September

18, 2017
1.05

LATE OB HEMORRHAGE, AMNIOTIC FLUID DISORDERS, PROM
Dra. Alicia Bautista, MD, FPOGS
Department of Obstetrics and Gynecology

TOPIC OUTLINE • UTZ: within 1 cm for internal os

I. LATE OBSTETRIC HEMORRHAGE
a. Placenta Previa

b. Abruptio Placeenta LOW LYING PLACENTA

c. Amniotic Fluid Embolism • Placenta is implanted in the lower uterine
d. Disseminated Intravascular Coagulation segment (same as isthmus during the prepregnant
II. AMNIOTIC FLUID DISORDERS state) such that placental edge actually does not
a. Hydramnios
reach the internal os but is in close proximity to it
b. Oligohydramnios

III. PREMATURE RUPTURE OF MEMBRANES VASA PREVIA

• The fetal vessels course through membranes and
LATE HEMORRHAGE
present at the cervical os
• Obstetrics is bloody business
• Serious hemorrhage may occur at any time throughout
pregnancy and the puerperium
• The time of bleeding is widely used to classify obstetrical
hemorrhage
• Williams does not exactly specify the delineation for early and
late hemorrhage, but some authors classify hemorrhage
occurring <20 weeks AOG as early antepartum hemorrhage, and
>20 weeks AOG as late antepartum hemorrhage (Suresh et al.
2013)
• If you have previous scar à defective blood supply – Dr. • Degree of placenta previa depends on the cervical dilatation at
Bautista the time of examination
PLACENTA PREVIA • Placenta previa that appears to be total before cervical
• · Previa- going before: placenta goes down before fetus dilatation may become partial at 4cm dilatation because the
• Placenta located over or very near the cervical os cervix dilates beyond the edge of the placenta
• Any bleeding on the 3rd trimester can be suspected for • Low lying placenta at 2cm dilatation may become partial at
placenta previa 8cm dilatation
• Not to be confused with vasa previa (fetal vessels course • Digital palpation to try to ascertain these changing relations
through membranes and present at the cervical - an between the edge of the placenta and the internal os as the
uncommon cause of antepartum hemorrhage and is associated cervix dilates can incite severe hemorrhage
with a high rate of fetal death) • Don’t ever attempt to do IE if the impression is Placenta Previa
• ABNORMAL IMPLANTATION of the placenta RISK FACTORS
• Normal placentation: more on the fundal area – Dr. Bautista • More common in multiparas, only 20% occur in primigravids
• Etiology: Unknown • Multiple induced abortion (permanent damage in the
PLACENTAL TROPHOTOPISM endometrium will be unsuitable for implantation)
• Dynamic migration of placenta at its insertion to an area of • Previous history of CS (previous uterine operation)
greater blood supply • Puerperal endometritis (defective vascularization of decidua as
• Tend to grow in areas of good blood supply and nutrition a result of inflammatory changes)
• Atrophies in areas with poor blood supply and poor nutrition • >35 years old
• Placental migration à the placenta does not move per se • Previous history of placenta previa
• Mechanism of movement is not understood • Malposition of fetus (breech or transverse)
• Large placenta (multiple fetus)/ Fetal erythroblastosis
DEGREES OF PLACENTA PREVIA (Old Classification) • Advancing maternal age (3x more common if more than 35
TOTAL PLACENTA PREVIA y/o)
• Internal cervical os is covered completely by • Smoking (causes hypoxemia leading to compensatory placental
placenta hypertrophy)
• Multiparity >5

PARTIAL PLACENTA PREVIA

• Internal os is partially covered by placenta

Placental localization based on POGS 2014:

MARGINAL PLACENTA PREVIA
1. UTZ at 20 weeks
• Edge of the placenta is at the margin of the 2. Follow-up 28-32 weeks is recommended if initial UTZ is
internal os; less than or equal to 2 cm away from
placenta previa
the internal os
3. Near internal os at 36 weeks

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*If at 32 weeks, <2cm from os, follow up at 36 weeks. If same at
36 weeks, consider it placenta previa
CAUSES
• Defective vascularization of the placenta secondary to atrophic
changes or inflammation
• Scarring of the endometrium with advancing maternal age as a
result of repeated pregnancies
• Changes in the vessels at the placenta that decrease the blood
supply to the endometrium and necessitate greater surface
area for placental attachment to probable adequate maternal
BF
• Erythroblastosis fetalis – because of large placenta
• Alteration in blood supply to the endometrium and changes in
the quality and depth of endometrium as a result of previous
incision
• Multiple pregnancies increase surface for placental
implantation so that lower portion of placenta may approach
internal os

CLINICAL PRESENTATION
• PAINLESS vaginal bleeding – classic symptom of PP
o Presumptive diagnosis (bleeding in 3rd trimester)
o Bleeding without warning
o Most characteristic sign
o Can occur at rest or during activity
o After coitus, trauma, internal exam
o Vaginal bleeding usually during the first time during the
3rd trimester when Lower Uterine Segment (LUS)
changes (cervical effacement and dilatation) that can
cause tearing of placenta
o Continued bleeding occurs because stretched fibers of Figure 2. Plan of Management for Placenta Previa
the LUS are unable to contract to compress the torn
vessels because of the undelivered pregnancy FACTORS TO CONSIDER:
o Sentinel bleed 1. Fetal Age
DIAGNOSIS 2. Stage of Labor
3. Bleeding
• Ultrasound
Expectant Management
o Simplest, most precise, safest
o 90-95% accurate • Rationale: Initial hemorrhage in placenta previa is rarely fatal;
Premature fetus can still grow
• Double Set-up
o All systems go • Surgical Management
o Pt. is in an operating room with preparations for o Elective CS (Planned or scheduled)
immediate cesarean delivery - Fetus is >2500 g
o Digital palpation of the placenta - Fetus is about 37 wks AOG by UTZ
o Not done unless delivery is planned (cause bleeding - L/S ratio is comparable with 37 wks (term
that necessitates immediate delivery even though the baby)
fetus is immature) o Emergency CS
o Delivery is completed at the time of examination - Vaginal bleeding present maternal threat
o Difficult to do it sa very premature - Viable fetus is in distress
- Tocolytics are ineffective in controlling labor
• Abruptio Placenta – premature separation of normally
Consider the following factors before sending the patient
implanted uterus
home:
• Marginal Sinus Rupture – blood vessel rupture at the margin of
placenta • Relatives have been well-informed about the patient’s
condition
• Placental Migration – placenta that is close to the internal os
during the 2nd trimester, usually • Proximity of home to hospital
o Vasa previa- rare anomaly of velamentous insertion, prone to • Patient’s financial resources
compression and laceration
• MRI • If presentation is placenta previa and patient has history of CS
delivery à manage as placenta accreta
• Suspected previa – color flow
• Previous CS, previous D&C, previous instrumentation, tignan
• Doppler UTZ
nyo baka ACCERA to
MANAGEMENT

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PROGNOSIS • Blood does not escape
• <1% maternal death externally but is
• Prematurity in the major cause of perinatal death retained between the
COMPLICATIONS detached placenta
• ↑ incidence of Placenta accreta because of the thinner and uterus
endothelium in LUS and inability to control the invasive • Presents with:
properties of trophoblast • Vaginal bleeding
• IUGR • Abdominal pain
• Severe postpartum hemorrhage (implantation is in LUS whose • Uterine tenderness
torn vessels hypertonicity
• Sheehan’s syndrome
• Acute Tubular Necrosis Combination
• As a consequence of Abnormal Decidua Basalis:
o Accreta – attach to myometrium
o Increta – invades the myometrium
o Percreta – penetrates the myometrium
o The implantation of the placenta should be up to
Nitabuch’s layer only; if it extends beyond, the above
conditions can be seen
o NITABUCH’S LAYER- fibrinoid layer that separates
normal placenta
o Implantation invades and and extends through
Nitabuch’s layer
• Types of Placenta Accreta:
o Total - all cotyledons
o Partial - few or several cotyledons
o Focal- one cotyledon

Figure 4. Types of Abruptio Placenta
Figure 3. Normal placenta, placenta accrete, increta and percreta
• INCIDENCE:
ABRUPTIO PLACENTA ü 1:200-300 pregnancies
ü 80% = Multipara
• Latin abruptio placentae, which means "rending asunder of
• CAUSE: UNKNOWN
the placenta," denotes a sudden accident, a clinical
characteristic of most cases of this complication • Timing of Placental Detachment
ü 50% at onset of labor
• Separation of a normally implanted placenta before the
ü 10-15% during the 2nd stage of labor
birth of the fetus (differentiated from placenta previa

because placenta is implanted over the cervical interna os)
Chronic abruptio: Oligohydramnios
• Premature separation of a normally attached placenta
Traumatic abruptio: motor or vehicle or physical
• Accidental hemorrhage assault
• Has been variously called placental abruption, abruptio RISK FACTORS
placentae, and in Great Britain, accidental hemorrhage ü Advanced maternal age > 40 yo and parity
• Sudden disturbances of vascular epithelium as in ü MATERNAL HYPERTENSION – M.C. CAUSE
vasodilation secondary to shock ü PROM
• Passive engorgement of the uterus and placenta ü Cigarette smoking - 2 fold increase
• Supine hypotension syndrome when IVC is compressed ü Cocaine abuse
TYPES ü External trauma
External Hemorrhage • d/t marginal ü Previous abruption
separation of placenta ü Race or ethnicity
• Bleeding insinuates ü Asian 1:300
itself between ü African-American 1:200
membranes and ü Latin American 1:450
uterus and then
ü Sudden decompression – ex: Polyhydramnios, sudden
escapes through the
rupture of water
cervix
ü Uterine leiomyomas- high pressure from enlarging mass
Concealed Hemorrhage • Associated with ü Short umbilical cord (normal length – 50-55 cm)
retroplacental ü Thrombophlebitis
bleeding

• Greater maternal
hazard

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PATHOLOGY
Hemorrhage into the decidua basalis
↓ *RETAINED OR CONCEALED TYPE is likely when:
Decidua splits • There is effusion of blood behind the placenta but its
↓ margins still remain adherent
Leaving a thin layer adherent to myometrium • Placenta completely separated yet the membranes retain
their attachment to the uterine wall
• Early Stage o may be no clinical symptoms • Blood gains access to the amnionic cavity after breaking
ü Discovered only on examination of the freshly through the membranes
delivered organ • Fetal head is so closely applied to the lower uterine segment
ü FINDINGS: circumscribed depression measuring a that the blood cannot make its way past it
few cm in diameter on its maternal surface covered SIGNS AND SYMPTOMS
by dark, clotted blood • PAINFUL vaginal bleeding
• Most frequent findings:
Decidual spiral artery ruptures
ü Abdominal pain
↓
ü Uterine tenderness
Retroplacental hematoma
↓ ü Uterine hypertonus
Expands ü Fetal distress
↓ ü Dead fetus
Disrupts more vessels to separate more placenta • May develop shock out of proportion to the amount of blood
↓ loss because of thromboplastin -> Thromboplastin from the
Area of separation rapidly becomes more extensive and decidua and placenta enter the maternal circulation at the
reaches the margin of the placenta site of placental
↓ • separation -> intravascular coagulation -> Acute cor
Uterus still distended w/ products of conception (unable to pulmonale -> DIC and hyperfibrigonemia -> Prolapse of the
contract sufficiently to compress the torn vessels that supply placenta
the placental site) CLASSIFICATION
↓ • Scanty to moderate
Escaping blood may dissect the membranes from the uterine 1. MILD vaginal bleeding
wall ->externally or may be completely retained within the • No fetal distress
uterus
• Stable maternal signs
CLASSIFICATION
• Lower abdominal
• Partial - only a part of it discomfort
1. As to EXTENT has separated
• Incomplete relaxation of
• Total - whole placenta uterus
separated

• Separation of ¼ - ½ of
• Acute abruption - 2. MODERATE placenta
2. As to ONSET sudden onset of signs • Continuous uterine pain
and symptoms
• Moderate vaginal
• Chronic abruption - bleeding and mild fetal
hemorrhage with
distress
retroplacental

hematoma formation is
• Separation of placenta >
somehow arrested
3. SEVERE ½
completely without
• Board-like, unrelaxed
delivery
uterus

• Fetal distress/death
• External - bleeding is
3. As to TYPE OF BLEEDING near cervical os • Shock, DIC, oliguria

• Internal os Retained or
DIAGNOSIS
Concealed* - much
greater maternal and • Suspect abruptio placenta in the ff cases:
fetal hazard because of ü Abnormal FHT of unknown cause
possibility of ü Unexplained bleeding
consumptive ü Ultrasonically visualized liquid or dark area behind the
coagulopathy and extent placenta
of the hemorrhage is not ü Portwine colored amniotic fluid
appreciated so that ü Decreasing serial hemoglobin
diagnosis is made later • Clot formation – retroplacental

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• Ultrasound - infrequently confirms the dx of abruption -> (-) Disproportion (CPD)
findings with ultrasound examination do not exclude • CS for DEAD FETUS:
placental abruption • Continuous bleeding
• MRI, Color Doppler • Progression of
abruption
DIFFERENTIAL DIAGNOSIS • If fibrinogen level
• Placenta previa progression falls -> DIC
• Labor accompanying placenta previa • Oxytocin
• Labor pain • If no rhythm
• Uterine rupture contractions are noted
• Abdominal pregnancy with intra-abdominal • Amniotomy
• Benefits: Decrease
• Hemorrhage
bleeding, decrease entry
• Ruptured Hemangioma
of thromboplastin in
• Hepatic Rupture implantation site
• Sickle cell rupture • Tocolysis: not been
used
MANAGEMENT
• Prevent hypovolemia
1. EMERGENCY MEASURES with IVF and blood
• Monitor vital signs, I&O
• Assess fetal if in distress
• Prepare properly typed
and cross-matched
blood
• IV using large bore
needle
• CBC with platelet count,
plasma fibrinogen,
fibrin degradation
products, aPTT
Figure 5. Causes of Fetal Distress from Placenta Abruptio and
• If dx is uncertain/term Their Treatment
2. ASSESS FETUS fetus alive and not in COMPLICATIONS
distress – Close MATERNAL
observation • Couvelaire uterus (uterine apoplexy)
• Term fetus in distress – • Severe form of abruptio
Immediate intervention • widespread extravasation of blood into the uterine
à CS • musculature and beneath the uterine serosa seeping of
• Delaying delivery may • blood through the myometrium of the uterus
prove beneficial in • Black and blue uteri
immature fetus but if w/ • Only diagnosed in CS
decelerations, oligo or
• Not an indication of hysterectomy except if with uterine
maternal deterioration
àterminate • atony not responding to treatment
• Renal Failure – ATN secondary to intrarenal vasospasm
• VAGINAL DELIVERY from massive hemorrhage and hypovolemia
3. SPECIFIC MEASURES • Dead fetus without • DIC
brisk hemorrhage or OB • Hemorrhagic Shock
complication
• Imminent
delivery/bleeding
minimal without signs
of fetal distress
• CS for LIVE FETUS if:
• Unsuccessful induction
of labor
• Fetal distress
• Failure of labor in 4hrs
• Other OB indications
sucj as Cephalopelvic

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6. Placental abruption or previa
7. Hydramnios

PATHOGENESIS

• Maternal exposure to various fetal elements during:
• Pregnancy termination
o Following amniocentesis
o Trauma
o Labor or delivery – more common
Figure 6. Couvelaire Uterus • Small lacerations develop in the lower uterine segment or
FETAL cervix
• Hypoxia • Cesarean delivery - mixture of maternal blood and fetal
• Death tissue
• Exposure initiates complex series of physiological reactions
mimicking those seen in human anaphylaxis and sepsis
• Complement levels - decreased uniformly
IUFD • Complement activation may play an important role
PATHOPHYSIOLOGY
UTERINE SPASM Pain
BLOOD LOSS
SHOCK Albuminuria Renal Failure

COAGULATION
DEFECT Massive bleeding Fibrinoysin release

AMNIOTIC FLUID EMBOLISM
• Responsible for 5% maternal deaths • Effects:
• Entry of amniotic fluid into the maternal circulation o uterine hypertonus
• Through: o cardiovascular collapse
1. Rent through the amnion and chorion • Complete cessation of uterine blood flow
2. Open uterine and endocervical veins o When intrauterine pressures exceed 35-40 mm Hg
3. Pressure gradient sufficient to force fluid o Thus, hypertonic contraction is the least likely time
4. Into the venous circulation for fetal–maternal exchange to take place
Classical Early 1. Hypotension CLINICAL FINDINGS
Characteristics (Abrupt 2. Hypoxia • Sudden dyspnea, cyanosis
Onset) 3. Consumptive coagulopathy • Profound shock that may lead to hemorrhage and death
Late 1. Begins gasping for air • Lethality of amniotic fluid due to a particular matter and esp.
2. Rapidly suffers seizure or if there is meconium
cardiorespiratory arrest AMNIOTIC FINDINGS
complicated by: • Amniotic cells, lanugo, meconium in the pulmonary arterial
o Consumptive system, right heart,
Coagulopathy • Thrombi in microcirculation in DIC
o Massive hemorrhage COMPLICATIONS
o Death
• Obstruction of pulmonary circulation ->right sided failure
Predisposing 1. Rapid labor
• Hypofibrinogemia due to DIC ->hemorrhage
conditions 2. Meconium-stained amniotic fluid
3. Tears into uterine and other pelvic • If the patient survives, she will have:
veins o Pulmonary hypertension
o RVH
Risk factor 1. Older maternal age
o Cardiac failure
2. Post-term pregnancy
DIFFERENTIAL DIAGNOSES
3. Labor induction or augmentation
4. Eclampsia • Septic shock
5. Cesarean, forceps or vacuum delivery • Eclampsia
• Emboli

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• Stroke
• Cardiac failure
• Toxic drug reaction
TREATMENT
• Treat shock
• Oxygenation
• Tourniquet to limit venous return
• Heparin for DIC isoproterenol to dilate microcirculation
• Insert CVP
• Deliver fetus w/o trauma if feasible
• Blood replacement therapy
DISSEMINATED INTRAVASCULAR COAGULOPATHY
• Consumptive Coagulopathy
• Abruptio Placenta – most common cause • During pregnancy
o The main mechanism is thromboplastin release o activation of platelet, clotting, and fibrinolytic
and activation of the extrinsic pathway (factor VII) mechanisms
due to ante partum placental separation o Significant increases in:
o When complicated by severe shock, DIC may be § fibrinopeptide A
exacerbated § β-thromboglobulin
by hypoxia and acidosis causing widespread § platelet factor 4
endothelial § fibrinogen–fibrin degradation products
damage, increasing endothelial surface expression o Compensated, accelerated intravascular
of tissue coagulation serves to maintain the uteroplacental
factor and activation of intrinsic pathway interface
• Pathological states
o coagulation may be activated via:
§ extrinsic pathway: thromboplastin from
tissue destruction
§ intrinsic pathway : collagen and other
tissue components when there is loss of
endothelial integrity
o Tissue factor III is released -> complexes with
factor VII -> activates tenase (factor IX) and
PREGNANCY HYPERCOAGUBILITY
prothrombinase (factor X) complexes
• Pregnancy normally induces ↑ in concentrations of o Common inciting factors in Obstetrics
coagulation factors:
§ thromboplastin from placental abruption
o I (fibrinogen), VII, VIII, IX, X
§ endotoxin
• Plasminogen levels are ↑ considerably but PAI-1 and PAI-2 § exotoxins
increase o Another mechanism is by direct activation of factor
o plasmin activity antepartum is normally decreased X by proteases
until after delivery § Example: as present in mucin or as
produced by neoplasms
§ Amniotic fluid
- contains abundant mucin from fetal
squames
- this causes rapid defibrination with
SIGNIFICANCE amniotic fluid embolism
• Bleeding and circulatory obstruction ->hypoperfusion -> • DIC almost always seen as a complication of an identifiable,
ischemia underlying pathological process against which treatment
• Microangiopathic hemolysis - caused by mechanical must bedirected to reverse defibrination
disruption of the erythrocyte membrane within small o Priority in txt: identification and prompt
vessels in which fibrin has been deposited elimination of the source
• Varying degrees of hemolysis with anemia, hemoglobinemia,
hemoglobinuria, and erythrocyte morphological changes are
produced.

PATHOLOGICAL ACTIVATION OF COAGULATION
• Normal circumstances
o No appreciable continuous physiological
intravascular
coagulation

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§ Nicks from shaving the perineum or
abdomen
§ Trauma from insertion of a catheter
§ Spontaneous bleeding from the gums or
nose

HYPOFIBRINOGENIMIA
• Late pregnancy
o Plasma fibrinogen levels: 300 to 600 mg/dL
o DIC, these high levels may sometimes serve to protect
against clinically significant hypofibrinogenemia
o To promote clinical coagulation, fibrinogen levels must
be about 150 mg/dL
o
FIBRIN AND FIBRINOGEN DERIVATIVES
• Monoclonal antibodies to detect D-dimers - commonly
used (always abnormally high)

THROMBOCYTOPENIA
• Petechiae are abundant
• Clinically significant thrombocytopenia - Purpuric areas at
pressure sites
• Clotted blood fails to retract over a period of an hour
• Confirmation: platelet count

PROTHROMBIN AND PARTIAL THROMBOPLASTIN TIME

• Prolongation of test

• Consequence of:
• Microangiopathic Hemolysis
o significant reductions in coagulants essential for
o Due to Another mechanism is by direct activation
generating thrombin
of factor X by proteases
o fibrinogen concentration < critical level of about 100
o Priority in txt: identification and prompt
mg/dL
elimination of the
o significant amounts of circulating fibrinogen–fibrin
source
degradation products
o Pathological activation of procoagulants that
trigger DIC -> • Prolongation time need not be the consequence of
consumptive coagulopathy
consumption of platelets and coagulation factors in

variable
quantities -> fibrin may be deposited in small CLINICAL FEATURES
vessels of Early • Generalized
virtually every organ system microvascular
o Mechanical disruption of erythrocyte membrane obstruction
within small vessels in which fibrin has been • Insufficient tissue
deposited oxygenation
o Effects: • Shock
§ Varying degrees of hemolysis with: • Myocirculatory
• Anemia damage in various
• Hemoglobinemia organs
• Hemoglobinuria • Myocardium:
• erythrocyte morphological arrhythmia, shock
changes • Lungs: respiratory
• Clinical and Laboratory Evidence of Defective distress
Hemostasis • CNS: tachypnea,
o Bioassay - excellent method to clinically detect or fever, convulsions
suspect • Kidneys: renal
significant coagulopathy insufficiency
o Excessive bleeding of modest trauma ◊ defective • Skin: infections
hemostasis • Adrenals: shock
o Signs of possible coagulation defects: (Waterhouse-
§ Persistent bleeding from venipuncture Friedrichsen
sites syndrome)

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• Consumption of o Control of hypertension and eclamptic states

coagulation factors o Replacement therapy
& platelets o Heparin – no benefit, dangerous intracerebral bleeding
• Generalized may occur especially in severe HPN
bleeding
Late • Organ dysfunction SUMMARY
• Kidneys: uremia PLACENTA PREVIA
• Liver: jaundice, liver • In placenta previa, the placenta is located over
insufficiency or very near the internal os
• Red cells: jaundice, • Classic symptom: painless vaginal bleeding
anemia • In the past, the double set-up exam has been
considered the first diagnostic procedure in the
management of placenta previa, however, since
MANAGEMENT placental localization thru ultrasonography is
• Since DIC results from an underlying disorder, correction of possible, it is now rarely necessary
the primary pathologic condition is the cornerstone of • Expectant management is recommended with
treatment a preterm fetus but with no active uterine
• If primary problem is: bleeding
• If pregnancy has reached term of lung maturity
1. Abruption placenta: has been documented, Caesarian Section is
• Problem: hemorrhage→ hypovolemic shock and renal indicated
insufficiency
• Management: ABRUPTIO PLACENTA
o Replacement of blood loss and prompt evacuation of the • Accidental haemorrhage
uterus • Premature separation of the normally implanted
o Cryoprecipitate to replace fibrinogen and factor VIII placenta
o Platelet to correct thrombocytopenia • The main pathology involved is the separation of
o Heparin not indicated because it may exacerbate decidual hematoma
bleeding • Painful bleeding are frequent findings

2. IUFD (Intrauterine Fetal Death) AMNIOTIC FLUID EMBOLISM
• Course of DIC is low grade • Re-entry of amniotic fluid into the maternal
• Elevated fibrin degradation products, platelet and fibrinogen circulation through a rent through the amnion,
become evident in the 3rd to 5th chorion, opened uterus, and endocervical veins,
• Management: pressure is sufficient to force fluid into the
o Successful deliver of fetus with minimal bleeding circulation
Replacement therapy • It may be responsible for some maternal deaths
o If laboratory parameters show a tendency to progressive
consumption, heparin should be administered before COAGULATION COAGULOPATHY OR
surgery DEFIBRINATION SYNDROME
• Happens when there is an imbalance between
3. Amniotic Fluid Embolization the coagulation cascade and fibrinolysis
• Very poor survival rates • Prothrombin time tests the integrity of the
• Those who survive may experience severe hemorrhage extrinsic pathway
within two hours after the onset of symptoms and • PTT: intrinsic pathway
fibrinolysis • PT: extrinsic pathway
• Management: • Treatment of DIC is controversial and is directed
o Correct hypoxia and shock towards specific conditions like abruption
o Heparin and anti-fibronlytic agents placenta, IUFD, AFE, pre-eclampsia/eclampsia,
o Replacement therapies infection, etc

4. Septic Abortion and Obstetric Sepsis
• Management: AMNIOTIC FLUID DISORDERS
o Appropriate antibiotic therapy

o Heparin may be given if DIC is found before clinical
manifestation became evident • Roles of amniotic fluid during pregnancy:
1) It creates a physical space for fetal movement, which is
o Prompt evacuation of the uterus
necessary for normal musculoskeletal development.
o Adequate replacement of depleted factors
2) It permits fetal swallowing—essential for

gastrointestinal tract development, and fetal
5. Pre-eclampsia/Eclampsia
breathing—necessary for lung development.
• Management:
o Termination of pregnancy

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3) Amnionic fluid guards against umbilical cord vessels on the placental surface, and thus into the
compression and protects the fetus from trauma. fetus.
4) It even has bacteriostatic properties. o This transfer reaches 400 mL per day and is a second
• Amnionic fluid volume abnormalities may reflect a problem regulator of fluid volume.
with fluid production or its circulation, such as underlying o In the setting of maternal dehydration, the resultant
fetal or placental pathology. increase in maternal osmolality favors fluid transfer
• These volume extremes may be associated with increased from the fetus to the mother, and then from the
risks for adverse pregnancy outcome. amnionic fluid compartment into the fetus.

NORMAL AMNIOTIC FLUID VOLUME 3) Respiratory tract.
• Amnionic fluid volume increases from approximately 30 mL o Approximately 350 mL of lung fluid is produced daily
at 10 weeks to 200 mL by 16 weeks and reaches 800 mL by late in gestation, and half of this is immediately
the mid-third trimester. swallowed.

• This fluid is approximately 98-percent water.
4) Fetal swallowing is the primary mechanism for
• A full-term fetus contains roughly 2800 mL of water, and the amnionic fluid resorption and averages 500 to 1000 mL
placenta another 400 mL, such that the term uterus holds per day.
nearly 4 liters of water. o Impaired swallowing, secondary to either a central
• Abnormally decreased fluid volume is termed nervous system abnormality or gastrointestinal tract
oligohydramnios obstruction, can result in an impressive degree of
• Abnormally increased fluid volume is termed hydramnios hydramnios.
or polyhydramnios.
• The other pathways—transmembranous flow and flow
PHYSIOLOGY across the fetal skin—account for a far smaller proportion
• Early in pregnancy, the amnionic cavity is filled with fluid of fluid transport in the second half of pregnancy.
that is similar in composition to extracellular fluid.
• During the first half of pregnancy, transfer of water and
other small molecules takes place across the amnion AMNIOTIC FLUID REGULATION IN LATE PREGNANCY
transmembranous flow, across the fetal vessels on placental Pathway Effect on Approximate Daily
surface—intramembranous flow, and across fetal skin. Volume Volume (mL)
• Fetal urine production begins between 8 and 11 weeks, Fetal Urination Production 1000
but it does not become a major component of amnionic fluid Fetal Swallowing Resorption 750
until the second trimester. Fetal Lung Fluid Production 350
o This latter observation explains why fetuses with lethal Secretion
renal abnormalities may not manifest severe Intramembranous Resorption 400
oligohydramnios until after 18 weeks. flow across fetal
• Water transport across the fetal skin continues until vessels on the
keratinization occurs at 22 to 25 weeks. placental surface
o This explains why extremely preterm infants can Transmembrane flow Resorption Minimal
experience significant fluid loss across their skin. across amniotic
membrane
AMNIOTIC FLUID REGULATION IN PREGNANCY
• With advancing gestation, four pathways play a major role in SONOGRAPHIC ASSESSMENT
amnionic fluid volume regulation. • Amnionic fluid volume evaluation is a component of every
standard sonogram performed in the second or third
1) Fetal urination is the primary amnionic fluid source by trimester.
the second half of pregnancy. • Volume is typically assessed semiquantitatively, by
o By term, fetal urine production may exceed 1 liter per measuring either a single pocket or the amnionic fluid
day—such that the entire amnionic fluid volume is index—AFI.
recirculated on a daily basis. • A qualitative or subjective estimate of amnionic fluid volume
is also considered acceptable when performed by an
2) Intramembranous flow across fetal vessels on the experienced examiner.
placental surface.
• One limitation of subjective estimation, however, is that it
o Fetal urine osmolality is significantly hypotonic to
does not permit a longitudinal assessment of trends in the
that of maternal and fetal plasma and similar to that
amount or adequacy of fluid volume.
of amnionic fluid.

o Osmolality of maternal and fetal plasma is
SINGLE DEEPEST POCKET (SDP)
approximately 280 mOsm/mL, whereas that of
amnionic fluid is about 260 mOsm/L. • This is also called the maximum vertical pocket.
o This hypotonicity of fetal urine—and thus of • The ultrasound transducer is held perpendicular to the floor
amnionic fluid—accounts for significant and parallel to the long axis of the pregnant woman.
intramembranous fluid transfer across and into fetal

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• In the sagittal plane, the largest vertical pocket of fluid is
identified.
• Fluid pocket may contain fetal parts or loops of umbilical
cord, but these are not included in the measurement.
• Normal range for single deepest pocket that is most
commonly used is 2 to 8 cm, with values above and below
this indicating hydramnios and oligohydramnios,
respectively.
• Other less commonly used thresholds to determine amnionic
fluid volume adequacy involve measurement of a single
pocket in both the vertical and transverse planes.
• Adequate fluid volume is defined as a 2 × 1 cm pocket, a 2 ×

2 cm pocket, or a pocket that is at least 15 cm2.
• When evaluating twin pregnancies and other multifetal Classification According to Degree
gestations, a single deepest pocket of amnionic fluid is
Mild Moderate Severe
assessed in each gestational sac, again using a normal range
AFI 25-29.9 cm 30-34.9 cm ≥ 35cm
of 2 to 8 cm.
SDP 8-9.9 cm 10-11.9 cm ≥ 12 cm

Most common
AMNIOTIC FLUID INDEX ~20% of cases ~15% of cases
~2/3 of cases
• Remains one of the most commonly used methods of

amnionic fluid volume assessment.
• These definitions fit the general rule that the AFI is
• As with the single deepest fluid pocket measurement, the
approximately three times the measurement of the
ultrasound transducer is held perpendicular to the floor and
single deepest fluid pocket.
parallel to the long axis of the pregnant woman.
• In general, severe hydramnios is far more likely to have
• The uterus is divided into four equal quadrants—the an underlying etiology and to have consequences for the
right- and left-upper and lower quadrants, respectively. pregnancy than mild hydramnios—which is frequently
• AFI is the sum of the single deepest pocket from each idiopathic and benign.
quadrant.
• A fluid pocket may contain fetal parts or umbilical cord Presents as:
loops, but these are not included in the measurement. • Dyspneic
• Color Doppler is generally used to verify that no umbilical • Edema
cord is included in the measurement. • Difficulty in auscultation of heart tones and fetal parts
o This may result in greater consistency and in reduction • Prolapse
of intraobserver variation. • Sudden decompression
o It has been reported, however, that color Doppler use • Uterine atony ⇾ overdistention
results in a lower AFI measurement, thus potentially
leading to overdiagnosis of oligohydramnios. Etiology
• Normal range for AFI that is most commonly used is 5 to 1. Fetal congenital anomalies
24 cm, with values above and below this indicating • Such as anencephaly, hydranencephaly, or
hydramnios and oligohydramnios, respectively. holoprosencephaly, can result in hydramnios due to
• Increased by high altitude impaired fetal swallowing
• Fetal neuromuscular disorders such as myotonic
HYDRAMNIOS dystrophy also may lead to excessive amnionic fluid.
• Also called polyhydramnios • Obstruction of the fetal upper gastrointestinal tract—
• Usually more than 2L; AFI > 24 cm esophageal or duodenal atresia—is often associated
o Normal AFI: 5-24 cm with hydramnios.
• This is an abnormally increased amniotic fluid volume, • Other obstructive causes include clefts, micrognathia,
and it complicates 1 to 2 percent of pregnancies. congenital high-airway obstruction sequence, and fetal
• Also termed polyhydramnios, hydramnios may be neck masses.
suspected if the uterine size exceeds that expected for • Severe fetal thoracic abnormalities, such as
gestational age. diaphragmatic hernia, cystic adenomatoid
• The uterus may feel tense, and palpating fetal small malformation, and pulmonary sequestration, may be
parts or auscultating fetal heart tones may be difficult. associated with hydramnios due to mediastinal shift
and impaired swallowing, occasionally with
development of hydrops.
• A common fetal renal anomaly, ureteropelvic junction
obstruction, may at times result in paradoxical
hydramnios.
• Although rare, tumors such as fetal sacrococcygeal
teratoma, fetal mesoblastic nephroma, and large

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placental chorioangiomas are frequently accompanied Complications
by abnormally increased amnionic fluid volume. • Maternal complications such as these are typically
associated with severe hydramnios from an underlying
2. Diabetes Mellitus etiology.
• The amnionic fluid glucose concentration is higher in • Maternal complications associated with hydramnios
diabetic women than in those without diabetes, and the include:
amnionic fluid index may correlate with the amnionic o placental abruption
fluid glucose concentration. o uterine dysfunction
• Such findings support the hypothesis that maternal o postpartum hemorrhage (from postpartum
hyperglycemia causes fetal hyperglycemia, with atony)
resulting fetal osmotic diuresis into the amnionic fluid
compartment. Pregnancy Outcomes
• Guarded because of fetal malformations
3. Multifetal gestation • Increased perinatal morbidity and mortality because of
• Hydramnios is generally defined in multifetal gestations increased risk of preterm labor
as a single deepest amnionic fluid pocket measuring 8 • Increased CS rate
cm or more. • Adverse perinatal outcomes if fetal growth restriction
accompanies hydramnios
4. Congenital infections and red blood cell alloimmunization
• Uterine dysfunction and postpartum hemorrhage result
• Less frequent reasons from uterine atony consequent to overdistention
• CMV, toxoplasmosis, syphilis, and parvovirus • Abnormal fetal presentations and operative
intervention are also common
5. Idiopathic
• Increased association with:

o Abruption placenta: shearing effect (because
Differential Diagnosis
of sudden release of amniotic fluid)
1. Multiple pregnancy o Uterine cord prolapsed: due to sudden gush
2. Ovarian cyst of fluid
3. H. mole o Umbilical cord prolapsed – due to
4. Full bladder overdistension
o Post partum hemorrhage – due to over
Symptoms distention.
• Unless hydramnios is severe or develops rapidly,
maternal symptoms are infrequent. Management
• With chronic hydramnios, fluid accumulates gradually, Amnioreduction
and a woman may tolerate excessive abdominal • Large-volume amniocentesis
distention with relatively little discomfort. • Risks of membrane rupture, preterm labor, and
• Acute hydramnios, however, tends to develop earlier in placental abruption
pregnancy.
o May result in preterm labor before 28 weeks OLIGOHYDRAMNIOS
or in symptoms that become so debilitating as An abnormally decreased amount of amnionic fluid.
to necessitate intervention. Oligohydramnios complicates approximately 1 to 2 percent of
• Symptoms may arise from pressure exerted within the pregnancies.
overdistended uterus and upon adjacent organs.
Unlike hydramnios, which is often mild and confers a benign
• When distention is excessive, the mother may suffer prognosis in the absence of an underlying etiology,
dyspnea and orthopnea to such a degree that she may oligohydramnios is a cause for concern.
be able to breathe comfortably only when upright.
Anhydramnios= When no measurable pocket of amnionic fluid
• Edema may develop as a consequence of major venous is identified
system compression by the enlarged uterus, and it
AFI ≤ 5 cm or on a single deepest pocket of amnionic fluid ≤ 2
tends to be most pronounced in the lower extremities,
cm
vulva, and abdominal wall.

• Rarely, oliguria may result from ureteral obstruction
Etiology
by the enlarged uterus.

Clinical Findings Early-Onset Oligohydramnios
• Difficulty in palpating fetal small parts • When amnionic fluid volume is abnormally decreased
from the early second trimester, it may reflect a fetal
• Difficulty in hearing the fetal heart tone
abnormality that precludes normal urination, or it
• Very tense uterine wall (unable to palpate fetal parts)
may represent a placental abnormality severe
• Greater fundic height measurement
enough to impair perfusion.
• Leads to labor before 28 weeks AOG
• In either circumstance, the prognosis is poor.
• Bulbar Edema
• Second-trimester rupture of the fetal membranes may

result in oligohydramnios—and should be excluded.

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• More commonly, membrane rupture presents with fluid • Complex fetal genitourinary abnormalities such as
leakage, vaginal bleeding, or uterine contractions. persistent cloaca and sirenomelia similarly may result
• Targeted sonography should be offered to assess for in lack of amnionic fluid.
fetal abnormalities. • If there is bilateral renal agenesis, no urine is produced,
and the resulting anhydramnios leads to:
Oligohydramnios After Midpregnancy o Limb contractures
• When amnionic fluid volume becomes abnormally o A distinctively compressed face
decreased in the late second or in the third trimester, it o Death from pulmonary hypoplasia
more likely is associated with fetal-growth restriction, • When this combination of abnormalities results from
a placental abnormality, or a maternal complication renal agenesis, it is called Potter syndrome, after Dr.
such as preeclampsia or vascular disease. Edith Potter, who described it in 1946.
• In such cases, the underlying etiology is often presumed • When this constellation stems from another etiology of
to be uteroplacental insufficiency, which can impair decreased amnionic fluid volume, it is generally called
fetal growth and reduce fetal urine output. Potter sequence.
• Normally, AF decreases in the second trimester. This is
due to the decrease in urine output which eventually Medications
leads to decrease in AF • Oligohydramnios has been associated with exposure to
• Exposure to selected medications has also been drugs that block the renin-angiotensin system.
linked with oligohydramnios as discussed subsequently. • Angiotensin-converting enzyme (ACE) inhibitors
• Investigation of third-trimester oligohydramnios o When taken in the second or third trimester,
generally includes evaluation for membrane rupture ACE inhibitors and angiotensin-receptor
and sonography to assess growth. blockers may create fetal hypotension,
• Umbilical artery Doppler studies may be performed if renal hypoperfusion, and renal ischemia,
growth restriction is identified. with subsequent anuric renal failure.
• Oligohydramnios is commonly encountered in o These adverse outcomes appear to be more
postterm pregnancies. prevalent following exposure to angiotensin-
• Amnionic fluid volume decreased by approximately 8 receptor blockers, but both medication types
percent per week beyond 40 weeks. are contraindicated in pregnancy.
• In postterm pregnancies, oligohydramnios has been • Nonsteroidal antiinflammatory drugs (NSAIDs).
associated with nonreassuring fetal heart rate patterns o NSAIDs have been associated with fetal
and adverse pregnancy outcomes. ductus arteriosus constriction and with
decreased fetal urine production.
Congenital Anomalies o In neonates, their use may result in acute and
chronic renal insufficiency.
• By approximately 18 weeks, the fetal kidneys are the
Pain reliever safe for pregnant: PARACETAMOL
main contributor to amnionic fluid volume.

• Among those with fetal abnormalities, most cases of
severely decreased amnionic fluid volume beginning Pregnancy Outcomes
early in gestation are secondary to genitourinary 1. Fetal stillbirth
anomalies. 2. Growth restriction
• Anomalies of other organ systems, aneuploidy, and 3. Nonreassuring fetal heart rate pattern
other genetic syndromes also have the potential to 4. Meconium aspiration syndrome
cause oligohydramnios indirectly, either from fetal
decompensation, fetal-growth restriction, or an Management
accompanying placental abnormality. • Initially, an evaluation for fetal anomalies and growth is
• Selected renal abnormalities that lead to absent fetal essential.
urine production include: • Close fetal surveillance
o Bilateral renal agenesis o In a pregnancy complicated by
o Bilateral multicystic dysplastic kidney oligohydramnios and fetal-growth restriction
o Unilateral renal agenesis with contralateral • Preterm delivery
multicystic dysplastic kidney o In many cases, evidence for fetal or maternal
o Infantile form of autosomal recessive compromise will override potential
polycystic kidney disease. complications from preterm delivery.
• Urinary abnormalities may also result in • Expectant Management with increased fetal
oligohydramnios because of fetal bladder outlet surveillance
obstruction o Oligohydramnios detected before 36 weeks in
o Posterior urethral valves the presence of normal fetal anatomy and
o Urethral atresia or stenosis growth
o Megacystis microcolon intestinal • Amnioinfusion,
hypoperistalsis syndrome o may be used intrapartum in the setting of
variable fetal heart rate decelerations

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o It is not considered treatment for membranes membranes that persists
oligohydramnios per se, although the for more than 24 hours
decelerations are presumed secondary to and prior to onset of
umbilical cord compression resulting from labor
lack of amnionic fluid.
o Amnioinfusion is not the standard of care for Latent Period • Interval between the
other etiologies of oligohydramnios and is not prelabor ROM and the
generally recommended. time of delivery
o
RISK FACTORS
BORDERLINE OLIGOHYDRAMNIOS

The term borderline AFI or borderline oligohydramnios is
Lower socioeconomic status
somewhat controversial. • Refers to AFIs between 5 and 8 cm
• Smoking
• Pregnancies between 24 and 34 weeks with an AFI between 5
• History of STI- weaken tensile strength of membrane
and 8 cm were not more likely than those with an AFI above 8 cm
to be complicated by maternal hypertension, stillbirth, or • Previous preterm delivery • History of vaginal bleeding
neonatal death. • Uterine distensions (polyhydramnios, multifetal pregnancy)

• Higher rates of preterm delivery, cesarean delivery for a
nonreassuring fetal heart rate pattern, and fetal-growth DIAGNOSIS
restriction were found. Study results evaluating pregnancy • History of fluid from vagina followed by persistent leak
outcomes with borderline AFI have been mixed. • Speculum examination (aseptic)
• There is insufficient evidence to support fetal testing or o Evaluate for any cervical dilatation and effacement
delivery in this setting. o Pooling of fluid in the vagina
o Leakage of fluid in the cervix
PREMATURE RUPTURE OF MEMBRANES • Ferning of dried fluid /Arborization
o amnionic fluid crystallizes to form a fernlike pattern due to the
PROM Prelabor rupture of relative concentrations of sodium chloride, proteins, and
membranes (Textbook of carbohydrates in the fluid)
Obstetrics 3rd ed. • Nitrazine or litmus paper o normal vaginal pH is 4.5-5.5 o
AWPTOG) amniotic fluid is 7.0-7.5
• Premature rupture of o pH above 6.5 is consistent of ROM
membranes (Williams o positive: color change from yellow to dark blue
24th ed.) • rupture of • Pooling of fluid
membranes prior to • Ultrasound
onset of labor • Amniocentesis - invasive
• Fetal fibronectin
COMPLICATIONS
• Perinatal complications (prematurity and infection)
o intrauterine infection is likely if delivery is delayed for more
than 24 hours
• Early delivery
o Malpresentation
PPROM • Preterm prelabor o Cord compression
rupture of membranes o Oligohydramnios
(AWPTOG) o Umbilical cord prolapse
• Preterm premature • Infections:
rupture of membranes o ENDOMETRITIS
(Williams) o CHORIOAMNIONITIS
• rupture of membranes
• Indicators:
prior to 37 weeks AOG o Fever ≥ 380C, Leukocytosis, Fetal and Maternal

tachycardia, foul smelling vaginal discharge,
SROM • Spontaneous Rupture uterine tenderness/uterine contraction
of Membranes o Definitive: (+) culture of membrane • Cord
• Rupture of membranes Prolapse
after or with the onset of • Cord Prolapse
labor o With support, push fetal head

MANAGEMENT
• Hospitalization
• Confirm diagnosis
• Management is based on AOG
• Delivery is obviously urgent for patient with advanced active
Prolonged rupture of • Any rupture of labor and signs of infection

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• At or near term:
o Induction of labor- induce labor (START the contractions) PRE-LEC CASE QUIZ
-Different from Augmentation (strengthen contraction 1-2. What are the risk factors present in the patient that lead to
AFTER labor begins à IMPROVE) the development of the disease?
o If with chorioamnionitis or fetal distress, prompt efforts to 3. What is the chief complaint?
effect delivery, not expected within few hours of CS 4. What is the fetal heart tone?
• Corticosteroids (for pregnancies less than 32 weeks accdg to 5. Definitive treatment for the patient?
Williams) 6. Working diagnosis?
o Betamethasone (Celestone) 12mg q 24h IM x 2doses 7. Fundic Height?
- Remember B, 2nd sa alphabet and T - welve 8. AOG of the patient?
o Dexamethasone (Decadrone) 6mg q 12h IM x 4 doses - 9. What is considered normal AFI body?
Remember D, 4th sa alphabet and si-X (bisaya daw) 10. This condition where the placental villi invades the
• Metaanalysis studies show that by giving these drugs: myometrium
o 20% vs 35% - RDS BONUS: how many pack years?
o 7.5% vs 15.9% - IVH
o 0.8% vs 4.6% - Necrotizing fasciculitis ANSWER:
1-2. smoking and maternal age
NIH RECOMMENDATIONS 3. painful uterine bleeding
• Recommends steroids before 30-32 weeks • 32-34wks- 4. 99bpm (bradycardia)
controversial 5. CS
• After 34wks-not recommended unless there are indication of 6. G1P0 PU 37 weeks abruptio placenta
fetal lung immaturity by amniocentesis 7. 32 cm
• Antibiotic: (to reduce bacterial complications) 8. 37 weeks AOG
o Recommended for Post-Term Endometritis 9. 5-24cm
o 2g ampicillin and 250 erythromycin q6h x8d 10. Placenta Increta
• Tocolytic treatment combined with steroids and antibiotics are BONUS: 12 pack years
beneficial (no studies)
o Short term Tocolytic POST LEC QUIZ
o Allow initiation of antibiotic, steroids administration 1-2. Differentiate placenta previa from abruptio based on
(maternal transport controversial) localization of placenta and type of bleeding.
o Long term Tocolytics in PROM not recommended 3. This refers to the phenomenon where there is dynamic
• Confirm the diagnosis migration of placenta and insertion thru gestation.
o Speculum 4. What is the definitive tx for a G1P0 PU 35 weeks with profuse
o Ferning bleeding diagnosed placenta previa
o Nitrazine/Lithmus Paper 5. A fibrinoid degeneration that seprates your superficial to the
o Ultrasound deeper layer of your decidua basalis
o Dye installation
6. What is the dose and route of admin of dexamethasone
• Basic Laboratory
7. What is the dose and route of admin of betametasone
o CBC
o ESR 8. What do you call a rupture of membrane after or with onset of
o CRP labor
o Urinalysis 9. What is the AFI of borderline oligo
o Gramstain 10. What is the pathway for DIC in abortion
o Chorioamniocentesis BONUS: no amniotic fluid
• General management
o Monitor vital sign q4h ANSWER:
o Color and smell of AF 1-2. placenta previa – near the os. Painless bleeding
o Observe S/Sx o Non- Stress Test (NST)
abruptio placenta - normal location. Painful bleeding

PROM Individualized 3. Placenta trophotropism
<24 Weeks (Acute management 4. CS
PROM) 5. Nitabuch Layer
6. 6mg q12h IM x 4 doses
PROM (24-32 weeks) Antibiotic, Steroids, 7. 12mg q24h IM x 2 doses
tocolysis 48 hrs, deliver 8. SROM
if 34-36 weeks 9. 5-8cm

10. Intrinsic Pathway
PROM (>34 weeks) Antibiotics, Delivery
BONUS: anhydramnios

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