Third Trimester Bleeds in Pregnancy

Presented By

Arpana Tewari

• Bleed occurring after 20th week of gestation is mid 2nd trimester to third trimester bleeds. However after 27th week is definitely third trimester bleeds.

• Requires medical evaluation in 5–10% of pregnancies.

• One of the 3 leading causes of maternal death and also a major cause of perinatal morbidity and mortality in the United States

Bleeding from the vagina after the 28th week of pregnancy is a true emergency.

The bleeding can range from very mild to extremely brisk and may or may not be accompanied by abdominal pain.

Hemorrhage (another word for bleeding) is the most common cause of maternal death in the United States. It complicates about 4% of all pregnancies.

Placenta Previa- 20% of third-trimester bleeding and happens in about 1 in 200 pregnancies.

About 70% of women have painless bright red blood from the vagina. Another 20% have some cramping with the bleeding, and 10% have no symptoms.

Uterine rupture :- Uterine rupture is an abnormal splitting open of the uterus causing the baby to be partially or completely expelled into the abdomen.

Symptoms are highly variable.

Classic uterine rupture is described as intense abdominal pain, heavy vaginal bleeding, and a "pulling back" from the birth canal of the baby's head.

Placental abruption - (10% recurrence risk)

occurs 1 in 200 pregnancies

About 80% of women have dark blood or clots from the vagina, but 20% have no external bleeding. More than one-third have a tender uterus. About two-thirds of women with placental abruption have the classic "pain and bleeding."

Vasa Previa. Occurs 1 in 5,000 pregnancies.

Fetal vessel rupture occurs in pregnancy.

Baby’s vessels may attach to the membranes instead of the placenta.

• Pregnant Woman

• Progressive increase in blood volume starting at 6-8 weeks gestation

• Reaches maximum at 32-34 weeks gestation

• Increase in plasma volume of 40-50%

• Increase in red blood cell mass of 20-30%

• Example• Pregnant woman who was 60kg (132lbs)

non-pregnant will have • 4.68-5.12L of whole blood of which• 3.08-3.3L will be plasma and • 1.68-1.82 will be erythrocytes

Obstetric Hemorrhage:- Late pregnancy

•Placenta previa

•Placental abruption

•Uterine rupture

•Vasa Previa

Abrputio Placenta

• Epidemiology – Most common cause of maternal death due to bleeding

– Incidence placental abruption

» All placental abruptions: 1-2%

» Severe placental abruption (Grade 3): 0.2%

– Risk of recurrence in future pregnancy

» One prior placental abruption: 5-16%

» Two or more prior placental abruptions: 25%

Placental Abruption ( Abruptio Placenta)

• Premature separation of the normally implanted placenta.

• Can be :- partial or complete• Bleeding may be revealed( vaginal bleed) or

occult • Can occur form mid trimester onwards• Incidence - 0.45- 1.3 % of deliveries

• In the majority of pregnancies with abruptio placentae, the pathogenesis is more likely to involve a chronic pathologic vascular process at the fetal-placental interface with abruption as the culmination of a long chain of events

• Grade 1: (Herald bleed) » Less than 100cc of uterine bleeding

» Uterus non-tender

» No Fetal Distress

– Grade 2 :- Uterus tender

» Fetal Distress

» Concealed hemorrhage

» Progresses to Grade 3 without delivery

– Grade 3 :- Fetal death

» Maternal shock

» Extensive concealed hemorrhage

» Coagulopathy

» Absent: 3A (66% of patients)

» Present: 3B (33% of patients)

• Ultrasound immediately – Placental abruption is a clinical diagnosis

» Do not delay definitive management for ultrasound

» Ultrasound should however be performed in all cases

– Ultrasound

» Inconsistent findings

» Sonolucent area between placenta and Uterus

» Rounding of placental edge

» Placenta appears thick (variably present)

• Associated factors:

• Maternal hypertensive disorders (present in 50% of women with placental abruption)

• Advanced maternal age

• Advanced maternal parity

• Abdominal trauma

• Cocaine use

• Maternal smoking

• Chorioamnionitis

• Sudden uterine decompression

• (rupture of membranes in polyhdramnios or between deliveries of multiple gestations)

• External cephalic version

• Placental abruption in a previous pregnancy (10% recurrence rate)

• Trauma may cause external compression-decompression induced stress at the placental-decidual interface.

• The presence of increased uterine activity, particularly tachysystole, after serious abdominal trauma warrants prolonged electronic fetal monitoring (up to 24 hours) and assessment for maternal coagulopathy

• A brief four to six hour monitoring period is sufficient in the presence of uterine quiescence, a reassuring fetal heart rate pattern, and absence of vaginal bleeding or uterine tenderness.

• Maternal hypertension — Severe, but not mild, abruption is strongly associated with chronic maternal hypertension, preeclampsia superimposed on chronic hypertension, and severe preeclampsia

• Hypertensive women had a five-fold increased risk of severe abruption compared to normotensive women. Unfortunately, antihypertensive therapy does not appear to reduce the risk of abruption among women with chronic hypertension

• Cigarette smoking — Smoking is associated with a 2.5 fold increased risk of abruption severe enough to result in fetal death; the risk increases by 40 percent for each pack per day smoked

• A possible mechanism is that ischemic peripheral necrosis of the decidua is observed in smokers and predisposes to vascular disruption

• The effects of cigarette smoking and hypertension are synergistic

• Maternal age and parity — Increasing parity is a risk factor for abruption

• The explanation for the association between increasing parity and abruption is unknown, but may be related to endometrial scarring, impaired decidualization, and aberrant uterine vasculature.

• Cocaine abuse — As many as 10 percent of women using cocaine in the third trimester will suffer an abruption

• The pathophysiologic effect of cocaine in the genesis of abruption is unknown, but may be related to cocaine-induced acute vasoconstriction leading to ischemia, reflex vasodilation, and disruption of vascular integrity

• Preterm premature rupture of the fetal membranes — Placental abruption occurs in 2 to 5 percent of pregnancies complicated by preterm premature rupture of membranes (PPROM)

• The risk is increased seven to nine-fold in those in which there is intrauterine infection or oligohyhydramnios associated with PPROM

• Abruption-induced decidual thrombin generation may promote increased protease production leading to both membrane compromise and vascular destabilization .

• Inherited thrombophilia — Inherited thrombophilias are associated with an increased risk of maternal venous thromboembolism, fetal death, fetal growth restriction, severe preeclampsia, and abruption

• The most common disorders are heterozygosity for the factor V Leiden .

• We screen women with recurrent abruptions for thrombophilic disorders. For those diagnosed with a thrombophilia, we recommend low molecular weight heparin prophylaxis or supplemental folate

• Previous abruption — A history of previous abruptio placentae increases the risk of recurrence in a subsequent pregnancy ten-fold, to 4 to 5 percent

• Multifetal gestation and polyhydramnios — Multifetal pregnancy is associated with a higher frequency of abruption

• This risk has been attributed to sudden rapid uterine decompression upon delivery of one twin. A similar mechanism has been implicated in abruption associated with rapid loss of amniotic fluid from membrane rupture or amnioreduction in pregnancies complicated by polyhydramnios.

• Signs

• Hallmark sign is painful vaginal bleeding .

• Colicky abdominal/back pain

• Non-reassuring fetal heart rate tracing

• Intrauterine fetal death

• Uterine tenderness/uterine irritability

• Contractions

• Uterine enlargement

• Couvelaire uterus –

• in a major abruption blood extravasates into myometrium causing uterus to become “woody hard” and fetal parts will no longer be palpable”

• DIC

• Maternal shock

• Possible mechanisms include:

• The placental margins remain adherent, despite an effusion of blood behind the center of the placenta. The resultant hematoma obliterates the intervillous space, leading to ischemia and destruction of the overlying placental tissue.

• The fetal membranes retain their attachment to the uterine wall during a marginal placental separation. This blood may then erode through the membranes to invade the amniotic cavity, leading to "port wine" discoloration of the amniotic fluid.

• The fetal head obstructs egress of blood through the cervical os.

• Blood may also extravasate into the myometrium to the serosal surface (called a Couvelaire uterus). This is typically diagnosed at cesarean delivery.

• Disseminated intravascular coagulation (DIC) occurs in 10 to 20 percent of cases of severe abruption with death of the fetus

• Rarely observed with a live baby

• DIC likely results from an infusion of tissue factor and/or other thromboplastic material from the disrupted decidua and damaged placental bed into the maternal circulation

• It may also be related to massive hemorrhage-induced dilution of coagulation factors.

DIAGNOSIS

• Sonography :- The echogenic appearance depended upon the timing of ultrasound examination relative to the onset of symptoms: acute hemorrhage was hyperechoic to isoechoic compared with the placenta, while resolving hematomas became hypoechoic within one week and sonolucent within two weeks.

• Laboratory :-The Kleihauer-Betke test for fetal hemoglobin and an elevated CA-125 have been suggested as markers of abruption, (Kleihauer-Betke sensitivity 17 percent)

• Coagulopathy, particularly hypofibrinogenemia, is suggestive of abruption. A plasma fibrinogen level below 200 mg/dL and thrombocytopenia (less than 100,000/microL) is highly suggestive of severe abruption.

• Labs: Initial – Complete Blood Count with platelets

– Blood type

– Kleihauer-Betke

– Urinalysis for Urine Protein

– Serum Creatinine

– Fibrinogen <150 mg/dl suggests coagulopathy

– Also consider

» Factor V Leiden

» Prothrombin gene mutation

» Urine drug screen

– Thrombomodulin

» New marker for placental abruption

– Coagulation studies

» ProTime (PT)

» Partial Thromboplastin Time (PTT)

» Fibrin split products (Fibrin Degradation Products)

» Fibrinogen as above

» Clot Test (4-8 minutes is normal clotting time)

» Coagulopathy if tube does not clot in 8 minutes

– Blood Type and Cross for 4 units

– Kleihauer-Betke Test (if Maternal blood Rh Negative)

» Indicated if positive sheep rosette test

» Not used to diagnose placental abruption

» Determines RhoGAM dose

– Thrombomodulin

» New marker for placental abruption

– Coagulation studies

» ProTime (PT)

» Partial Thromboplastin Time (PTT)

» Fibrin split products (Fibrin Degradation Products)

» Fibrinogen as above

» Clot Test (4-8 minutes is normal clotting time)

» Coagulopathy if tube does not clot in 8 minutes

– Blood Type and Cross for 4 units

– Kleihauer-Betke Test (if Maternal blood Rh Negative)

» Indicated if positive sheep rosette test

» Not used to diagnose placental abruption

» Determines RhoGAM dose

• Management

• Delivery (with preparations for massive postpartum hemorrhage)

• If mother symptomatic /deteriorating, urgent delivery regardless of fetal maturity

• If fetus very immature and maternal and fetal vital signs are stable, tocolytics for uterine quiescence may be considered.

• If fetus alive and viable urgent delivery by cesarean section unless vaginal delivery imminent (vaginal delivery preferred unless contraindications)

• Resuscitation/correction of hypovolemia

• Correction of coagulopathy

• Monitor maternal hemodynamic status

• Hct, platelet count, fibrinogen conc., PT, APTT, Type and Rh.

• Continuous fetal monitoring

• Transfusions if ongoing hemorrhage or anemia. The hematocrit should be kept above 30 percent and hourly urine output should be maintained above 30 mL/hour

• If the PT and PTT exceed 1.5 times the control value, the patient should be transfused with two units of fresh frozen plasma.

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• Tocolysis is generally contraindicated in the setting of a severe abruption with coagulopathy or evidence of fetal compromise. It may be of value in mild cases with active preterm labor prior to 33 weeks of gestation to delay delivery long enough to administer corticosteroids when there is no evidence of fetal compromise or maternal coagulopathy.

• Delivery is the optimal treatment in such patients as DIC and hemorrhage will resolve over approximately 12 hours when the placenta is removed and the uterus involutes.

• Labor —Meticulous attention to the fetal heart rate, serial coagulation evaluation, and aggressive maternal hemodynamic surveillance are the major components of labor management in these pregnancies

• Amniotomy - careful monitoring of the fetal heart rate pattern.

• Intrauterine pressure catheter - resting tonus higher than 25 mmHg may be associated with abnormal uterine blood flow and decreased oxygenation of the fetus

• Delivery — Cesarean birth is appropriate in the presence of a nonreassuring fetal heart rate pattern and severe hypertonus, life-threatening hemorrhage, or DIC

• Recommended carrying out expeditious cesarean birth after rapid maternal hemodynamic and clotting factor stabilization

• Vaginal delivery may be attempted if there is significant cervical dilation in a parous woman,

• Maternal complications » Prolonged hypovolemic shock

» Renal Cortical necrosis

» Coagulopathy

» Consumptive Coagulopathy

» Disseminated Intravascular Coagulation

» Amniotic Fluid Embolism

» Maternal Death

» Uteroplacental apoplexy (Couvelaire uterus)

» Bleeding into myometrium results in hypotonic wall

» Risk of Postpartum Hemorrhage

– Fetal complications

» Intrauterine Growth Retardation

» Preterm Labor

» Intrauterine Fetal Demise

• Placental separation occurring in the second trimester, especially when accompanied by oligohydramnios, has a very poor prognosis

Placenta Previa

• Epidemiology – Incidence

» Second trimester (16-20 weeks): 5%

» Term: 0.5% (90% of low placentas resolve by term)

• Types – Type 1: Low Implantation

» Lower placenta margin dips into lower uterine segment

– Type 2: Marginal Placenta

» Placenta reaches internal os, but does not cover it

– Type 3: Partial Previa

» Placenta covers internal os when closed

» Placenta does not cover os when fully dilated

– Type 4: Complete Previa (Central Previa)

» Placenta covers internal os even when fully dilated

• Malposition of the placenta in the lower uterine segment

• Complete – body of placenta overlaps the entirety of the cervical os, Partial – placental edge covers (totally or partially), Marginal – Edge of placenta near, but not over the cervical os.

• Additional independent risk factors include maternal smoking, residence at higher altitudes, male fetus, and multiple gestation

• These associations suggest that the need for increased placental surface area to compensate for a reduction in uteroplacental oxygen or nutrient delivery promotes previa formation.

• Development of the lower uterine segment relocates the stationary lower edge of the placenta away from the os.

• Progressive unidirectional growth of trophoblastic tissue toward the fundus within the relatively stationary uterus (trophotropism) results in upward migration of the placenta.

• Associated Conditions – Abnormal presentation (placenta raises presenting part)

» Oblique Lie

» Transverse Lie

– Placental Abruption

– Intrauterine Growth Retardation

– Placenta accreta (especially if prior ceserean section)

– Postpartum Hemorrhage

• Associated Factors

• Multiparity

• Maternal age >35

• Previous placenta previa

• Previous uterine surgery (including c/s)

• Multiple gestation

• Smoking

• Signs

• Hallmark sign is painless vaginal bleeding with sudden onset

• Bleeding usually occurs in third trimester (but can start second trimester)

• Malpresentation

• The initial bleeding episode typically occurs at about 34 weeks of gestation, necessitating emergency or scheduled delivery at a mean gestational age of 36 weeks

• Approximately one-third of affected pregnancies develop bleeding prior to 30 weeks of gestation.

• Malpresentation and preterm premature rupture of the membrane (PPROM) are clearly associated with placenta previa

• Placenta previa is characterized by placental separation and hemorrhage due to an abnormally located placenta, rather than a normally located one. It is typically associated with less pain and different risk factors than placental abruption

• DIAGNOSIS —

• Ultrasound examination

• Placenta previa should be suspected in any woman beyond 24 weeks of gestation who presents with painless vaginal bleeding

• Absence of abdominal pain and uterine contractions, distinguishing feature between placenta previa and abruptio placentae

• Exclusion of placenta accreta

• Magnetic resonance imaging (MRI) has been used to provide a more precise method of placental localization.

• Serial Obstetric Ultrasound – General evaluation

» Interval Fetal Growth

» Evaluate for resolution or partial previa

» Evaluate for placenta acreta if prior ceserean

– Visualization aids

» Anterior placenta previa

» View placental edge with full, then empty bladder

» Posterior placenta previa

» Transducer lateral and angled toward midline

» Consider slight trendelenberg position

» Consider gentle Transvaginal Ultrasound

» Insert probe only partially into vagina

• Management- Ultrasound to try to determine placental placement. Avoid digital exams, Expectant management if no symptoms/no active bleeding

• If active bleeding, management determined by gestational age, severity of bleeding, fetal status. If active bleeding and mother, baby symptomatic for blood loss delivery indicated via c/s.

• Active Mgmt of symptomatic placenta previa. :- Monitoring mother’s hemodynamic status.

• Fetal heart monitoring.• Apt test or Kleihauer-Betke analysis

• Tocolysis is not administered to actively bleeding patients.

• Delivery is indicated if: life threatening refractory maternal hemorrhage, any bleeding after 34 weeks in the presence of known fetal pulmonary maturity, nonreassuring fetal heart rate tracing unresponsive to maternal oxygen therapy

» No sexual intercourse

» Avoid digital cervical exam

» Gentle speculum exam is permitted (insert 90 degrees) and pelvic rest.

– Cesarean section at tertiary care center recommended

» Delay delivery until mature lung studies if possible

» Tocolysis with Magnesium Sulfate

» Regional (spinal) anesthesia preferred over general

» General anesthesia may increase bleeding risk

» Marginal previa may allow vaginal delivery

» Double set-up is mandatory for vaginal exam

» NSVD indications

» Head engaged: Can tamponade marginal previa and

» No brisk bleeding on exam and

» Close monitoring and In-house OR team for stat Ceserean

• Conservative management of stable preterm patients

• Placenta previa between 24 and 37 weeks of gestation :- Bed rest

• Type and cross

• Corticosteroid single course

• Rh D Ig if negative

• Tocolysis

• Fetal heart monitoring

• Ultrasongraphic evaluation

• Antepartum hemorrhage is a major risk factor for preterm premature rupture of membranes (PPROM).

• An abdominal delivery is always indicated when there is sonographic evidence of a complete placenta previa

• If demonstrated a low-lying placenta or descent of the fetal head beyond an intact placental edge, vaginal delivery may be considered

• Women who have never bled are followed as outpatients

• Outpatient management :- If bleeding has stopped for more than one week , no other pregnancy complications such as IUGR, Patient lives near the hospital , is reliable and understands the risks involved.

• A prospective randomized clinical trial suggested outpatient management of women with placenta previa was safe, after the initial bleeding episode had subsided.

• The presence of a placenta previa does not preclude second trimester pregnancy termination

• Velamentous umbilical cord

• The association of velamentous cord insertions with placenta previa and multiple gestation has led to the theory that relative trophoblastic growth toward the well-vascularized uterine fundus (trophotropism) is responsible for this condition

• The ultrasound evaluation of a woman with a possible placenta previa should also include identification of the umbilical cord's insertion site at the chorionic surface of the placenta

Vasa previa

• Epidemiology – Very rare cause of Late Pregnancy Bleeding

– Incidence: 1 in 2500 pregnancies

• Presentation – Bleeding onset at Rupture of Membranes

• Risk Factors – Low-lying placenta in second trimester

– Velamentous insertion

– Bilobed or succenturiate lobe of placenta

– Multiple pregnancy (e.g. Twin Gestation)

– IVF pregnancy

• Symptoms and signs – Vaginal Bleeding immediately after membrane rupture

– Fetal Distress

– Vessel may be palpable on cervical ex

• Labs – Modified Apt Test

– Wright's stain

• Radiology – Transvaginal Ultrasound with color flow doppler

» Differentiate from umbilical cord

• Management – Requires immediate delivery if bleeding

• A vasa previa can be distinguished from a funic presentation antenatally by changing the mother's position (eg, Trendelenburg): the umbilical cord will move while a vasa previa is fixed.

• Antenatal examination with TVU and color Doppler of women at risk, those with low-lying placentas; bilobed, multi-lobed and succenturiate-lobed placentas; multiple pregnancies; and pregnancies resulting from in vitro fertilization, may be useful for antenatal diagnosis of vulnerable vessels proximate to the cervical os.

Optimal management of antenatally diagnosed vasa

previa.• Hospitalization

• Antepartum fetal surveillance - to detect compression of vessels. Sinusoidal pattern

• of fetal heart rate.

• Antenatal corticosteroids.

• Elective cesarean delivery at 35 to 36 weeks of gestation.

• Overall perinatal mortality - 36%

Uterine rupture

• Catastrophic tearing open of the uterus into the abdominal cavity.

• Prolonged, late, or variable decelerations and bradycardia seen on fetal heart rate monitoring are the most common and often the only manifestation of uterine rupture.

• No reliable predictors or unequivocal clinical manifestations of rupture

• Maintain a high index of suspicion.

• The rate of true uterine rupture with one prior low-transverse scar has been reported by ACOG to be between 0.2 and 1.5 percent

• Two or more prior cesareans, the rate of rupture rises as high as 3.9 percent.

• History of a successful prior vaginal delivery was found to reduce the risk of rupture from 1.1 to 0.2 percent (one of 511 women).

• Rupture of an unscarred uterus occurs in one of 8,000 to 17,000 deliveries

Conditions Associated with Uterine Rupture

• Uterine scars – Prior cesarean section – Prior rupture – Trauma – Injury from instrumentation during an abortion – Significant myomectomy – Any cause of uterine perforation

• Uterine anomalies (i.e., undeveloped uterine horn)

• Prior invasive molar pregnancy

• History of placenta percreta or increta

• Difficult forceps delivery

• Malpresentation

• Fetal anomaly

• Obstructed labor

• Induction of labor (suspected association)

• Excessive uterine stimulation – Prostaglandin E1 (misoprostol [Cytotec])

– Prostaglandin E2 (dinoprostone [Cervidil])

– Oxytocin (Pitocin), especially high infusion rates – Alkaloidal/crack-cocaine abuse

Presenting Manifestations of Uterine Rupture

• Bradycardia as sole manifestation 5 of 5 ruptures (100)

• Bradycardia, fetal distress 9 of 11 ruptures (82)

• Abnormal fetal heart rate tracing 23 of 70 ruptures (33)

• Failure to progress 15 of 70 ruptures (21)3 Pain 13 of 99 ruptures (13)

• Vaginal bleeding 11 of 99 ruptures (11)

• Unhelpful signs (not reliable and often absent): sudden tearing uterine pain, vaginal hemorrhage, cessation of uterine contractions, and regression of the fetus.

• Timely management depends on prompt detection.

• Fetal heart rate monitoring.

• If a prolonged deceleration to 90 beats per minute or less lasting more than one minute occurs during a trial of labor, you should perform an immediate cesarean operation

• Do not waste time performing an ultrasound examination

Management

• Urgent delivery

• Cesarean delivery.

• Although many infants delivered after uterine rupture do well, management often includes admission to a neonatal intensive care unit and, possibly, mechanical respiratory support.

Thank You