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-Dr. N.N.CHAVAN
 Placental abruption (also referred to as abruptio
placentae) refers to partial or complete placental
detachment prior to delivery of the fetus.
 The diagnosis is typically reserved for
pregnancies over 20 weeks of gestation.
 Abruption is a significant cause of both maternal
morbidity and neonatal morbidity and mortality,
particularly when it occurs preterm
 Placental abruption complicates
approximately 1 in 100 to 120 pregnancies,
with two-thirds classified as severe based
on associated maternal, fetal, and
neonatal morbidity
https://www.uptodate.com/contents/placental-abruption-pathophysiology-
clinical-features-diagnosis-and-consequences/abstract/1
 The immediate cause of the premature placental
separation is rupture of maternal vessels in the
decidua basalis.
 Rarely, the bleeding originates from the fetal-
placental vessels.
 The accumulating blood splits the decidua, separating
off a thin layer of decidua with its placental
attachment.
 Complete or nearly complete placental separations
are caused by high pressure arterial hemorrhage in
the central area of the placenta that extensively
dissect through the placental-decidual interface
 Thrombin plays a key role in the clinical consequences of
placental abruption, and may be important in its
pathogenesis, as well.
 It is formed via two pathways:
-Decidual bleeding leads to release of tissue factor
(thromboplastin) from decidual cells, which generates
thrombin
-Decidual hypoxia induces production of vascular
endothelial growth factor (VEGF), which acts directly on
decidual endothelial cells to induce aberrant expression of
tissue factor, which then generates thrombin
 Uterine hypertonus and contractions
 Enhanced expression of matrix metalloproteinases, up-
regulation of genes involved in apoptosis , and induced
expression of inflammatory cytokines (predominantly
interleukin-8), leading to tissue necrosis and degradation of
extracellular matrix
 Triggering of coagulation
 Functional progesterone withdrawal by reduced expression
of progesterone receptors in decidual cells
 The prevalence is more with
(a) high birth order pregnancies with gravida 5 and above —
three times more common than in first birth
(b) advancing age of the mother
(c) poor socio-economic condition
(d) Malnutrition
(e) smoking (vaso-spasm).
 Hypertension in pregnancy is the most important predisposing
factor. Pre-eclampsia, gestational hypertension and essential
hypertension, all are associated with placental abruption.
 The association of pre-eclampsia in abruptio placenta varies
from10-50 percent.
 The mechanism of the placental separation in pre-
eclampsia is : Spasm of the vessels in the utero placental
bed (decidual spiral artery) → anoxic endothelial damage →
rupture of vessels or extravasation of blood in the decidua
basalis (retroplacental hematoma).
 Trauma:Traumatic separation of the placenta usually
leads to its marginal separation with escape of blood
outside. The trauma may be due to: (i) Attempted external
cephalic version specially under anesthesia using great force
(ii) Road traffic accidents or blow on the abdomen (iii)
Needle puncture at amniocentesis
 Sudden uterine decompression: Sudden decompression of
the uterus leads to diminished surface area of the uterus
adjacent to the placental attachment and results in
separation of the placenta.This may occur following—(a)
delivery of the first baby of twins (b) sudden escape of liquor
amnii in hydramnios and (c) premature rupture of
membranes.
 Short cord, either relative or absolute, can bring about
placental separation during labor by mechanical pull.
 Placental anomaly: Circumvallate placenta .
 Sick placenta: Poor placentation, evidenced by abnormal
uterine artery Doppler waveforms is associated with
placental abruption.
 Folic acid deficiency even without evidence of overt
megaloblastic erythropoiesis — this has been observed to be
associated.
 Uterine factor: Placenta implanted over a septum (Septate
Uterus) or a submucous fibroid.
 Torsion of the uterus leads to increased venous pressure and
rupture of the veins with separation of the placenta.
 Cocaine abuse is associated with increased risk of transient
hypertension, vasospasm and placental abruption.
 Thrombophilias inherited or acquired have been associated
with increased risk of placental infarcts or
abruption.
 Prior abruption: Risk of recurrence for a woman with
previous abruption varies between 5 to 17%.
RCOG Green top Guideline 63
 Blood may accumulate behind the placenta when it is
totally separated from the uterine wall except at the margin
— concealed type.
 Blood may dissect downwards in between the membranes
and the uterine wall and ultimately escapes out through
the cervix or may be kept concealed by the pressure of
the fetal head on the lower uterine segment
— revealed type.
 Blood may gain access to the amniotic cavity after rupturing
the membranes
 Blood may percolate through the layers of myometrium
upto the serous coat – couvelaire uterus
 Grade—0: Clinical features may be absent.The diagnosis is
made after inspection of placenta following delivery.
 Grade—1 (40%): (i)Vaginal bleeding is slight (ii) Uterus:
irritable, tenderness may be minimal or absent (iii) Maternal
BP and fibrinogen levels unaffected (iv) FHS is good.
 Grade—2 (45%): (i)Vaginal bleeding mild to moderate (ii)
Uterine tenderness is always present (iii) Maternal pulse ↑,
BP is maintained (iv) Fibrinogen level may be decreased (v)
Shock is absent (vi) Fetal distress or even fetal death occurs.
 Grade—3 (15%): (i) Bleeding is moderate to severe or may be
concealed (ii) Uterine tenderness is marked (iii) Shock is
pronounced (iv) Fetal death is the rule (v) Associated
coagulation defect or anuria may complicate.
 Women with an acute abruption classically present with the
abrupt onset of vaginal bleeding, mild to moderate
abdominal and/or back pain, and uterine contractions
vaginal bleeding ranges from mild and clinically insignificant
to severe and life-threatening
 Adominal pain, hypotension, and fetal heart rate (FHR)
abnormalities suggest clinically significant separation that
could result in fetal death and severe maternal morbidity
 Identification of a retroplacental hematoma is the classic
ultrasound finding of placental abruption. Retroplacental
hematomas have a variable appearance; they can appear
solid, complex, and hypo-, hyper-, or iso-echoic compared
with the placenta. Hypoechogenicity and sonolucency are
features of resolving rather than acute hematoma.
 The sensitivity of ultrasound findings for diagnosis of
abruption is only 25 to 60 percent but the positive predictive
value is high (88 percent) when ultrasound findings
suggestive of abruption are present
 Serious maternal consequences of abruption include:
Excessive blood loss and DIC, which generally necessitate
blood transfusion and can lead to hypovolemic shock, renal
failure, adult respiratory distress syndrome, multiorgan
failure, peripartum hysterectomy and, rarely, death.
 In addition to these acute consequences, the mother is at
increased long-term risk of premature cardiovascular disease
and doubling of the risk of death after coronary artery
revascularization.These increased risks may reflect
underlying maternal vascular abnormalities that manifest
during pregnancy as abruption.
 Serious fetal and neonatal consequences of abruption
include:
Increased perinatal morbidity and mortality related to
hypoxemia, asphyxia, low birth weight, and/or preterm
delivery.
 Fetal growth restriction (with chronic abruption)
 Fetal asphyxia, preterm birth, and growth restriction can be
associated with short- and long-term sequelae, and
abruption appears to compound the risk
 Initiate continuous fetal heart rate monitoring
 Secure intravenous access
 Closely monitor the mother's hemodynamic status
 Quantify blood loss
 Draw blood for a complete blood count including platelet
count, blood type and screen (cross-match if transfusion is
likely), and coagulation studies
 Notify the anesthesia team
 Administer standard medications to women likely to
deliver: magnesium sulfate for neuroprotection for
pregnancies <32 weeks of gestation, antenatal
corticosteroids for pregnancies <34 weeks of gestation
The most important factors impacting the decision to deliver
a patient with placental abruption versus expectant
management are:
 Gestational age
 Fetal and maternal status, which reflect the severity of the
abruption.
 The optimal route of delivery in these cases minimizes the
risk of maternal morbidity or mortality, since fetal well-being
is no longer a factor.
 Blood and blood product replacement is often necessary and
expeditious delivery is desirable because the frequency of
coagulopathy and continuous heavy bleeding is much higher
in abruptions in which fetal death has occurred.
 Placental separation is often greater than 50 percent.
 Caesarean delivery is often the best option when vaginal
delivery is not imminent and rapid control of bleeding is
required because of
 maternal hemodynamic instability or
 significant coagulopathy, or
 the mother is unwilling to accept adequate blood
replacement therapy and is therefore likely to develop
hemodynamic instability or
 coagulopathy during labour.
 Blood and blood products for correction of coagulopathy
should be replaced prior to and during the caesarean delivery
 When the fetus and mother are both stable, the decision to
deliver depends primarily on gestational age, with
consideration of ongoing maternal symptoms
 Less than 34 weeks of gestation —When the fetus and
mother are both stable and there is no evidence of ongoing
major blood loss or coagulopathy, conservative
management with the aim of delivering a more mature fetus
is the main goal before 34 weeks of gestation .
We take the following approach:
 Administer corticosteroids – Corticosteroids to promote
fetal lung maturation and reduce complications of
prematurity are administered to pregnancies at 23 to 34
weeks of gestation, given the increased risk of need for
preterm delivery.
 Tocolysis – For women in preterm labor, we administer a 48-
hour course of nifedipine to enable administration of a full
course of corticosteroids.
 In severe abruptions, blood may extravasate into the
myometrium (called a Couvelaire uterus), and this can be
seen at cesarean.
 The Couvelaire uterus is atonic and prone to postpartum
hemorrhage.
 Aggressive management of atony is needed to prevent
disseminated intravascular coagulation and exsanguination;
however, atony in this setting is less likely to respond to
standard therapies for postpartum hemorrhage than atony
from other causes; thus, these women are at high risk for
requiring hysterectomy
 Naked eye features:
The uterus is of dark port wine colour which may be patchy
or diffuse.
It tends to occur initially on the cornua before spreading to
other areas, more specially over the placental site.
Subperitoneal petechial haemorrhages are found
under the uterine peritoneum and may extend into the broad
ligament.
There may be free blood in the peritoneal cavity or
broad ligament hematoma.
 Microscopic appearance:
The uterine muscles over the affected area are necrosed and
there is infiltration of blood and fluid in between the muscle
bundles.
The serosa may split on occasions, to allow the blood to
enter the peritoneal cavity.
The blood vessels show acute degenerative changes with
thrombosis.
Uterus as observed during cesarean section is not an
indication per se for hysterectomy.
 Postpartum, we administer an intravenous oxytocin infusion
as the first-line uterotonic agent.
 Maternal vital signs, blood loss, urine output, uterine size
and consistency, and laboratory results are monitored
closely to ensure that bleeding has been controlled and that
coagulopathy (if present) is resolving, and to guide
replacement of fluids and blood products, as needed.
 Women with placental abruption are at several fold higher
risk of abruption in a subsequent pregnancy.
 3 to 15 percent of women have a recurrence, compared with
a baseline incidence of 0.4 to 1.3 percent in the general
population.
 In one longitudinal population-based study, the risk of
placental abruption in a subsequent pregnancy was about 6
percent in women with an abruption in their first pregnancy
versus 0.06 percent in women without an abruption.
Abruptio placentae
Abruptio placentae

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Abruptio placentae

  • 2.
  • 3.  Placental abruption (also referred to as abruptio placentae) refers to partial or complete placental detachment prior to delivery of the fetus.  The diagnosis is typically reserved for pregnancies over 20 weeks of gestation.  Abruption is a significant cause of both maternal morbidity and neonatal morbidity and mortality, particularly when it occurs preterm
  • 4.  Placental abruption complicates approximately 1 in 100 to 120 pregnancies, with two-thirds classified as severe based on associated maternal, fetal, and neonatal morbidity https://www.uptodate.com/contents/placental-abruption-pathophysiology- clinical-features-diagnosis-and-consequences/abstract/1
  • 5.  The immediate cause of the premature placental separation is rupture of maternal vessels in the decidua basalis.  Rarely, the bleeding originates from the fetal- placental vessels.  The accumulating blood splits the decidua, separating off a thin layer of decidua with its placental attachment.  Complete or nearly complete placental separations are caused by high pressure arterial hemorrhage in the central area of the placenta that extensively dissect through the placental-decidual interface
  • 6.  Thrombin plays a key role in the clinical consequences of placental abruption, and may be important in its pathogenesis, as well.  It is formed via two pathways: -Decidual bleeding leads to release of tissue factor (thromboplastin) from decidual cells, which generates thrombin -Decidual hypoxia induces production of vascular endothelial growth factor (VEGF), which acts directly on decidual endothelial cells to induce aberrant expression of tissue factor, which then generates thrombin
  • 7.  Uterine hypertonus and contractions  Enhanced expression of matrix metalloproteinases, up- regulation of genes involved in apoptosis , and induced expression of inflammatory cytokines (predominantly interleukin-8), leading to tissue necrosis and degradation of extracellular matrix  Triggering of coagulation  Functional progesterone withdrawal by reduced expression of progesterone receptors in decidual cells
  • 8.  The prevalence is more with (a) high birth order pregnancies with gravida 5 and above — three times more common than in first birth (b) advancing age of the mother (c) poor socio-economic condition (d) Malnutrition (e) smoking (vaso-spasm).  Hypertension in pregnancy is the most important predisposing factor. Pre-eclampsia, gestational hypertension and essential hypertension, all are associated with placental abruption.  The association of pre-eclampsia in abruptio placenta varies from10-50 percent.
  • 9.  The mechanism of the placental separation in pre- eclampsia is : Spasm of the vessels in the utero placental bed (decidual spiral artery) → anoxic endothelial damage → rupture of vessels or extravasation of blood in the decidua basalis (retroplacental hematoma).  Trauma:Traumatic separation of the placenta usually leads to its marginal separation with escape of blood outside. The trauma may be due to: (i) Attempted external cephalic version specially under anesthesia using great force (ii) Road traffic accidents or blow on the abdomen (iii) Needle puncture at amniocentesis
  • 10.  Sudden uterine decompression: Sudden decompression of the uterus leads to diminished surface area of the uterus adjacent to the placental attachment and results in separation of the placenta.This may occur following—(a) delivery of the first baby of twins (b) sudden escape of liquor amnii in hydramnios and (c) premature rupture of membranes.  Short cord, either relative or absolute, can bring about placental separation during labor by mechanical pull.
  • 11.  Placental anomaly: Circumvallate placenta .  Sick placenta: Poor placentation, evidenced by abnormal uterine artery Doppler waveforms is associated with placental abruption.  Folic acid deficiency even without evidence of overt megaloblastic erythropoiesis — this has been observed to be associated.  Uterine factor: Placenta implanted over a septum (Septate Uterus) or a submucous fibroid.
  • 12.  Torsion of the uterus leads to increased venous pressure and rupture of the veins with separation of the placenta.  Cocaine abuse is associated with increased risk of transient hypertension, vasospasm and placental abruption.  Thrombophilias inherited or acquired have been associated with increased risk of placental infarcts or abruption.  Prior abruption: Risk of recurrence for a woman with previous abruption varies between 5 to 17%.
  • 13. RCOG Green top Guideline 63
  • 14.  Blood may accumulate behind the placenta when it is totally separated from the uterine wall except at the margin — concealed type.  Blood may dissect downwards in between the membranes and the uterine wall and ultimately escapes out through the cervix or may be kept concealed by the pressure of the fetal head on the lower uterine segment — revealed type.  Blood may gain access to the amniotic cavity after rupturing the membranes  Blood may percolate through the layers of myometrium upto the serous coat – couvelaire uterus
  • 15.  Grade—0: Clinical features may be absent.The diagnosis is made after inspection of placenta following delivery.  Grade—1 (40%): (i)Vaginal bleeding is slight (ii) Uterus: irritable, tenderness may be minimal or absent (iii) Maternal BP and fibrinogen levels unaffected (iv) FHS is good.
  • 16.  Grade—2 (45%): (i)Vaginal bleeding mild to moderate (ii) Uterine tenderness is always present (iii) Maternal pulse ↑, BP is maintained (iv) Fibrinogen level may be decreased (v) Shock is absent (vi) Fetal distress or even fetal death occurs.  Grade—3 (15%): (i) Bleeding is moderate to severe or may be concealed (ii) Uterine tenderness is marked (iii) Shock is pronounced (iv) Fetal death is the rule (v) Associated coagulation defect or anuria may complicate.
  • 17.
  • 18.
  • 19.  Women with an acute abruption classically present with the abrupt onset of vaginal bleeding, mild to moderate abdominal and/or back pain, and uterine contractions vaginal bleeding ranges from mild and clinically insignificant to severe and life-threatening  Adominal pain, hypotension, and fetal heart rate (FHR) abnormalities suggest clinically significant separation that could result in fetal death and severe maternal morbidity
  • 20.  Identification of a retroplacental hematoma is the classic ultrasound finding of placental abruption. Retroplacental hematomas have a variable appearance; they can appear solid, complex, and hypo-, hyper-, or iso-echoic compared with the placenta. Hypoechogenicity and sonolucency are features of resolving rather than acute hematoma.  The sensitivity of ultrasound findings for diagnosis of abruption is only 25 to 60 percent but the positive predictive value is high (88 percent) when ultrasound findings suggestive of abruption are present
  • 21.
  • 22.  Serious maternal consequences of abruption include: Excessive blood loss and DIC, which generally necessitate blood transfusion and can lead to hypovolemic shock, renal failure, adult respiratory distress syndrome, multiorgan failure, peripartum hysterectomy and, rarely, death.  In addition to these acute consequences, the mother is at increased long-term risk of premature cardiovascular disease and doubling of the risk of death after coronary artery revascularization.These increased risks may reflect underlying maternal vascular abnormalities that manifest during pregnancy as abruption.
  • 23.  Serious fetal and neonatal consequences of abruption include: Increased perinatal morbidity and mortality related to hypoxemia, asphyxia, low birth weight, and/or preterm delivery.  Fetal growth restriction (with chronic abruption)  Fetal asphyxia, preterm birth, and growth restriction can be associated with short- and long-term sequelae, and abruption appears to compound the risk
  • 24.  Initiate continuous fetal heart rate monitoring  Secure intravenous access  Closely monitor the mother's hemodynamic status  Quantify blood loss  Draw blood for a complete blood count including platelet count, blood type and screen (cross-match if transfusion is likely), and coagulation studies  Notify the anesthesia team  Administer standard medications to women likely to deliver: magnesium sulfate for neuroprotection for pregnancies <32 weeks of gestation, antenatal corticosteroids for pregnancies <34 weeks of gestation
  • 25. The most important factors impacting the decision to deliver a patient with placental abruption versus expectant management are:  Gestational age  Fetal and maternal status, which reflect the severity of the abruption.
  • 26.  The optimal route of delivery in these cases minimizes the risk of maternal morbidity or mortality, since fetal well-being is no longer a factor.  Blood and blood product replacement is often necessary and expeditious delivery is desirable because the frequency of coagulopathy and continuous heavy bleeding is much higher in abruptions in which fetal death has occurred.  Placental separation is often greater than 50 percent.
  • 27.  Caesarean delivery is often the best option when vaginal delivery is not imminent and rapid control of bleeding is required because of  maternal hemodynamic instability or  significant coagulopathy, or  the mother is unwilling to accept adequate blood replacement therapy and is therefore likely to develop hemodynamic instability or  coagulopathy during labour.  Blood and blood products for correction of coagulopathy should be replaced prior to and during the caesarean delivery
  • 28.  When the fetus and mother are both stable, the decision to deliver depends primarily on gestational age, with consideration of ongoing maternal symptoms  Less than 34 weeks of gestation —When the fetus and mother are both stable and there is no evidence of ongoing major blood loss or coagulopathy, conservative management with the aim of delivering a more mature fetus is the main goal before 34 weeks of gestation .
  • 29. We take the following approach:  Administer corticosteroids – Corticosteroids to promote fetal lung maturation and reduce complications of prematurity are administered to pregnancies at 23 to 34 weeks of gestation, given the increased risk of need for preterm delivery.  Tocolysis – For women in preterm labor, we administer a 48- hour course of nifedipine to enable administration of a full course of corticosteroids.
  • 30.
  • 31.  In severe abruptions, blood may extravasate into the myometrium (called a Couvelaire uterus), and this can be seen at cesarean.  The Couvelaire uterus is atonic and prone to postpartum hemorrhage.  Aggressive management of atony is needed to prevent disseminated intravascular coagulation and exsanguination; however, atony in this setting is less likely to respond to standard therapies for postpartum hemorrhage than atony from other causes; thus, these women are at high risk for requiring hysterectomy
  • 32.  Naked eye features: The uterus is of dark port wine colour which may be patchy or diffuse. It tends to occur initially on the cornua before spreading to other areas, more specially over the placental site. Subperitoneal petechial haemorrhages are found under the uterine peritoneum and may extend into the broad ligament. There may be free blood in the peritoneal cavity or broad ligament hematoma.
  • 33.  Microscopic appearance: The uterine muscles over the affected area are necrosed and there is infiltration of blood and fluid in between the muscle bundles. The serosa may split on occasions, to allow the blood to enter the peritoneal cavity. The blood vessels show acute degenerative changes with thrombosis. Uterus as observed during cesarean section is not an indication per se for hysterectomy.
  • 34.  Postpartum, we administer an intravenous oxytocin infusion as the first-line uterotonic agent.  Maternal vital signs, blood loss, urine output, uterine size and consistency, and laboratory results are monitored closely to ensure that bleeding has been controlled and that coagulopathy (if present) is resolving, and to guide replacement of fluids and blood products, as needed.
  • 35.  Women with placental abruption are at several fold higher risk of abruption in a subsequent pregnancy.  3 to 15 percent of women have a recurrence, compared with a baseline incidence of 0.4 to 1.3 percent in the general population.  In one longitudinal population-based study, the risk of placental abruption in a subsequent pregnancy was about 6 percent in women with an abruption in their first pregnancy versus 0.06 percent in women without an abruption.