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OBSTETRICAL HEMORRAGE

AIDA V. SAN JOSE, MD


2. ABRUPTIO PLACENTA
Causes of obstetrical hemorrhage  Separation of the placenta located elsewhere (normally
 Happening in the first half of pregnancy and those occurring implanted) in the uterine cavity
in the second half of pregnancy. For the causes of bleeding  The normal implantation of the placenta is where? Upper
for the first half of pregnancy: fundal (antero fundal, sabi ni dra)
 Abortion, ectopic pregnancy, gestational trophoblastic… and  Severe abruption placenta = >50% separation of the
of course the two important causes of Antepartum placenta
hemorrhage we have abruptio placenta and placenta previa,
we also include vasa previa, and these are the cause of 3. VASA PREVIA
bleeding for the first half.  Velamentous insertion of the umbilical cord with rupture
of a fetal vessel at the time of rupture of the membranes
Antepartum Hemorrhage (2nd half of pregnancy) resulting to fetal hemorrhage
 Placental abruption  Somewhat rare; fatal
 Placenta previa
 Vasa previa cause these three entities cause more bleeding ABRUPTIO PLACENTA
late in to the 2nd trimester or in to the early trimester  DEFINITION:
o “Ablation” - separation
Postpartum Hemorrhage o The premature separation of the normally implanted
 Uterine atony (most common) placenta (at upper uterine segment)
 Hemorrhage from retained placental fragments o Other terms are: ABLATIO PLACENTA or rendering
 Placenta accreta, increta, and percreta asunder biglang nag seseparateang placenta
 Inversion of the uterus o Accidental hemorrhage
o Maybe total or partial
 Genital tract laceration
o Total – entire placenta has separated, most severe type,
 Puerperal hematomas
accompanied by fetal death
 Rupture of the uterus o Partial – can cause death sometimes
 Rupture of the scarred uterus  FREQUENCY: 1 in 200 deliveries
 INTENSITY: depends on the promptness in consultation and
OBSTETRICAL HEMORRHAGE management
 Obstetrical hemorrhage, along with hypertension and
 PERINATAL MORBIDITY AND MORTALITY:
infection, is one of the infamous “triad” of causes of maternal
o Perinatal mortality: 25% (119/1000)
deaths
o Stillbirths- 10-12%
 The single most important cause of maternal death; half of all o With fetal survival, there may be adverse sequelae 
postpartum death significant neurologic sequelae within the first year of
 Acceptable obstetric care requires facilities that allow prompt life (15%)
administration of blood
 Coombs et al. 1991 defined hemorrhage as postpartum drop
of 10 volume percent or by a need for transfusion ->
incidence was 3.9%

CAUSES OF PREGNANCY- RELATED DEATHS DUE TO


HEMORRHAGE
CAUSE OF PERCENTAGE (%)
HEMORRHAGE
Uterine atony 19%
Placental abruption 17%
DIC 16%
Laceration 14%
Placenta accreta/ 12%
increta/percreta
(3rd stage hemorrhage)
Uterine placental bleeding 6%
Placenta previa 7%  Chronic Hypertension – MOST COMMON
Retained placenta 4%  Multifetal Gestation –d/t very large placenta, delivery of the 1st
of twin
ANTEPARTUM HEMORRHAGE  Prior abruption - possibility of recurrent, problem with this is
1. PLACENTA PREVIA the timing of delivery or onset of abruption. Difficult to tell and
 Separation of the placenta which is implanted in the manage. 40 years or more are more prone to develop abruption
immediate vicinity of the cervical canal  Increased age and parity (Elderly primigravida)- 1st time
 Refers to implantation of the placenta of the lower pregnancy of a >35 y.o. woman; Best age to get pregnant: 20
uterine segment either totally or partially covering the to 25 years old
internal os  Uterine leiomyoma- Placenta implanted over a submucous type
of leiomyoma
1|O B S T E T R I C S , 2 0 1 4
Trans by: Macasaet, T. Edited By CK Lorenzo, Kaisoo, Dedeem, Grallohnll
RECURRENCE: ABRUPTIO PLACENTA CLINICAL DIAGNOSIS:
 The risk is high in subsequent pregnancies SIGNS AND SYMPTOMS:
 Management is difficult  Vaginal bleeding
o Most prominent manifestation
PATHOLOGY: o Profuse external
 Initiated by hemorrhage into the decidua basalis which then o Scanty external bleeding
splits and leaves a thin layer adherent to the myometrium o Characteristic of blood is said to be dark appearance
 The earliest stage is the development of a decidual hematoma which can be clotted blood or dark black as compared
 separation of the basal portion  compression  to placenta previa wherein the bleeding is red and fresh
destruction of adjacent placenta  Uterine tenderness, back pain
 There maybe no clinical symptoms in the early stages  Frequent uterine contraction or persistent uterine hypertonous
 A circumscribed area of depression on examination – (tetanic uterine contraction without adequate time for uterine
location where hematoma was used to be relaxation)
confirm the dx of abruption P = Blod clot = will create  Fetal distress esp. if there is a complete separation of
depression on maternal surface of the placenta placenta
 Idiopathic preterm labor
ABRUPTIO PLACENTA TYPES:  Dead fetus after complete separation
1. EXTERNAL HEMORRHAGE o We call these uterine tenderness, back pain, abdominal
 Bleeding that insinuates between the membranes and pain = painful bleeding, where as in previa is generally
uterus and escapes through the cervix as painless hge.
o Px complaint of vaginal bleeding
2. CONCEALED HEMORRHAGE (MORE DANGEROUS) Signs and symptoms Frequency (%)
 Blood that does not escape externally but is retained Vaginal bleeding 78
between the detached placenta and uterus Uterine tenderness 66
 Carries a greater maternal danger due to: Fetal distress 60
o Extent of bleeding cannot be appreciated Preterm labor 22
o Risks of consumptive coagulopathy or DIC High- frequency 17
 Could lead to shock; previous description of contraction
this type is “shock out of proportion to Hypertonus 17
amount of bleeding” Dead fetus 15
From Hurd and associates (1983)
CONCEALED/RETAINED HEMORRHAGE
1. Blood effused behind the placenta but its margins are still ULTRASOUND:
adherent  Highly dx of placenta previa
2. Placenta is completely separated but the membranes remain
 If findings (-) previa, or if placenta is N located then
adherent to the uterine wall
probably it is abruption P
3. Blood enters the amniotic cavity after breaking through
 Negative findings DO NOT exclude placental abruption; 24%
membranes –most acceptable reason
sensitivity
4. A closely related applied fetal head in the lower uterine
 In most cases, diagnosis is based on clinical grounds
segment so that blood is prevented from escaping. Usually
though the membrane are gradually detached from the uterine  Usually requested right away, and usually abdominal UZ, but
wall and blood eventually escapes – not credible the abdominal UZ will not give us an accurate dx of
abruption placenta. It cannot determine the presence of clot
CHRONIC PLACENTAL ABRUPTION of the maternal surface of the placenta because the clot
brought about by the abruption and cotyledons can have the
 Occurs in a few cases in which hemorrhage with
same echogenicity on UZ. So it is not recognized by UZ often
retroplacental hematoma is formed and is arrested completely
times, unless there is a big clot. Diagnosis is usually made on
without delivery; CAOS (chronic abruption oligohydramnios
clinical grounds but UZ is usually requested to rule out the
sequence): > MSAF (elevated)
possibility of placenta previa. Internal examination is not
 Incidence rate is low
performed because it can cause torrential hge. If you already
ruled out placenta previa you can now perform I.E to
FETAL TO MATERNAL HEMORRHAGE
determine if px. Is in labor, often times abruption is
 Blood in the retroplacental hematoma is almost always accompanied by labor, uterine contraction, hypertonous.
maternal but sometimes it can be fetal
 Non-traumatic PA – evidence of feto-maternal hge in 20% SHOCK
(<10ml) – more on maternal origin  May be due to massive or torrential hge; can develop with
 Traumatic PA- significant fetal bleeding, more on fetal in concealed abruption
origin  Prompt treatment of hypotension of crystalloid and blood
infusion to restore vital signs and reverse oliguria
 Can cause renal failure requiring dialysis
 AKI can lead to tubular necrosis

2|O B S T E T R I C S , 2 0 1 4

Trans by: Macasaet, T. Edited By CK Lorenzo, Kaisoo, Dedeem, Grallohnll


CONSUMPTIVE COAGULOPATHY  TOCOLYSIS
 Defibrination syndrome or DIC: 30% of cases of severe o Clinically evident placental abruption is
abruption with fetal death will have overt contraindication to tocolytic therapy except in selected
hypofibrinogenemia (<150 mg/dl of plasma) along with cases of extreme prematurity in which the separation is
elevated levels of fibrinogen- fibrin degradation products, d- minor and maternal hemodynamic status is stable-
dimer, and variable decreases in other coagulation factors- ACOG 1993
despite increase in levels, they will NOT be able to
compensate for the hypofibrogenemia  AMNIOTOMY
 Major mechanism: intravascular and retroplacental induction o Early amniotomy was advocated because the escape of
of coagulopathy amniotic fluid might:
 Important consequence of intravascular coagulation:  Decrease bleeding from the implantation site
activation of plasminogen to plasmin  lysis of fibrin  Reduce the entry into the maternal circulation of
microemboli  maintenance of microcirculation patency thromboplastin and perhaps activated coagulation
 Pathologic levels- >100ug/ml of fibrinogen-fibrin factors from the retroplacental clot – more
degradation products in maternal serum- not clinically useful important function

ACUTE KIDNEY INJURY  VAGINAL DELIVERY


 Renal dysfunction that develops in severe forms of abruption o The preferred route if the fetus is already dead unless
especially when hypovolemia is not promptly corrected- in ¾ the hemorrhage is brisk and there are other obstetrical
of cases, reversible acute tubular necrosis accounts for the complication precluding vaginal delivery
Renal Failure o Course of labor is shorter in cases of placenta previa
 Major factors in its development
o Impaired renal perfusion- massive bleeding  reduces  CEASAREAN SECTION
cardiac output o Often management of abruption placenta
o Coexisting hypertensive disordered can cause renal o Done to deliver the live distress fetus rapidly
vasospam o If fetus is alive but CS is not carried out there must be
 Prompt and vigorous treatment of hemorrhage with blood and continuous fetal monitoring and delivered once signs of
electrolyte solution will often prevent significant renal distress manifest
dysfunction o Serious coagulation defect may prove difficult during
CS
UTEROPLACENTAL APOPLEXY (COUVELAIRE  The longer the interval between admission and
UTERUS) delivery, the higher the mortality
 In severe form of abruption placenta
 Widespread extravasation of blood into the uterine PLACENTA PREVIA
musculature and beneath the uterine serosa, tubal serosa,  Implantation of the placenta on the lower uterine segment
between the leaves of the broad ligament, ovarian substance,  The degree depends on the cervical dilatation
peritoneal cavity  Cervical examination to determine dilatation can incite
 Demonstrated conclusively at laparotomy torrential hemorrhage and is therefore not usually carried out
 Seldom interfere with uterine contraction and is not an unless there is a “double set up”
indication for hysterectomy o The patient and facility is ready for either CS or
o Color of the uterus is similar to that of an eggplant due vaginal delivery
to extravasation of blood to the serosa o Rarely done d/t presence of UZ
o Apoplexy- it means stroke  IE: no low lying uterine segment  abruptio placenta
vaginal delivery
CAUSES OF FETAL DISTRESS  IE: with low lying uterine segment placenta previa
 Placental separation  prompt delivery cesarean section
 Maternal hemorrhage  vigorous transfusion and prompt  Placenta previa usually does not become symptomatic until
deliver the late second or early third trimester when bleeding ensues
 Fetal hemorrhage immediate delivery and fetal transfusion which is classically but not always painless
 Uterine hypertonus prompt delivery
PLACENTA PREVIA DEGREE
MANAGEMENT:  TOTALIS- internal OS is completely covered by placenta
 Varies depending on fetomaternal status and AOG  PARTIALIS- internal OS is partially covered by placenta
 Massive bleeding intensive blood replacement and prompt  MARGINALIS- edge of placenta is at the margin of the
delivery internal OS - fall under the low lying
 With lesser and slower blood loss, mgt. is influenced by fetal  LOW-LYING- placenta is implanted in the lower uterine
status, live uncompromised fetus (esp. if immature), no segment such that the placental edge does not reach the os but
serious maternal hypovolemia or anemia close watch, is in close proximity to it
immediate intervention if condition deteriorates (immediate
cesarean section)

3|O B S T E T R I C S , 2 0 1 4

Trans by: Macasaet, T. Edited By CK Lorenzo, Kaisoo, Dedeem, Grallohnll


ETIOLOGY:
1. Multiparity – 5 or more DIAGNOSIS:
2. Advancing age – age 40 and up or age 35 elderly  An I.E is not done because of risk of torrential hemorrhage
primigravida unless there are provision for immediate CS (double set-up)
3. Prior CS or induced abortion and delivery is planned
4. Inflammatory or atrophic changes  Localization by SONOGRAPHY: simplest, most precise
5. Smoking (90%) and safest method of placental localization
6. Cocaine use  Magnetic resonance imaging: unlikely to replace ultrasound
7. Large placentas- erythroblastosis. Twin etc in placental localization
8. Association- accreta, increta, percreta  poorly
developed decidua in the lower uterine segment MANAGEMENT:
FOUR CONDITIONS IN PREVIA
CLINICAL FINDINGS: 1. Women with preterm fetuses but no pressing need for delivery
PAINLESS BLEEDING (no active bleeding)- observe, confine in hospital meanwhile
 The most characteristic event which takes place in the late 2. Women with reasonably mature fetuses- PARKLAND:
second or early third trimesters recommend termination at 37-38wks by CS
 Without warning and prior prenatal course may be uneventful 3. Women in labor – double set-up – baka naman hndi placenta
 Initial bleeding is often not profuse and ceases spontaneously previa, sometimes can do vaginal delivery
but RECURS 4. Women with severe hemorrhage that delivery is mandated
 Usual presenting history: mother waking up in the middle of painless of AOG- CS right away
the night lying on a pool of blood  Procrastination but in hospital setting although the
 Formation of LUS (lower uterine segment) and cervical women maybe discharge if bleeding stops and fetus is
dilatation tearing of placental attachment torn vessels healthy
which cannot be constricted because myometrial fibers in  Delivery: CS  preferred method
LUS are unable to contract bleeding

DIFFERENTIATION BETWEEN PLACENTA PREVIA AND ABRUPTIO PLACENTA


DIFFERENTIATION ABRUPTIO PLACENTA PLACENTA PREVIA
HISTORY Frequent association of preeclampsia or hypertension No association with preeclampsia
from any cause
A single attack of vaginal bleeding which usually Repeated “warming” hemorrhage, often occurring over a
continues until delivery period of weeks
Abdominal pain Usually no abdominal pain
Abdominal  Local uterine tenderness, hypertonic “woody” uterus  Normal uterine tone and usually no tenderness
examination in a concealed abruption  Patient rarely in labor
 Patient usually in labor  Presenting part above brim, malpresentation frequently
 Presenting part often engaged found
 Fetal parts may be difficult to palpate  Fetal parts usually palpable
 Fetal heart tone often absent  Fetal heart tones present
Ancillary (ultrasound)  Placenta in upper uterine segment  Placenta in lower uterine segment
Vaginal examination  Double-set up reveals no placenta within 5cm of  Double-set up reveals placenta implanted on the lower
internal OS uterine segment
Management  No place for expectant treatment when this is  If bleeding stops and fetus is less than 36 weeks old,
diagnosis is made expectant treatment may be indicated
NOTE: pain cannot be the basis of differentiation bet abruption P and P previa, although painfull bleeding is more common in P previa, it may
also occur on abruption P, depending on the case..

4|O B S T E T R I C S , 2 0 1 4

Trans by: Macasaet, T. Edited By CK Lorenzo, Kaisoo, Dedeem, Grallohnll

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