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Obstetrical Hemorrhage

Maternal Deaths

 Infamous triad
 Obstetrical hemorrhage (single most important cause)
 Hypertension
 Infection
Mechanism of Hemostasis

 Near term
 At least 600mL/min
 Intervillous space
 Flows through spiral arteries, which average 120 in number
 These vessels have no muscular layer because of their modeling by trophoblasts, which creates a low
pressure system
 Placental separation
 Vessels at the implantation avulsed, and hemostasis is achieved first by myometrial contraction,
which compresses this formidable number of large vessels.
 Compression → clotting → obliteration of vessels lumen
Postpartum Hemorrhage

 > 500 mL blood loss


 American College of Obstetricians and Gynecologists
 >1000 mL + hypovolemia
 Estimated blood loss is commonly only approximately half of the actual loss.
 Blood volume of a pregnant women with normal pregnancy induced hypervolemia usually
rises by half, but increases from 30-60& (1500-2000 mL) for an average sized woman
Blood Loss

 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 + 500 mL for each 3% volume decline hematocrit
Risk
Timing

 Antepartum
 Placenta previa
 Placental abruption
 Postpartum
 Atony
 Genital tract laceration
Antepartum Hemorrhage

 First half of pregnancy  After Midpregnancy


 Abortion/ Ectopic pregnancy  Placental abruption
 Active Labor  Previa
 “bloody show”  Cervical bleeding
 Above the cervix
 Placenta previa
Despite this, any pregnancy with antepartum
 Placental abruptio
bleeding remains HIGHER risk for an
 Uterine Tear adverse outcome even though bleeding has
 Vasa Previa (rarely) stopped and placenta previa has been
 Near Term excluded sonographically
 Source is not identified
Postpartum Hemorrhage

 Uterine atony with placental site bleeding


 Boggy, soft uterus during bimanual examination, expression of clots and hemorrhage during
uterine massage
 Genital tract trauma
 Important exceptions
 Unrecognized intrauterine and intravaginal blood accumulation
 Uterine rupture with intraperitoneal or retroperitoneal bleeding
 Vulvar or vaginal hematoma
 Late Postpartum Hemorrhage
 Bleeding after the first 24 hours
Blood Loss Estimation

 Atony
 moderate→ HYPOVOLEMIA
 Episiotomy/ Vaginal Lacerations
 Minimal→ Moderate → BLOOD LOSS
 Uterine Cavity (1000mL)
 A treacherous feature of postpartum hemorrhage is the failure of he pulse and blood pressure to undergo
more than moderate alterations until large amounts of blood have been lost
 Small women
 Blood volume expansion is less than expected
 Severe Preclampsia or Eclampsia
 They do not have a normal blood volume accrual
 Crystalloid and blood
UTERINE ATONY
Uterine Atony

 Failure of the Uterus to contract sufficiently after delivery and to arrest bleeding from
vessels at the implantation site.
 Duncan Mechanism
 Blood from implantation site may escape into the vagina immediately
 Schultze Mechanism
 Remains concealed behind the placenta and membranes until placenta is delivered
 Separation and delivery of the placenta by cord traction, especially when he uterus is
atonic, may cause uterine inversion
Manual Placental Removal

 Heavy bleeding after delivery of the newborn and while the placenta remains partially or
totally attached.
 Analgesia is mandatory and aseptic surgical technique should be used
 Another method is to wipe out the uterine cavity with gauze-wrapped hands.
 Ampicillin or Cefazolin prophylaxis after manual removal (WHO)
 Fundal Massage
 Oxytocin 20 units in 1000 mL of crystalloid solution IV at 10 ml/min for a dose of 200
mU/min
Risk Factors

 Primiparity and High Parity


 Overdistended Uterus
 Large fetus, multiple fetuses or hydramnios
 Labor Abnormalities
 hyper- or hypotonic labor
 Labor induction or augmentation
 Either prostaglandins or oxytoxin
 Prior to postpartum hemorrhage
Evaluation and Management

 Uterus is massage and uterotonic agent are administered


 Uterotonic Agents
 Oxytocin (IV/IM)
 Methergine (IM/IV)
 Stimulate tetanic uterine contractions and act for approximately 45 mins
 O.2 mg (IM), can be repeated at 2-4 hour intervals
 IV causes hypertension especially with pre-eclampsia

 Ergometrine + oxytocin
 Carboprost tromethamine (Hemabate)
 0.25 mg IM, 15-90 mis intervals max of 8 doses
 Cannot be given to asthmatic and suspected amniotic fluid embolism
 Uterotonic Agents
 Dinoprostone
 20 mg suppository

 Misoprostol (rectally, orally or SL)


 600-1000 ug (ACOG)
Bleeding Unresponsive to Uterotonic Agents

 Bimanual Uterine Compression  Balloon Tamponade


 The posterior uterine wall is massaged by  Uterine packing to treat refractory uterine
one hand on the abdomen, while the atony fell from favor because of concerns
other hand is made into a fist and placed regarding concealed bleeding and
into the vagina infection

 Surgical Procedures
 Uterine compression sutures
 Pelvic vessel ligation
 Angiographic embolization
 Hyterectomy
UTERINE INVERSION
Uterine Inversion

 Puerperal Inversion (classic hemorrhagic disaster)


 Risk Factors
 Fundal placental implantation
 Uterine atony
 Cord traction applied before placental separatin
 Abnormally adhered placentation such as with accrete syndromes
Recognition and Management

 Immediate recognition of uterine  If initially unrecognized continued


inversion improves the chances of quick hemorrhage likely will prompt closed
resolution and good outcomes examination of the birth canal
Steps

1. Immediate assistance (OB and Anesthesia)


2. Blood preparations
3. Evaluation for general anesthesia
 Large-bore IV are secured to begin rapid crystalloid infusion (hypovolemia)
4. If the recently inverted uterus has not contracted and retracted completely and if placenta
has already separated, the the uterus may often be replaced by simply PUSHING UP the
inverted fundus with the palm of the hand and fingers in the direction of the long axis of
the vagina
 Some use two fingers rigidly exended to push the center of the fundus upward
5. If the placenta is attached, then attempts are made to reposition the uterus with the placenta in situ.
 IV tocolytic drugs (terbutaline, MgSO4 or nitroglycerine) for uterine relaxation and repositioning
 Halogenated inhalation agent
6. If uterine reposistioning fails with the placenta attached, then it is peeled off and steady pressure with the
fist, palm or fingers is applied to the inverted fundus in an attempt to push it up into and through the
dilated cervix
7. Once the uterus is restored to its normal configuration
 Tocolysis is stopped
 Oxytocin and other uterotonic may be given
 Operator
 Maintains the fundus in its normal anatomical position while applying bimanual compression to control further
hemorrhage until the uterus is well contracted
 Monitor the uterus transvaginally for evidence of subsequent inversion
 Bakri balloon has been used to maintain the repositioned uterus
Surgical Intervention

 Laparotomy
 Dense myometrial constriction ring
 Huntington Procedure
 Application of atraumatic clamps to each round ligament and upward traction
 In some cases, placing a deep traction suture in the inverted fundus or grasping it with tissue forceps may be
of aid
 Haultain Incision
 Sagital surgical cut, if a constriction ring still prohibits reposistioning
 Made posteriorly through the muscular ring to release it
 After uterine replacement, tocolytics are stopped, oxytocin and other utertonics are given
and the uterine incision is repaired
 In some cases, the uterus will again invert almost immediately after repositioning
 Uterine compression sutures can be used to prevent another inversion
 Chronic puerperal uterine inversion may become apparent weeks after delivery
Injures to the Birth Canal
Vulvovaginal Lacerations

 80% sustain some type of laceration at vaginal delivery


 Small tears of the anterior vaginal wall near the urethra (common)
 Sutures for hemostasis
 Large enough to require extensive repair can be associated by short-term voiding difficulty
 Deeper perineal lacerations
 Outer third of vaginal vault
 Some extend to involve anal sphincter
 Lacerations involving the middle and upper third of the vaginal vault
 Injuries of the perineum or cervix
Management

 Extensive vaginal or cervical tears should prompt a careful search for evidence of
retroperitoneal hemorrhage or of peritoneal perforation with hemorrhage.
 Intrauterine exploration is considered to exclde uterine tears or rupture
 Laparotomy
 Peritoneal perforation or uterine rupture
 Imaging and potential embolization
 Large retroperitoneal hematomas
Cervical Lacerations

 Superficial Lacerations (<0.5 cm)


 Deeper laceration
 Colporrhesis
 Cervix may be entirely or partially avulsed from the vagina in the anterior, posterior or lateral
fornices
 Annular or circular detachment (rare)
 When the entire vaginal portion of cervix is avulsed
 Forceps delivery due to incompletely dilated cervix
 Lower uterine segments
 Uterine artery and its major branches
 Peritoneal Cvaity
Management

 Transfer to the OR
 Assistant
 Firm doenward pressure on the uterus
 Operator
 Gentle traction on the lips of the cervix with ring forceps
 Second Assistant
 Provide better exposure with R-angle vaginal wall retractors (Breisky vaginal retractors)
 Suction device
 1 and 2 cm – not repaired unless they are bleeding
 Such tears heal rapidly and ultimately create an irregular, sometimes stellate appearing, external
cervical os that indicated previous delivery.
 Deep Cervical Tears
 Suturing the cervix after bringing it into view
 Any associated vaginal lacerations or an episiotomy maybe
tamponade with gauze packs to arrest their bleeding
 Upper angle of the wound (2-0 chromic or polyglactin)
 Interrupted or continous locking sutures are serially placed
outward or toward the operator
Puerperal Hematomas

CLASSIFICATION RISKS
 Anatomical  Vaginal or perineal laceration
 Vulvar  Episiotomy
 vestibular bulb  Operative delivery
 branches of pudendal artery (inferior rectal, perineal
and clitoral arteries
 Stretch and rupture of a blood vessel (forceps
delivery)
 Vulvovaginal
 Underlying coagulopathy
 Paravaginal
 Descending branch of uterine artery

 Retroperitoneal
 Supralevator
 Torn vessels lie about the pelvic fascia
Diagnosis

 Excruciating Pain
 Perineal, Vular and paravaginal hematoma
 Prompt Evaluation
 Pelvic pressure
 Pain
 Inability to void
 Supralevator extension
 Hematoma extends upward in paravaginal space and between the leaves of braod ligament
 Abdominal palpation
 Assess for hypovolemia
 Ultrasound or CT-scan
Clinical Course

 Small hematomas often remained contained and show minimal expansion


 Rupture from pressure necrosis
 Profuse hemorrhage
 Drains in form of large clots and old blood
 Retroperitoneal bleeding
 Paravaginal space and extends above the levator sling
 Massive and occasionally fatal
 Rebleeding up to 2 weeks postpartum
Management

 Vulvovaginal hematomas
 Size, location, duration since delivery and expansion
 Small o moderate size maybe treated expectantly until absorbed
 Surgical exploration
 Severe pain or if hematoma continues to enlarge
 Repair
 Incision is made at the point of maximal distension
 Blood clots are evacuated
 Bleeding points are ligated
 Cavity may then be obliterated with absorbable sutures
 Evacuated hematoma cavity is surgically closed and the vagina is packed for 12-24 hours
 Supralevator hematomas
 Difficult to treat
 Can be evacuated by vulvar or vaginal incisions
 Laparotomy or interventional embolization
 Angiographic embolization
 For supralevator or retroperitoneal hematomas
 Primarily or secondarily if surgical attempts at hemostasis have failed or if hematoma is difficult
to access surgically
 Bakri balloon
 Paracervical hematoma
 Ultrasound guided drainage
 Recurrent supralevator hematoma
Uterine Rupture

 Primary
 Occuring in a previously intact or unscarred uterus
 Secondary
 Preexisting insicion
 Injury
 Anomaly of myometrium
Pathogenesis

 Rupture of the previously intact uterus during labor most often involves the thinned out
lower uterine segment
 If it is immediate vicinity of the cervix, it frequently extends transversely or obliquely
 Portion of the uterus adjacent to the broad ligament, the tear is longitudinal
 Develop primarily in the lower uterine segment
 Upward into the active segment
 Downward into the cervix and vagina

 Bladder laceration
 If the rupture is of sufficient size, the uterine contents will usually excape into the
peritoneal cavity
 Fetal prognosis
 Degree of placental separation
 Magnitude of maternal hemorrhage
 Hypovolemia
 Some cases overlying peritoneum remans intact, accompanied by hemorrhage that extends
into the broad ligament to cause a large retroperitoneal hematoma
 Following vaginal delivery in an unscarred uterus
 Incomplete tear inside the uterus that extends vertically into active segment and is a source of
profuse hemorrhage
 Found at the time of hysterectomy for intractable bleeding despite a contracted uterus, bleeding is
not usually slowed until uterine artery pedicles are clamped bilaterally
Placental Abruption

 Abruptio Placentae
 Separation of placenta either partially or totally from its implantation site before delivery
 “rendering asunder of the placenta”
 Premature separation of the normally implanted placenta
pathogenesis
 Hemorrhage into the decidua basalis → splits leaving a thin layer adhered to the
myometrium
 Decidual hematoma and expands to cause separation and compression of the adjacent placenta
 Begins with rupture od a decidual spinal artery then an expanding retroplacental hematoma
 Early stages (symptoms maybe absent)
 External hemorrhage
 Bleeding typically insinuates itself between the membranes and the uterus, ultimating excapes
through the cervix
 Concealed hemorrhage
 Blood retained between the detached placenta and the uterus
 Consumptive coagulopathy is elevated
 Increased pressure within the intervillous space, caused by expanding retroplacental clot, forces
more placental thromboplastin into the maternal circulation
 Maternal
 Non traumatic placental abruption
 Retroplacental hematoma
 Separation of maternal decidua and
placental villi are usually intact
 Placenta as circumscribed depression
 Measured as few cm in diameter
 Dark, clotted blood
 Severe abruption (1 or more)
1. Maternal sequelae that inckude DIC, shock, transfusion, hysterectomy, renal failure or death
2. Fetal complications such as non reassuring fetal status, groth restriction or death
3. Neonatal outcomes that includes death, preterm delivery or growth restriction
Traumatic Abruption

 Placental separation
 Motor vehicular accidents or aggravated assault
 Fetomaternal hemorrhage
 Most common
 Concomittant placental tears or fractures
Chronic Abruption

 Early in pregnancy
 Abnormally
 elevated maternal serum aneuploidy markers and subsequent abruption
 Elevated serum levels of alpha-fetoprotein
 Placenta-specific RNAs
 Chronic abruption-oligohydramnios sequence (CAOS)
 Subsequent oligohydramnios
 Hemorrhage with retroplacental hematoma formation
 Occassionally arrested completely without delivery
Perinatal Morbidity and Mortality

 Influenced by gestational age


 Rises in the 3rd trimester
 More common with earlier abruptions
 Neonatal Deaths (15%)
 Perinatal Morbidity
 Cerebral palsy
 Severe acidemia
 Cord arterial blood pH <7.0 or base deficit of > 12 mmol/L
Predisposing Factor

 Advance maternal age


 Race
 Black and white (most common) 1 in 200
 Asian 1 in 300
 Latin-American 1 in 350
 Familial association
 Woman had severe abruption, the risk for
her sister was doubled
Pregnancy Associated Hypertension

 Gestational hypertension
 Pre-eclampsia
 Chronic hypertension

 Risk
 Fetal demise
 Elevated cardiovascular mortality risk prior, with or without chronic hypertension
Preterm Prematurely Ruptured Membranes

 20 and 36 weeks (5%)


 Risk if with comorbid infection
 Inflammation
 Infection
 Preterm delivery
 Hydramnios >34 weeks
 Abrupt uterine decompression during membrane rupture
Prior Abruption

 Fetal death (12%)


 Recurrence at a gestational age of 1 to 3 weeks (22%)

 Labor induction at 37 weeks


Other Associations

 Cigarette Smoking
 Antepartum Vitamin C and E
 Cocaine abuse
 Uterine Leiomyomas
 Isolated single umbilical artery
Clinical Findings and DIagnosis

 Abdominal pain
 Vaginal bleeding
 Uterine tenderness
 Others
 Frequent contractions
 Persistent hypertonus
Hypovolemic Shock

 Placenta abruption is one of several notable obstetrical entities that may be complicated by
massive and sometimes torrential hemorrhage
 Blood loss often amounted to atleast half of their pregnant blood volume
 Blood loss and shock can develop

 Treatment
 Crystalloid
 Blood transfusion
 resuscitation
Consumptive Coagulopathy

 Defibrination syndrome
 Placental abruption and amnionic fluid embolism
 Consumptive coagulopathy or DIC
 Major mechanism causing proagulant consumption is intravascular activation of clotting
 Activation of plasminogen to plasmin → lyses fibrinmicroemboli to maintain microcirculatory patency
 Fibrinogen level of <150 mg/dL
 Severe enough to kill the fetus
Couvelaire Uterus

 Widespread exravasation of blood into the


uterine musculature and beneath the serosa
 Uteroplacental apoplexy
 Seldom cause uterine atony and alone they
are not indication for hysterectomy
 Effusions of blood
 Tubal serosa
 Between leaves of the broad ligaments
 Substance of ovaries
 Free in the peritoneal cavity
End Organ Injury

 Acute Kidney Injury


 Treatment of hemorrhage with blood and crystalloid solution usually prevents clinical significant
renal dysfunction
 Reversible
 Acute Cortical Necrosis
 Irreversible
 Sheehans Syndrome (rarely)
Management

 Emergency Cesarean Delivery


 Living viable-aged fetus
 Vaginal delivery not imminent
 Prompt intensive resuscitation with blood plus crystalloid
 Vaginal Delivery
 Fetus has died
 Uterotonics and Uterine Massage
 Early amniotomy
 Better spinal artery compression to diminish implantation site bleeding and reduce thromboplastin infusion
 Preterm Fetus
 Cs delivery ca be perfomed
 Tocolysis is advocated by some suspected abruption
Placenta Previa
Previa means “going before”
Placental Migration

 Apparent movement of placenta away from internal os


1. Apparent movement of the low-lying placenta relative to the internal os is related to the
imprecision of 2D sonography
2. As pregnancy progresses, growth of the lower and upper uterine segments differs.
 Trophotropism- With greater blood flow in the upper uterus, placental growth is more likely
directed toward the fundus
Classification

 Placenta previa
 Internal os is covered partially or completely by placenta
 Low-lying placenta
 Implantation in the lower uterine segment is such that the placental edge does not cover the
internal os but lies within 2cm wide perimeter around the os
 Cervical dilation
 2cm low lying → 4cm partial
 Vasa Previa
 Fetal vessels course through membranes and present at the cervical os
Factors

RISK CLINICAL
 Maternal age  Prior CS
 > 35 y/o  Ptior uterine incision and placenta previa
 Multiparity  Maternal Serum alpha fetoprotein
 Cigarette smoking (MSAFP)
 Elevated
 Uterine leimomyoma
 Assisted Reproductive Technology
(ART)
Clinical Features

 Painless bleeding
 Sentinel bleed
 Bleeding from a previs usually begins without warning and without pain or contractions in a
women who has had an uneventful prenatal course
 Morbidly adherent placentas
 Frequent and serious complication
 Coagulation defects (rare)
Diagnosis
 22 -28 weeks with vaginal beeding
 Sonography
 Transabdominal
 Excellent sensitovity and negative predictive value
 If the placenta clearly overlies the cervix or lies away from the lower uterine segment

 Transvaginal
 Obese
 Full bladder

 Double set-up technique


 Finger be passed through the cervix and the placenta palpated
 Placental edge is <2cm from internal os, but not covering it (low lying)
 MRI
 Excellent in visualizing placental abnormalities
Management
 Factors
 Fetal age and maturity
 Fetus is immature and active bleeding subsides – close observation
 Tocolytic administration is limited to 48 hours of administration

 Labor
 Bleedig severity
 After bleeding has ceased for approximately 2 days and fetus is healthy
 Discharged home with pelvic rest
 Emergency delivery (25-40%)
 Near Term and eho are not bleeding
 Scheduled CS
Delivery
 Cesarean delivery
 Vertical laparotomy incision
 Rapid entry in cases with torrential bleeding
 Hysterectomy (operating space)
 Low transverse hysterotomy
 Fetal bleeding if placenta is implanted anteriorly and incised
 0-chromic sutures
 Uncontrollable bleeding
 1cm intervals to form a circle around the bleeding portion of he lower segment to control hemorrhage
 Bakri or Foley balloon tamponade
 Bilateral uterine or internal iliac ligation
 Pelvic artery embolization
Hysterectomy

 Conservative methods fail and bleeding is brisk


 Placenta previa with abnormally adherent placenta (most frequent)
 Women whose placenta previa is implanted anteriorly at he site of a prior uterine incision,
the likelihood of an associated morbidly adherent placenta and need for hysterectomy is
increased.
Morbidly Adherent Placenta
Accrete syndromes
Ac- + crescere – to adhere or become attached to
Accrete syndromes

 1 in 20,000 births
 Leading cause of hemorrhage and emergency peripartum hysterectomy
 High risk recurrence in subsequent pregnancies
 Abnormal placental adherence to the myometrium stems in part from partial or total
absence of the decidua basalis and imperfect development of the fibrinoid or Nitabuch
layer
 Decidua spongy layer is lacking (partially or totally)
 Physiological line of cleavage is absent
 Decidual deficiency then prevents normal placental separation after delivery
 The surface area of the implanation site involved and the depth of trophoblastic tissue in
growth are variable between women
Classification
 Placenta accrete
 Villi attached to the myometrium
 Placenta increta
 Villi actually invade the myometrium
 Placenta Percreta
 Villi that penetrate through the
myometrium
 Total placenta accrete
 Abnormal adherence may involve all
lobules
 Focal placenta accrete
 All part of a single lobule is abnormally
attached
Risk Factors

 Associated previa
 A prior cesarean delivery
 Classical hysterotomy incision (high risk)
 Dysfunctional decidual formation
 Curettage or endometrial ablation
 Widespread use of MSAFP and HCG
Clinical presentation and Diagnosis
 1st and 2nd Trimester
 Hemorrhage
 Sonography
 1st trimester- smallest myometrial thickness
 Loss of the normal hypoechoic retroplacental zone between the placenta and uterus, placenta
vascular lacunae and placental bulging into the posterior bladder wall
 3D sonography and power Doppler (better results)
 Highly predictive of myometrial invasion
 MRI
 Outline anatomy and to identify invasion of adjacent structures, including possible ureteral
involvement
 Uterine bulging
 Heterogenous signal intensity within the placenta indicative of lacunae
 Dark intraplacental bands on T@ weighted imaging
Management
 Preoperative assessment
 OB surgeon or gyne oncologist and surgical,
urological and intervenional radiological
consultants should be available
 Tertairy facility
 Timing of delivery
 (ACOG) elective delivery without fetal lung
maturity after 34 wks
 (SMFM) between 34-37 weeks
 Preoperative Prophylactic Catheterization
 Aid in dissection of identification and repair of injury
 Balloon-tipped intraarterial catheters
 To mitigate blood loss and thereby enhance surgical visibility

 Cesarean Delivery and Hysterectomy


 Confirmation of percreta or incretaa always mandates hysterectomy
 Wider bladder flap before making the hysterotomy incision
 Round ligament are divided, and the lateral edges of the peritoneal reflection are dissected downward
 The incisions are extended to encircle the entire placental implantation site that visbly occupies the
prevesical space and posterior bladder wall
 Conservative Management
 Maybe possible to trim the umbilical cord, repair the hysterotomy incision, leave the placenta in
situ and not pursue hysterectomy.
 For women whom abnormal placentation was not suspected before cesarean delivery and In
whom uterine closure stops bleeding
Obstetrical Coagulopathies
Consumptive coagulopathy
Dilutional coagulopathy
Disseminated intravascular coagulation In
pregnancy
 Second most common severe maternal  Sepsis
morbidity indicator  Thrombotic microangiopathis
 Nearly a 4th maternal deaths  Acute kidney injury
 Acute fatty liver
 Severe pre eclampsia
 Hemolysis
 Elevated liver enzymes
 Low platelet count
 HELLP syndrome
Pregnancy-Induced Coagulation Changes

 ↑ in the plasma concentration factors ( I, VII, VIII, IX and X)


 ↑ plasminogen levels
 Net results are greater levels of
 Fibrinopeptide A
 B-thromboglobulin
 Platelet factor 4
 Fibrinogen-fibrin degradation products
 D dimers
Diagnosis

 Bioassay
 Excellent method to detect or suspect clinically significant coagulopathy
 Laboratory
 Fibrinogen
 Fibrin
 Degradation product levels
 PT/PTT (standard coagulation tests)
 Thrombocytopenia
 Petechiae or clotted blood fails to retract within an hour
 Thromboelastometry and thromboelastgraphy
General Management

 Defibrination
 Prompt identification
 Removal of the inciting source of coagulopathy
 Rapid replacement of procoagulants
 Severe hemorrhage
 Adequate perfusion restores hepatic and endothelial synthesis of procoagulants and permits
promt removal of activated coagulation factors, fibrin and fibrin degradation products by
the reticuloendothelial system
Specific Comorbid Conditions
 Placental abruption (most common)
 Fetal death and Delayed Delivery
 Amniotic Fluid Embolism
 Sepsis syndrome
 E. coli
 Purpura Fulminans
 Abortions
 Septic abortion
Amniotic Fluid Embolism
 TRIAD- abrupt hemodynamic and respiratory compromise along with DIC
 Rapid labor, meconium stain fluid and tears into uterine and other large pelvic veins that permit
an exchange of fluids between maternal and fetal compart
 Diagnosis
 Women in the late stage of labor or immediately postpartum begins gasoing for air
 Seizures or cardiorespiratory arrest rapidly follows accompanied by massive hemorrhage
Amniotic Fluid Embolism
 Pathophysiology
 Disruption of the maternal and fetal interface, which allows material from the fetal compartment
to enter maternal circulation
 Abnormal activation of proinflammatory mediator suystems, similar to SIRS
 Initial transient pulmonary vasoconstriction and hypertension
 Acute right ventricular failure is then followed by hemodynamic collapse from right ventricular
infarction coupled with interventricular septum displacement to the left and ultimately decreases left
sided cardiac output.
 Acute respiratory failure with severe hypoxemia from shunting develops.
 Management
 Immediate high quality cardiopulmonary resuscitation and ACLS
 Temp 36 C and MAP 65mmHg
 Intubation (supportive)
 Dobutamine- R- ventricular failure
 Norepinephrine- systemic hypotension
MANAGEMENT OF HEMORRHAGE
 Recognition of obstetrical hemorrhage severity is crucial to its management
 A prudent rule is that anytime 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
 Hourly ( 30 ml or > 50mL/hr
Hypovolemic Shock

 Massive bleeding, MAP, SV, CO, central enous pressure and pulmonary capillary wedge
pressure decline
 When the blood volume exceeds approximately 25%, compensatory mechanisms usually
are inadequate to maintain CO and BP
 Total oxygen extraction by maternal tissue, maldistribution of blood flow results in local
tissue hypoxia and metabolic acidosis
 Creates vicious cycle of vasoconstriction, organ ischemia and cellular death
Fluid Resuscitation

 Undelivered
 Restoration of blood volume is beneficial to mother and fetus
 Prepare for emergent delivery
 Postpartum
 Identify cause
 Administration of crystalloid solutions
 Initial fluid is infused in a volume 2-3x the estimated blood loss

 Ready OR, surgical and anesthesia team


Blood Replacement
Rapid blood infusion when hematocrit is <25 volume ercent
Blood Component Products
 Whole blood
 Ideal for treatment of hypovolemia from catastrophic hemorrhage
 40 days
 70% transfused Red Cells for atleast 24 hours
 1 unit - ↑ hematocrit by 3% - 4%
 Packed RBC and Crystalloid
 Combination of Red Cells, Plasma, cryoprecipitate and platelets
 Platelet count- >50,000/uL by infusion platelet concentrates
 Fibrinogen level <150 mg/dL or prolonged PT/PTT
 Fresh frozen plasma 10-15 mL/kg or alternatively cryoprecipitate is infused
Dilutional Coagulopathy

 A major drawback of treatment for massive hemorrhage with crystalloid solutions and
packed red blood cells is depletion of platelets and clotting factors
 Thrombocytopenia
 Most frequent coagulation defect found with blood loss and multiple transfusions
Type and Screen Vs Crossmatch
 Crossmatching involves the use of actual donor erythrocytes rather than standardized red
cells
 Administration of Screened blood rarely results in adverse clinical sequelae
 PRBC
 1 unit derived from 1 unit of whole blood to have HCT of 55-80%
 1 unit – 3-4 volume percent
 Platelet
 1 bag (sigle donor apheresis) = 6 units from 6 individual donors
 1 bag - ↑ 20,000/uL
 Fresh Frozen Plasma
 Treatment of women with consumptive or dilutional coagulopathy
Cryoprecipitate and Fibrinogen Concentrate

 10-15 mL unit – 200mg of fibrinogen along with factor VIII: C, factor VIII: von Willebrad
factor, factor XIII and fibronectin
 Pool of bag using an aliquot of fibrinogen concentrate taken from 8-120 donors.
 Ideal source of fibrinogen when levels are dangerously low and there is oozing from
surgical incisions
 Each gram raises the plasma fibrinogen level approximately 40mg/dL
Recombinant Activated Factor VII

 Synthetic Vitamin K- dependent protein (NovoSeven)


 Help to control hemorrhage from surgery, trauma and obstetrical causes
 Not effective
 Plasma fibrinogen lvel <50 mg/dL
 Platelet count < 30,000/uL
Tranexamic Acid Massive Transfusion Protocols
 Inhibits clot lysis to help forestall  Speed blood product delivery to the
bleeding by preventing plasmin from bedside or OR
degrading fibrin  Permits product infusion early in
 Associated with high incidence of renal resuscitation process
cortical necrosis  To prevent adverse effect of aggressive
resuscitation solely with crystalloid and
packed RBC
 Viscoelastic Assays
 Thromboelastography (TEG)
 Rotational thromboelastometry
 Cell Salvage and Autologous Transfusion
 Preoperative patients phlebotomy and autologous storage
 Intraoperative blood salvage with reinfusion (safe)
Transfusion Complications
 Transfusion of an incompatible blood component may result to acute hemolysis
 DIC, AKI and death
 Transfusion reaction
 Fever, hypotension, tachycardia, dyspnea, chest or back pain, fushing, severe anxiety and
hemoglobinuria
 Stop transfusion, treat hypotension and hyperkalemia, diuretics and alkalinizing the urine
 Transfusion-related acute lung injury (TRALI)
 Most common develop within 6 hours of transfusion
 Cause severe dyspnea, hypoxia and non cardiogenic pulmonary edema
 Bacterial Infectios
 Yersinia, pseudomonas, serratia, Acinetobacter, e.coli
 Viral infection
Adjunctive Surgical Procedures
 Uterine Artery Ligation
 Uterine Compression Sutures
 Internal Iliac Artery Ligation
 Adequate exposure is obtained opening the peritoneum over the common iliac artery and
dissecting down to the bifurcation of the external and internal iliac arteries
 Ligation of internal iliac artery 5cm distal to the common iliac bifurcation will usually avoid the
posterior division branches
 Suture is nonabsorbable
 85 % resuction in pulse pressure
 Angiographic embolization
 Used for many causes of intractable hemorrhage when surgical access is difficult
 Pelvic Packing
 Significant bleeding refractory to suture or topical hemostats
 Pelvic packing with gauze and termination of the operation may be considered
 Roll of gauze are packed to provide constant local pressure
 This may serve as a temporizing step prior to interventional embolization
 Left for 24-48 hours
 Umbrella or parachute pack
 Removed after 24 hours

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