
04:08
and may involve surrounding
04:09
organs, such as the bladder,
04:11
as shown in the ultrasound
04:12
image.
04:13
04:16
Placenta previa is included
04:18
in the differential diagnosis
04:20
for third trimester bleeding.
04:22
Other conditions that cause
04:23
third trimester bleeding include
04:25
placental abruption, which
04:27
is a premature separation
04:29
of the placenta
04:30
from the uterus; vasa previa,
04:34
when fetal vessels course
04:35
the internal cervical os;
04:37
uterine rupture; and lastly,
04:39
vaginal, cervical, or uterine
04:41
pathology.
04:44
The diagnosis of placenta previa
04:46
is made by localizing
04:48
the placenta
04:49
on diagnostic imaging.
04:51
Transabdominal ultrasound
04:53
is the safest, simplest,
04:54
and most accurate way
04:56
to localize the placenta.
04:58
Transvaginal ultrasound is safe
05:00
and offers
05:01
excellent visualization
05:02
of the internal cervical os.
05:05
Transperineal sonography
05:07
is reported to be accurate,
05:09
but is not routinely used
05:11
for placental localization.
05:13
Magnetic resonance imaging
05:14
is not routinely used
05:16
for placental localization,
05:17
but is often used when there is
05:19
a strong suspicion for accreta
05:21
based on ultrasound findings.
05:23
Magnetic resonance imaging
05:25
findings suggestive of accreta
05:27
are uterine bulging,
05:29
heterogeneous signal intensity
05:31
within the placenta,
05:32
and the presence
05:33
of dark intraplacental bands.
05:35
05:38
Now we will review management
05:40
of placenta previa.
05:42
Asymptomatic patients
05:44
with placenta previa
05:45
are followed with repeat
05:46
ultrasounds
05:47
through the third trimester,
05:49
as the placenta may become
05:50
farther
05:51
from the internal cervical os
05:52
as the uterus expands
05:54
and the lower uterine segment
05:55
develops.
05:56
These patients are instructed
05:57
to continue pelvic rest,
05:59
and then nothing should be put
06:00
in the vagina.
06:02
This includes
06:02
vaginal intercourse as well as
06:05
digital cervical examinations
06:07
by their physician.
06:08
After an episode
06:09
of vaginal bleeding, patients
06:11
are hospitalized for close
06:12
inpatient monitoring.
06:14
If they are stable and have
06:15
no further bleeding
06:17
for several days,
06:18
they may be discharged.
06:20
Before discharge, patients must
06:22
understand that they should be
06:23
able to reliably return
06:25
to the hospital quickly
06:27
should they develop
06:28
further vaginal bleeding.
06:30
Importantly, the plan
06:31
is
06:32
contingent on gestational age,
06:34
as it may be more
06:35
prudent to move toward delivery
06:36
after a significant bleed
06:38
if the patient is over 34 weeks,
06:41
while conservative management is
06:43
preferred in earlier
06:44
gestational ages given
06:45
the risks of morbidity
06:47
associated with premature birth.
06:48
06:51
In the setting
06:52
of acute vaginal bleeding,
06:54
patients must have adequate IV
06:56
access, often two large bore
06:58
IVs,
06:59
in case aggressive resuscitation
07:00
is required.
07:02
Patients should receive
07:03
antenatal steroids to promote
07:05
fetal lung maturity if they are
07:07
less than 34 weeks
07:08
gestational age,
07:09
as delivery may be imminent
07:11
depending on the severity
07:12
of the hemorrhage.
07:13
A blood type and antibody screen
07:15
should be obtained for Rh
07:17
status,
07:18
as patients should receive Rh
07:20
immune globulin
07:21
after the initial bleed
07:22
if they are Rh negative.
07:24
This should also be sent
07:25
in anticipation
07:26
of possible blood transfusion
07:28
if required.
07:30
The fetus should be monitored
07:31
continuously as any signs
07:33
of nonreassuring fetal status
07:35
suggest fetal anemia
07:36
and/or hypoxemia.
07:39
Ultimately, providers should
07:40
move toward delivery
07:42
if fetal status is nonreassuring
07:44
despite resuscitative measures,
07:46
if hemorrhage is
07:47
life-threatening, if the patient
07:49
is in active labor,
07:51
or if significant bleeding
07:52
occurs after 34 weeks
07:54
gestational age.
07:55
Cesarean delivery
07:57
is necessary in nearly all women
07:59
with placenta previa.
08:00
In the case of placenta accreta,
08:03
special precautions should be
08:04
taken as there is a very
08:06
significant chance of hemorrhage
08:07
at the time of surgery.
08:09
These precautions include
08:11
pre-operative arterial catheter
08:13
placement for possible uterine
08:14
artery embolization,
08:16
coordination with the blood bank
08:18
for transfusion services,
08:20
and consultation
08:21
with gynecologic oncology
08:23
for surgical assistance
08:24
if cesarean hysterectomy is
08:25
required.
08:26
08:29
In conclusion, placenta previa
08:32
occurs when there is
08:33
abnormal placental implantation
08:35
at or near the internal cervical
08:37
os.
08:38
It classically presents
08:39
with painless vaginal bleeding
08:42
and is diagnosed by imaging
08:44
with ultrasound
08:45
and magnetic resonance imaging
08:47
follow-up if necessary
08:49
when there is concern
08:50
for placenta accreta.
08:52
Placenta previa can be managed
08:54
as an outpatient if the patient
08:56
is asymptomatic
08:57
or after one episode
08:59
of bleeding.
09:01
Active bleeding in placenta
09:02
previa should be considered
09:04
a potential obstetric emergency.
09:06
Mode of delivery
09:08
should be by cesarean section.

00:01
Today, we’ll be talking
00:02
about placental abruption.
00:03
00:07
At the end of this presentation
00:08
students should be
00:09
able to describe
00:09
the clinical presentation
00:11
of placental abruption,
00:12
describe the epidemiology
00:14
and risk factors
00:14
for placental abruption,
00:16
describe the diagnosis
00:17
of third trimester bleeding,
00:19
understand the pathogenesis
00:20
of placental abruption,
00:22
describe treatment options
00:23
for a placental abruption,
00:25
and understand the range
00:26
of possible outcomes.
00:27
00:30
We’ll start with a case
00:31
vignette.
00:32
Our first patient is
00:33
a 23-year-old gravid 2 para 001
00:36
at 37 weeks and four days,
00:38
gestational age, who presents
00:39
to labor and delivery triage
00:41
with intense cramping, which
00:42
started approximately one hour
00:44
ago.
00:45
In the last 15 minutes,
00:46
she’s developed
00:46
profuse vaginal bleeding.
00:48
Her physical exam reveals
00:49
increased uterine tone
00:50
and fetal tachycardia.
00:53
This case just demonstrates
00:55
that the clinical presentation
00:56
of abruption can vary.
00:57
Our patient here has
00:58
the classical presentation
00:59
of painful third trimester
01:00
bleeding.
01:01
01:04
Abruption presents with varying
01:05
degrees of severity.
01:07
Acute onset vaginal bleeding
01:09
with painful contracting uterus
01:10
in the third trimester
01:11
is classic.
01:12
In these cases, the blood
01:14
in the uterus has an irritating
01:15
effect causing hearing
01:16
contractions.
01:18
Additionally, the mother
01:19
experiences abdominal or lower
01:20
back pain,
01:21
secondary to this irritation.
01:23
The fetus
01:24
can be without effects,
01:25
but, most likely,
01:26
will demonstrate tachycardia
01:27
and decreased variability.
01:29
Of note, vaginal bleeding is not
01:31
required for the diagnosis
01:32
as the bleeding can be trapped
01:33
behind the placenta.
01:35
Additionally,
01:35
a couvelaire uterus can occur,
01:37
which is when the bleeding
01:38
passes through the uterine wall
01:40
into the perinatal cavity
01:41
or retroperitoneum.
01:44
Acute abruption is thought to be
01:45
secondary to an arterial bleed
01:47
at the utero-placental junction.
01:49
Conversely, placental abruption
01:51
can also present
01:52
with light chronic bleeding.
01:54
This bleeding can be
01:54
difficult to differentiate
01:56
from other etiologies
01:57
of third trimester bleeding,
01:59
and a careful search
01:59
for the most common cause
02:01
must ensue.
02:03
As there is decreased
02:04
placental oxygen in transfer,
02:05
fetal effects include
02:06
oligohydramnios, fetal growth
02:08
restriction, and preeclampsia.
02:11
Of concern is
02:11
that this chronic type bleeding
02:13
can rapidly convert
02:14
to an acute abruption
02:15
with catastrophic consequences.
02:16
02:20
Placental abruption is quite
02:21
simply the premature separation
02:23
of the placenta
02:24
from the uterine wall.
02:25
As mentioned earlier,
02:26
there are many risk factors
02:27
and events which can lead
02:28
to this.
02:30
The most recent theories argue
02:31
that the majority
02:32
of placental abruption
02:33
is related
02:34
to chronic pathologic vascular
02:35
processes, hence the association
02:38
with smoking,
02:39
maternal hypertension,
02:40
and ischemic placental disease.
02:42
Traumatic events can also cause
02:44
abruption by creating shear
02:46
forces between the placenta
02:47
and the uterus.
02:48
These lead
02:49
to a common final pathway
02:50
involving
02:51
retroplacental hemorrhage.
02:53
This separation causes impaired
02:55
maternal-fetal oxygen
02:56
and nutrient exchange leading
02:58
to fetal hypoxemia
03:00
and eventual metabolic acidosis.
03:02
Additionally, this bleeding
03:04
can activate
03:05
the maternal coagulation cascade
03:07
leading
03:07
to disseminated intravascular
03:09
coagulation, hemorrhage, ARDS,
03:12
renal failure,
03:13
multi-organ system failure,
03:15
and eventually death,
03:16
if rapid aggressive treatment is
03:18
not pursued.
03:19
03:22
There are many risk factors
03:23
for placental abruption,
03:25
however, the most important
03:26
is pregnancy, meaning this can
03:28
happen to any pregnant woman
03:29
regardless of risk factors.
03:32
Risk factors can be separated
03:33
into several themes.
03:35
First, are acute events
03:36
associated with rapid uterine
03:37
decompression.
03:39
When the uterine volume rapidly
03:40
decreases, such as with trauma,
03:42
rupture of membranes,
03:43
or delivery of the first twin,
03:45
shear forces
03:46
between the placenta
03:47
and the uterine wall ensue,
03:48
which can cause separation.
03:50
Another theme
03:51
is maternal hypertensive
03:52
disorders.
03:53
Maternal hypertension
03:54
and cocaine use
03:55
lead to increased vascular
03:56
pressure, which can cause
03:57
vascular rupture and ensuing
03:59
hemorrhage.
04:00
Finally, smoking
04:01
and ischemic placental disease
04:03
can cause microvascular damage,
04:05
which can lead
04:05
to retro-placental bleeding.
04:07
04:10
The differential diagnosis
04:11
of third trimester bleeding
04:12
is long.
04:13
Placental abruption
04:14
is the first and presents
04:15
with painful vaginal bleeding.
04:18
Placenta previa occurs when
04:19
the placenta is implanted
04:20
on or near the cervix,
04:22
and bleeding occurs
04:22
with cervical dilation
04:24
or cervical manipulation.
04:26
This is classically painless
04:27
vaginal bleeding.
04:29
Uterine rupture is a rarer
04:30
event, but can occur in labor
04:32
when the uterine muscle tears
04:33
open.
04:34
This typically occurs
04:35
at the site
04:36
of a previous uterine scar
04:37
such as cesarean scar
04:38
or myomectomy scar.
04:41
Vasa previa occurs when there is
04:42
a marginal cord insertion
04:44
into the placenta and the cord
04:45
comes across the cervical os.
04:48
Of note, this is often bleeding
04:49
of fetal blood, which can be
04:50
catastrophic as the fetal blood
04:52
volume is very small.
04:54
Other cervical
04:55
or vaginal pathology
04:56
can lead to vaginal bleeding,
04:57
including
04:58
cervicitis cervical cancer,
05:00
cervical laceration,
05:01
or vaginitis.
05:03
Finally, vaginal bleeding
05:05
can be physiologic and occur
05:06
with cervical dilation.
05:07
This is referred to as bloody
05:08
show.
05:09
05:12
Placental abruption is primarily
05:14
a clinical diagnosis.
05:15
Diagnosis is based
05:16
on patient history and risk
05:18
factors, as mentioned earlier.
05:19
Physical exam is performed
05:21
rapidly, yet thoughtfully.
05:23
Abdominal exam will likely
05:24
reveal uterine tenderness
05:25
and hypertonicity.
05:27
Speculum exam should always
05:28
be performed prior
05:29
to digital exam.
05:30
This is used to rule out
05:31
placenta previa.
05:33
If a digital exam is performed
05:35
in the face of placenta previa,
05:36
then the placenta can be further
05:38
disturbed leading
05:38
to fetal hemorrage.
05:40
Historically, speculum exam
05:42
was performed
05:42
under double set-up,
05:44
meaning that the exam was
05:45
performed in the operating room,
05:46
with the capability
05:47
of performing
05:47
both vaginal or cesarean
05:49
delivery expediently.
05:52
Now bedside ultrasound has been
05:53
added to the obstetricians’
05:55
armamentarium.
05:56
Although ultrasonographic
05:57
examination is
05:58
insensitive for the diagnosis
06:00
of placental abruption,
06:01
it can be used to rule out
06:03
other pathology,
06:03
such as placenta previa or vasa
06:05
previa.
06:07
If ultrasound does demonstrate
06:08
a retroplacental blood
06:09
collection or clot,
06:10
then the diagnosis is confirmed.
06:12
06:16
Management
06:16
of placental abruption.
06:18
If abruption is suspected
06:19
or diagnosed at greater than 34
06:21
weeks, an expeditious delivery
06:23
should be pursued.
06:25
In the absence of signs
06:26
of fetal distress,
06:28
and if the mother is
06:28
hemodynamically stable,
06:30
then vaginal delivery
06:31
is optimal.
06:33
Labor augmentation in the form
06:34
of intravenous Platosin
06:36
and artificial rupture
06:37
of membranes
06:37
should be undertaken.
06:39
In the event of fetal distress
06:41
or maternal hemodynamic
06:42
instability,
06:43
then emergent Cesarean delivery
06:45
may be necessary.
06:46
In either case, blood products
06:48
should be prepared
06:48
for rapid delivery, particularly
06:50
packed red blood cells,
06:51
fresh frozen plasma, platelets,
06:53
and cryofibrinogen.
06:57
In the pre-term gestation
06:59
complicated by placenta previa,
07:01
the risks of prematurity
07:02
must be balanced with the risks
07:03
of reduced maternal fetal oxygen
07:05
and nutrient exchange.
07:07
If there are no signs
07:08
of fetal distress and the mother
07:09
is hemodynamically
07:10
stable without evidence
07:12
of coagulopathy,
07:13
then expectant management
07:14
is the optimal course.
07:17
Regular fetal assessment
07:18
with non-stress testing
07:19
and ultrasonography
07:20
should be performed and delivery
07:22
pursued if fetal distress is
07:24
uncovered.
07:25
RhoGAM should be administered
07:26
if the mother is Rh negative.
07:29
Likewise,
07:30
maternal hemodynamic status
07:31
and coagulation should be
07:32
regularly monitored
07:34
and, if abnormal, then a move
07:35
should be made toward delivery.
07:37
If neither of these occur
07:38
and the pregnancy
07:39
continues to progress, delivery
07:41
should occur at or before 37
07:43
weeks, with the exact timing
07:44
being provider dependent
07:46
and ranging from 34 to 37 weeks.
07:48
07:51
Tragically, fetal demise
07:53
secondary to hemorrhage
07:54
or asphyxia does occur.
07:56
In these instances,
07:57
the care of the mother
07:58
becomes the primary concern
07:59
of the obstetrical team.
08:01
In these situations,
08:02
expeditious delivery should
08:04
occur no matter
08:04
the gestational age.
08:07
Vaginal delivery is ideal
08:08
because of the decreased
08:09
maternal morbidity associated
08:10
with this procedure.
08:12
In these cases,
08:13
the risk
08:13
of maternal coagulopathy
08:15
is greatly increased.
08:17
DIC is a frequent occurrence
08:19
and should be managed by rapid
08:20
and aggressive blood product
08:21
replacement.
08:22
The latest data derived
08:24
from the trauma literature
08:25
indicate
08:26
that massive transfusion should
08:27
include both PRBCs, FFP,
08:29
platelets, and cryoprecipitate.
08:32
Blood products should be
08:33
administered based
08:33
on the clinical exam,
08:35
as laboratory of coagulopathy
08:37
often lags
08:37
behind the clinical situation
08:39
which can lead
08:40
to catastrophic hemorrhage.
08:42
Finally, Cesarean delivery,
08:44
referred to as a hysterotomy,
08:45
in the case of fetal demise,
08:47
should be used
08:47
for maternal indications
08:49
such as uncontrolled hemorrhage.
08:50
08:53
Outcomes for placental abruption
08:55
are widely varied and largely
08:56
dependent on the degree
08:57
of placental separation.
09:00
In cases where there is
09:01
minimal or marginal separation
09:02
at term, there may be
09:03
no adverse maternal
09:05
or fetal affects.
09:07
Chronic abruption can lead
09:08
to pre-term birth
09:09
and intrauterine growth
09:10
restriction which carry a range
09:11
of neonatal outcomes ranging
09:13
from NICU admission
09:14
to permanent, neurologic sequela
09:15
or death.
09:17
Maternal mortality is generally
09:18
low, but morbidity can be high.
09:21
Emergent DIC can lead
09:22
to renal failure
09:23
and multi-organ failure.
09:25
Even when blood products are
09:26
aggressively supplemented,
09:27
ICU admission is common.
09:29
Hysterectomy may also be
09:31
performed if uterine bleeding
09:32
cannot be controlled in any
09:33
other way.
09:34
09:36
In summary,
09:37
painful third trimester bleeding
09:39
is placental abruption
09:40
until proven otherwise.
09:42
Risk factors
09:43
for placental abruption
09:44
are varied.
09:44
Both acute and chronic abruption
09:46
can occur.
09:48
Treatment is
09:48
dependent on gestational age.
09:51
And outcomes depend
09:52
on the degree
09:53
of placental separation.
09:54
09:56
Here are a list of references
09:58
for further reading.