Obstetrical Hemorrhage
Reynold John D. Valencia
Obstetric Hemorrhage
One of the “triad” of maternal death causes
along with hypertension and infection
Leading reason for admission of pregnant
women to intensive care units
In developing countries, the single most
important cause of maternal death
worldwide
Mechanism of Normal Hemostasis
Blood flow through the intervillous space:
600mL/min
1. Myometrial contraction
2. Clotting
3. Obliteration of vessel lumens
An intact coagulation system is not
necessary for postpartum hemostasis
unless there are lacerations in the uterus,
birth canal, or perineum.
Definition
Postpartum Hemorrhage- episode of
bleeding of >500mL after completion of the
third stage of labor
Estimated 5% of women lose >1000mL in
first 24 hours
Late pospartum hemorrhage describes
bleeding after the first 24 hours. (found in
1% of women)
Studies show that estimated blood loss is
commonly only approximately half of the
actual loss.
Blood volume of a Pregnant woman
Blood volume of a Pregnant woman
Usually rises by half (30-60% increase) or
1500 to 2000mL for an average-sized
woman
Whenever the postpartum hematocrit is
lower than one obtained on admission for
delivery, blood loss can be estimated as the
sum of the calculated pregnancy-added
volume plus 500mL for each 3 volume
percent decline of the hematocrit.
Causes
Antepartum Hemorrhage
Placental Abruption (32%)
Placenta Previa (21%)- vasa previa
Cervical Bleeding (6.6%)
Postpartum Hemorrhage
Uterine atony (most common)
Genital Tract Lacerations
Retained products of conception
Coagulopathy
Uterine Inversion
Immediate Management
Establish Cause
Volume Replacement
Monitor Vital signs and urine output
Uterine atony
Failure of the uterus to contract sufficiently
after delivery and to arrest bleeding from
vessels at the placental implantation site
Third stage Management
Separation and delivey of the placenta by
cord traction, especially when the uterus is
atonic, may cause uterine inversion.
Manual Removal of Placenta
Risk factors for Uterine Atony
Primiparity and high parity
Overdistended uterus (women with a large
fetus, multiple fetuses, or hydramnios)
Labor abnormalities
Labor induction or augmentation
Prior postpartum hemorrhage
Evaluation
Careful inspection is done to exclude birth
canal laceration
Inspection of the placenta after delivery
should be routine
The uterus may be boggy, soft and
enlarged to palpation above the umbilicus
Management
Uterotonics
Oxytocin
Ergot Alkaloids- methylergonovine
(Methergine) and ergonovine
Severe hypertension
F-series prostaglandins- Carboprost
tromethamine (Hemabate)
diarrhea, hypertension, vomiting, fever, flushing,
and tachycardia
E-series Prostaglandins- Dinoprostone
Diarrhea- rectal route, vigorous vaginal bleeding-
per vaginum
Bleeding Unresponsive to
Uterotonic Agents
1. Begin bimanual uterine compression
2. Immediately mobilize the emergent-care obstetrical team to the delivery
room and call for whole blood or packed red cells
3. Request urgent help from the anesthesia team
4. Secure at least two large-bore intravenous catheters so that crystalloid
with oxytocin can be continued simultaneously with blood products.
Insert an indwelling Foley catheter for continuous urine output
monitoring
5. Begin volume resuscitation with rapid intravenous infusion of crystalloid.
6. With sedation, analgesia, or anesthesia established and no with optimal
exposure, once again manually explore the uterine cavity for retained
placental fragments and for uterine abnormalities, including lacerations
or rupture
7. Thoroughly inspect the cervix and vagina again for lacerations that may
have escaped attention.
8. If the woman is still unstable or if there is persistent hemorrhage, then
blood transfusions are given.
Bimanual Compression
Balloon Tamponade
Surgical Procedures
Uterine compression sutures
Pelvic vessel ligation
Angiographic embolization
Hysterectomy
Uterine Inversion
1 :2000 incidence
associated bleeding often is massive
Risk factors include alone or in
combination:
1. Fundal placental implantation,
2. uterine atony,
3. cord traction applied before placental
separation, and
4. abnormally adhered placentation such as
with the accrete syndromes
Recognition and
Management
Inability to palpate
endometrial cavity
and/or beefy red,
bleeding mass
protruding into the
vagina
partially inverted
uterus can be
mistaken for a
uterine myoma,
and sonography
can aid
diferentiation
Management
1. Immediate assistance is summoned,
including obstetrical and anesthesia
personnel.
2. Blood is brought to the delivery suite for
potential use.
3. The woman is evaluated for emergency
general anesthesia. Large-bore intravenous
infusion systems are secured to begin rapid
crystalloid infusion to treat hypovolemia
while awaiting arrival of blood products.
4. If the recently inverted uterus has not
contracted and retracted completely and if
the placenta has already separated-pushing
Management
5. If the placenta is still attached- tocolytics . If
these fail to provide suficient relaxation, then
a rapidly acting halogenated inhalational
agent is administered. After the uterus is
replaced, the placenta is carefully manually
removed.
6. If uterine repositioning fails with the placenta
attached- back to step 4
7. Once the uterus is restored to its normal
configuration, tocolysis is stopped. Maneuvers
for uterine contractions are done. (oxytocin,
Bimanual compression)
Surgical Intervention
Laparotomy
Huntington procedure
Haultain incision
Injuries to the Birth Canal
Vulvovaginal lacerations
Cervical lacerations
Puerperal Hematomas
Uterine Rupture
Vulvovaginal lacerations
Vulvovaginal lacerations
Vulvovaginal lacerations
Cervical Lacerations
Colporrhexis
Annular or circular detachment
As with vulvovaginal lacerations, cervical
tears can be more fully appreciated with
adequate exposure, which may be best
attained with transfer to an operating room
Cervical Laceration
Puerperal Hematomas
Diagnosis
tense, tender swelling of varying size
rapidly develops, encroaches on the vaginal
lumen, and causes overlying skin or
epithelium to become ecchymotic.
Pelvic pressure, pain, or inability to void
Management
Vulvovaginal hematomas are managed
according to their size, location, duration
since delivery, and expansion.
May be treated expectantly until absorbed
Or may have surgical exploration.
For repair, an incision is made at the point
of maximal distention, blood and clots are
evacuated, and bleeding points ligated.
Supralevator or retroperitoneal hematomas-
laparotomy or interventional embolization
Uterine Rupture
Diagnosis
most common sign of uterine rupture is a
nonreassuring fetl heart rate pattern with
variable decelerations that may evolve into
late decelerations and bradycardia.
If the fetal presenting part has already
entered the pelvis with labor, loss of station
may be detected by pelvic examination.
Management
Immediate delivery of the baby
Laparotomy
Hysterectomy
Placental Abruption
abruptio placentae- refers to "rending asunder
of the placenta”
Placental abruption is initiated by hemorrhage
into the decidua basalis. The decidua then
splits, leaving a thin layer adhered to the
myometrium. Consequently, the process
begins as a decidual hematoma and expands
to cause separation and compression of the
adjacent placenta
Most blood in the retroplacental hematoma in a
nontraumatic placental abruption is maternal
Placental Abruption
Severe abruption is defined as
displaying one or more of the
following:
1. maternal sequelae that
include disseminated
intravascular coagulation,
shock, transfusion,
hysterectomy, renal failure, or
death
2. fetal complications such as
nonreassuring fetal status,
growth restriction, or death; or
3. neonatal outcomes that
include death, preterm
delivery, or growth restriction
Placental Abruption
Traumatic Abruption- fetomaternal
hemorrhage is more common
Chronic Abruption- may develop chronic
abruption-oligohydramnios sequence(CAOS)
Abruption is the most common cause of
clinically profound consumptive
coagulopathy in obstetrics
Couvelaire uterus- widespread extravasation
of blood into the uterine musculature and
beneath the serosa at the time of cesarean
delivery
Placental Abruption
Diagnosis
Most women with a placental abruption
have sudden-onset abdominal pain, vaginal
bleeding, and uterine tenderness.
Nonreassuring fetal status, frequent
contractions, hypertonus
With abruption, some degree o f
intravascular coagulation is almost
universal.
Painful bleeding vs painless bleeding of
placenta previa
Complications
Acute kidney injury
Sheehan syndrome
Management
Cesarean Delivery
Vaginal Delivery- if the fetus had died
Placenta Previa
previa means going before- and in this
sense, the placenta goes before the fetus
into the birth canal
placenta that is implanted somewhere in
the lower uterine segment, either over or
very near the internal cervical os.
Classification
Placenta previa- the internal os is covered partially or
completely by placenta. In the past, these were further
classified as either total or partial previa.
Low-lying placenta- implantation in the lower uterine
segment is such that the placental edge does not cover
the internal os but lies within a 2-cm wide perimeter
around the os. A previously used term, marginal previa,
described a placenta that was at the edge of the internal
os but did not overlie it
Digital palpation in an attempt to ascertain these changing
relations between the placental edge and internal os as
the cervix dilates usually causes severe hemorrhage
Vasa previa - fetal vessels which course through
membranes and present at the cervical os
Risk Factors
Maternal age
Multiparity
Cigarette smoking
Uterine myoma
Prior cesarean delivery
Clinical Features
Painless bleeding- most characteristic event
A specific sequence of events leads to bleeding in cases
in which the placenta is located over the internal os:
1. the uterine body remodels to form the lower uterine
segment.
2. the internal os dilates, and some of the implanted
placenta inevitably separates.
3. Bleeding that ensues is augmented by the inherent
inability of myometrial fibers in the lower uterine
segment to contract and thereby constrict torn vessels.
Similarly, bleeding from this lower segment implantation
site also frequently continues ater placentl delivery.
4. there may be lacerations in the friable cervix and lower
segment.
Complications
Morbidly adherent placenta
Coagulation defects
Diagnosis
Whenever there is uterine bleeding after
midpregnancy, placenta previa or abruption
are always considered.
Usually diagnosed sonographically
If not available, double set-up technique
Even the gentlest examination can cause
torrential hemorrhage.
Transvaginal vs Transabdominal
sonography?
Management
By
Fetal age and maturity,
labor, and
bleeding severity
43% had emergency delivery (practically all by CS)
if the fetus is immature and active bleeding - close
observation in an obstetrical unit is indicated
If near term and who are not bleeding - for scheduled
cesarean delivery
If suspected morbidly adherent placenta, delivery is at
34 to 35 completed weeks (NIH) or 36 weeks (Parkland)
Surgery
Vertical Incision
Abnormally adherent placenta- most
frequent indication for peripartum
hysterectomy
Maternal mortality ratio is increased
approximately threefold for women with a
placenta previa
Morbidly Adherent
Placent
Also referred to these disorders collectively
as accrete syndromes which comes from
the Latin ac- + crescere- to adhere or
become attached to
Have greater risks for previa, uterine
rupture, and hysterectomy
Risk Factors
associated previa,
prior cesarean delivery
Diagnosis
• Sonography
• 3D sonography + power doppler
• MR imaging
Management
Management
Timing- usually 34 to 37 weeks, some after
36 weeks
Confirmation of a percreta or increta almost
always mandates hysterectomy
Pregnancy Outcomes
Obstetrical
Coagulopathies
An event related to actual consumption of pro coagulants
within the intravascular tree results in a consumptive
coagulopathy.
In contrast, massive loss of procoagulants from hemorrhage
results in a dilutional coagulopathy
Found in virtually all cases of
placental abruption and
amnionic fluid embolism
Also found in
sepsis,
Thrombotic microangiopathies,
acute kidney injury,
acute fatty liver,
severe preeclampsia, and
HELLP
Pregnancy-Induced Coagulation
Changes
procoagulant state during normal
pregnancy
Plasmin activity usually declines after
delivery
Mean platelet count drops by 10% during
pregnancy -> platelet activation is
enhanced
Coagulation Pathway
Activation of Pathological
Coagulation
Release of tissue factor by pathological entities.
With generalized endothelial activation, diffuse
activation of coagulation follows. This pathological
cycle of coagulation and fibrinolysis becomes clinically
important when coagulation factors and platelets are
sufficiently depleted to create consumptive
coagulopathy.
The best known and most common is placental
abruption with its significant release of
thromboplastin.
Another is embolization of amnionic fluid and debris
into the maternal circulation.
Diagnosis
Bioassay
fibrinogen, fibrin, and degradation product levels
CBC
Prothrombin time (PT) and partial
thromboplastin time (PTT)
Thromboelastomety and thromboelastography
persistent bleeding from venipuncture sites,
nicks from shaving the perineum or abdomen,
trauma from bladder catheterization, and
spontaneous bleeding from the gums, nose, or
gastrointestinal tract
General Management
prompt identification and removal of the
inciting source of the coagulopathy
rapid replacement of procoagulants
Vigorous restoration and maintenance of
the circulation to treat hypovolemia
Amnionic Fluid Embolism
classic triad of abrupt hemodynamic and respiratory
compromise along with DIC underpins its diagnosis
Predisposing conditions are
rapid labor,
meconium-stained fluid, and
tears into uterine and other large pelvic veins that permit an
exchange of fluids between the maternal and fetal compartment
older maternal age;
postterm pregnancy;
labor induction or augmentation;
eclampsia;
Cesarean, forceps, or vacuum delivery;
placental abruption or previa; and
hydramnios
Diagnosis
Pathophysiology
1. disruption of the maternal-fetal interface, which allows material
from the fetal compartment to enter maternal circulation.
2. abnormal activation of proinflammatory mediator systems,
similar to the systemic inflammatory response syndrome (SIRS) ,
and
3. initial, transient pulmonary vasoconstriction and hypertension.
4. Acute right ventricular failure is then followed by hemodynamic
collapse from right ventricular infarction coupled with
interventricular septum displacement to the let and ultimately
decreased leftsided cardiac output.
5. cardiogenic pulmonary edema and systemic hypotension.
Concurrently in this process, acute respiratory failure with severe
hypoxemia from shunting develops.
6. consumptive coagulopathy. material from the fetal compartment
containing tissue factor activates factor VII . This leads to the
development of DIC
Management
Immediate high-quality cardiopulmonary
resuscitation and advanced cardiac life
support must be initiated without delay.
A suitable goal for temperature is 36°C and
for MAP is 65 mm Hg.
Supportive care
Inotropic agents, vasopressors
Avoid excess fluid administration
Coagulation parameters
Clinical outcomes
Death is rapid, within 30 minutes
~25% maternal mortality rate
70% neonatal survival rate, ½ suffering
neurological impairment
Sepsis syndrome
E. coli
Antepartum pyelonephritis
Puerperal infections
Consumptive coagulopathy usually not
severe
Purpura fulminans
Severe, often lethal-form of consumptive coagulopathy
caused by micro thrombi in small blood vessels leading to
skin necrosis and sometimes vasculitis
Debridement of large areas of skin over the extremities
and buttocks
Abortion
can incite coagulation and worsen hemorrhage, especially
with midtrimester abortions.
sepsis syndrome accompanied by intravascular
coagulation accounts for 25 percent of abortion-related
deaths.
Another source is from instillation of hypertonic solutions
to effect mid trimester abortions.
Management of
Hemorrhage
True blood loss is often two to three times the clinical
estimate.
After pregnancy hypervolemia is lost at delivery,
blood loss can be estimated by calculating 500 mL
loss for each 3 volume percent drop in hematocrit.
A prudent rule is that any time blood loss is
considered more than average, then the hematocrit
is determined and plans are made for close
observation for potential physiological deterioration.
Urine output measured hourly is one of the most
important "vital signs. " Urine low of at least 30 mL,
and preferably : 50 mL per hour, should be
maintained.
Hypovolemic Shock
Early in the course of massive bleeding, mean arterial pressure, stroke
volume, cardiac output, central venous pressure, and pulmonary capillary
wedge pressure decline.
Increases in arteriovenous oxygen. -> compensatory rises in heart rate,
systemic and pulmonary vascular resistance, and myocardial contractility,
perfusion to the kidneys, splanchnic beds, muscles, skin, and uterus is
diminished, more blood flow is diverted to the heart, brain, and adrenal
glands.
When the blood volume deficit exceeds approximately 25 percent,
compensatory mechanisms usually are inadequate.
local tissue hypoxia and metabolic acidosis -> vicious cycle of
vasoconstriction, organ ischemia, and cellular death.
activation of lymphocytes and monocytes, which in turn causes endothelial
cell activation and platelet aggregation. These then can incite DIC.
extracellular luid and electrolyte shifts involved in both the genesis and
successful treatment of hypovolemic shock.
Survival is enhanced in acute hemorrhagic shock if blood plus cystalloid
solution is given compared with blood tranusions alone.
Fluid Resuscitation
Identify the bleeding source and to begin resuscitation.
If she is undelivered, restoration of blood volume is beneficial to
mother and fetus, and it also prepares for emergent delivery.
If she is postpartum, it is essential to immediately identify uterine
atony, retained placental fragments, or genital tract lacerations.
At least one and preferably more large-bore intravenous infusion
systems are established promptly with rapid administration of
crystalloid solutions, while blood is made available.
An operating room is readied, and a surgical and anesthesia team
are assembled immediately.
Only 20 percent of crystalloid remains intravascularly in critically
ill patients after 1 hour.
Initial fluid is infused in a volume two to three times the
estimated blood loss.
Blood Replacement
Dilutional Coagulopathy
depletion of platelets and clotting factors
can lead to a dilutional coagulopathy that is
clinically indistinguishable from DIC
Thrombocytopenia is the most frequent
coagulation defect
In addition, packed red cells have only very small
amounts of
soluble clotting factors, and
stored whole blood is deficient in platelets and in
factors V, VIII, and XI. distinction between dilutional
and consumptive coagulopathy can be confusing
treatment for both is similar.
Blood replacement
Recombinant activated Factor VI
Tranexamic Acid
Massive transmission protocols
Viscoelastic Assays
Topical Hemostatic Agents
Cell Salvage and Autologous Transfusion
Transfusion complications
Acute hemolysis
Transfusion-related acute lung injury
(TRALI)
Bacterial infections
Viral infections
Adjunctive Surgical
Procedures
Uterine Artery Ligation
Uterine Compression Sutures
Internal Iliac Artery Ligation
Angiographic embolization
Pelvic Packing
Adjunctive Surgical
Procedures
