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Obstetrical Hemorrhage
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
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
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
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
Surgical Procedures
Uterine compression sutures
Pelvic vessel ligation
Angiographic embolization
Hyterectomy
UTERINE INVERSION
Uterine Inversion
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
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
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
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
Gestational hypertension
Pre-eclampsia
Chronic hypertension
Risk
Fetal demise
Elevated cardiovascular mortality risk prior, with or without chronic hypertension
Preterm Prematurely Ruptured Membranes
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
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
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
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
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
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