Placental Abruption: Symptoms, Causes, Types & Treatment
Guest Author
Guest Author: Dr. Vineshree Govender, MBChB, MMed, FCOG(SA), PhD
The lecture below was written and created by guest author Dr. Vineshree Govender who is an OB/GYN physician.
All medical illustrations were created and provided by EZmed.
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Placental Abruption: Definition
Placental abruption occurs when a normally situated placenta partly or completely separates from the wall of the uterus in a viable fetus (after 24 weeks gestation) and prior to the delivery of the fetus.
Placental abruption is most common in the third trimester, but can occur any time after 20 weeks gestation.
Placental abruption is also known as abruptio placentae.
Placental Abruption vs Placenta Previa
Placenta previa occurs when the placenta covers all or part of the cervix.
Even though the placenta is covering the cervix, the placenta is still attached to the uterus in placenta previa.
Alternatively, placental abruption occurs when the placenta partially or completely detaches from the uterus.
Placental Abruption: Causes and Risk Factors
The cause of placental abruption is often unknown, however there are risk factors that can play a role.
Risk factors for placental abruption include:
Short umbilical cord
External trauma
Sudden decompression of the uterus. For example, uncontrolled rupture of membranes with polyhydramnios - The sudden decrease in uterine size results in shearing of the placenta of the uterine wall.
Uterine abnormalities, for example, uterine septum
Uterine tumors, for example, fibroids
Preeclampsia – Spiral arterioles do not contain an internal elastic lamina. Therefore, sudden changes in blood pressure can lead to rupture of these vessels.
Intrauterine growth restriction (IUGR)
Smoking
Cocaine abuse – The associated release of catecholamines with cocaine use is thought to cause vasospasm of the arteries in the decidua.
Placental infarcts
Previous abruption – Recurrence varies from 6% to 17% after 1 previous placental abruption. Recurrence increases to 25% after 2 previous abruptions.
Advanced maternal age – 35 years or older
Low socio-economic status
Male fetus
Elevated second trimester alpha-fetoprotein (associated with an up to 10 fold increased risk of abruption)
Chorioamnionitis
Placental Abruption: Types and Grades
Placental abruption can be classified into different grades (grade 0-3) based on its severity.
**The grading scale can vary among countries and institutions.
Grade 0 (Asymptomatic)
Grade 0: Asymptomatic; This is a retrospective diagnosis
There are no signs or symptoms of a placental abruption present.
The fetus and placenta are delivered and only upon inspection of the placenta is the retroplacental clot found.
Grade 1 (Mild)
Grade 1: No signs of maternal or fetal distress.
Mild symptoms may be present including: Minimal to no vaginal bleeding; Slight uterine tenderness.
There are no signs of maternal distress, and the maternal blood pressure and heart rate are normal.
There are no signs of fetal distress.
Grade 2 (Moderate)
Grade 2: No signs of maternal shock, but fetal distress present.
Symptoms are more severe compared to a grade 1 and include: No vaginal bleeding to a moderate amount of vaginal bleeding; Significant uterine tenderness; Increased uterine activity.
There are no signs of maternal shock.
However, there may be slight changes to maternal vital signs such as increased heart rate (tachycardia).
Although the fetal heart beat is present, there are signs of fetal distress as well.
Cardiotocograph (CTG) changes may include possible decelerations and a sinusoidal pattern.
Grade 3 (Severe)
Grade 3: Maternal shock and fetal death present
SUBTYPE A: No coagulopathy present
There are obvious signs and symptoms of placental abruption present.
For example, vaginal bleeding is typically present which may be dark in color.
The amount of blood loss varies, but may be heavy.
Usually there is a sudden onset of pain in the lower abdomen and back.
The uterus is often “woody hard” and tender.
No fetal heart is heard, and the fetal parts may be difficult to palpate.
Maternal shock is present.
SUBTYPE B: Coagulopathy present
Clinically, the presentation may be identical to subtype A but there is a coagulopathy present.
Types
There are several different types of placental abruption based on:
Degree of separation
Presence or absence of vaginal bleeding
Site of bleeding
1. Degree of separation:
Partial Placental Abruption - Placenta does not completely detach from the uterine wall
Complete or Total Placental Abruption - Placenta completely detaches from the uterine wall
2. Presence or absence of vaginal bleeding:
Revealed Placental Abruption - Vaginal bleeding visible
Concealed Placental Abruption - Little to no visible vaginal bleeding
3. Site of bleeding:
Subchorionic Abruption - Bleeding between myometrium and placental membranes
Retroplacental Abruption - Bleeding between myometrium and placenta
Preplacental Abruption - Bleeding between placenta and amniotic fluid
Intraplacental Abruption - Bleeding within or inside the placenta
Pathophysiology of Placental Abruption
The process of placental abruption begins with uterine vasospasm followed by relaxation, and subsequent venous engorgement and arterial rupture (decidual arteries).
A hematoma forms which may initially be concealed but with expansion of the hematoma, progressive placental separation occurs.
When there has been intravasation of blood into the myometrium, the uterus becomes purplish in color - The so called Couvelaire uterus.
The infiltration of blood between muscle fibers causes a tonic contraction which makes the uterus “woody hard” and tender.
The increase in intra-uterine pressure compromises the placental circulation, adding to the fetal hypoxia which has already started due to the placental separation.
Coagulopathy in Placental Abruption
Severe coagulopathy can occur with fetal demise.
The decidua is rich in thromboplastin.
As the decidua degenerates, it releases thromboplastin into the maternal circulation leading to disseminated intravascular coagulation (DIC).
This in turn results in:
The systemic consumption of coagulation factors and the presence of abnormal blood clotting. This cascading effect interferes with the clotting mechanism.
The presence of small clots in the micro-circulation plugs small blood vessels. This in turn results in the ensuing ischemia of organs.
Placental Abruption: Symptoms
History
The patient may present with a history of vaginal bleeding, abdominal pain, back pain, and decreased fetal movements.
A review of the patient’s antenatal history is required i.e. a history of hypertension in pregnancy, previous placental abruption, presence of placenta previa, smoking, cocaine use, or trauma.
The classic triad of placental abruption is the following:
Vaginal bleeding
Uterine tenderness/contractions
Decreased fetal movements
Vaginal bleeding occurs in 80% of patients.
Bleeding may compromise fetal and maternal health in a short period of time.
Uterine activity is a sensitive marker of placental abruption, and in the absence of vaginal bleeding, should suggest the possibility of an abruption especially if there is a history of trauma.
The presenting complaint may be decreased fetal movements, which may indicate fetal compromise or even fetal death.
Clinical Presentation
The clinical presentation may vary.
A high index of suspicion may be required to make a diagnosis.
If the separation is early and near the placental margin, vaginal bleeding occurs early, the pain is minimal, and the tenderness mild.
This may be mistaken for a heavy bloody show, and the diagnosis is less obvious.
With severe abruptions signs include heavy vaginal bleeding, abdominal pain, back pain, anemia, hypovolemia, a tender “woody hard” uterus, decreased fetal movements and difficulty palpating fetal parts.
With a posteriorly situated placenta, back pain initially dominates.
If the patient presents with hypovolemic shock, there may be hypotension, tachycardia and decreased urine output.
The patient may progress from alert to an obtunded state.
Fetal monitoring may reveal a prolonged fetal bradycardia, repetitive late decelerations on CTG, decreased variability on CTG, or even a sinusoidal pattern.
The uterine fundal height may increase with a rapidly developing concealed hematoma.
Placental Abruption: Diagnosis
Laboratory Studies
Complete blood count (CBC) - May reveal anemia and thrombocytopenia
Fibrinogen - Pregnancy is associated with hyperfibrinogenemia. Even a mildly decreased fibrinogen level may represent significant coagulopathy. Aim to keep the fibrinogen level above 100mg/dl.
Prothrombin time/Partial thromboplastin time (PT/PTT) - Imperative to know if this is abnormal as a cesarean section may be required.
Urea and Creatinine - Hypovolemia and organ ischemia may lead to renal dysfunction. Fluid resuscitation may be required.
Kleihauer-Betke (KB) Test - Detects fetal red blood cells in the maternal circulation. Rhesus (Rh factor) iso-immunization will occur in women who are rhesus negative (Rh-negative mother).
Blood Type - The patient must be typed and screened as a blood transfusion may be required.
Ultrasound
Ultrasound may be used to diagnose placental abruption.
Ultrasound is important to exclude other causes of ante-partum hemorrhage, e.g. placenta previa.
Ultrasound may reveal a retroplacental hematoma.
The hematoma is seen on ultrasound as a hypoechogenic area between the placenta and myometrium.
The fetal heart can also be seen as present or not.
Cardiotocograph (CTG)
CTG is a recording of fetal heart rate and uterine contractions.
CTG with placental abruption may show:
Late decelerations
Decreased beat-beat variability
Fetal bradycardia
Sinusoidal pattern
An increased uterine resting tone and increasing frequency of contractions that may progress to hyperstimulation may be noted.
Placental Abruption: Treatment
Management of placental abruption includes the following:
Resuscitation is essential.
Monitor blood pressure (BP), heart rate (HR), oxygen saturation every 30 minutes. In the shocked patient this must be done every 15 minutes.
The patient should be monitored in a high risk ward or ICU if needed.
Insert 2 large bore peripheral IV lines. A central venous pressure (CVP) is required for the shocked patient.
Correct hypovolemia using crystalloid/colloids.
Type and cross-match blood.
Correct anemia with packed red blood cells (PRBCs).
Correct coagulopathy if present – May require FDPs , platelets, whole blood, etc.
Insert a foley catheter and monitor for renal output and possible failure.
Administer Rhesus immunoglobulin if the patient is rhesus negative (Rh-negative).
Provide appropriate analgesia.
Input from an ICU specialist may be required in very severe cases.
**Resuscitation is ongoing
Delivery of the Fetus
A vaginal delivery is preferable for a fetus that has demised secondary to placental abruption.
The ability of the patient to undergo vaginal delivery is dependent on the patient’s hemodynamic stability and if there is a contra-indication to vaginal birth e.g. previous cesarean section, a major malpresentation or an extremely unfavorable cervix.
Cesarean delivery may be required to save both mother and child.
Whilst cesarean delivery may allow rapid access to the uterus and its vasculature, it may be complicated by an underlying coagulopathy which would then need to be corrected/stabilized prior to delivery.
The type of uterine incision is dependent on the gestational age of the fetus.
A classical cesarean section (C-section) may be required if the fetus is less than 28 weeks gestation.
A cesarean hysterectomy may be required for uncontrolled hemorrhage - This may be lifesaving.
Placental Abruption and Postpartum Hemorrhage
The patient must be closely monitored post-delivery as postpartum hemorrhage may result from uterine atony following intravasation of blood into the myometrium or from an uncorrected coagulopathy.
Summary
In conclusion, a placental abruption is a major cause of maternal-fetal morbidity and mortality and is an obstetric emergency.
Intense monitoring is required in the mother and ongoing resuscitation.
Summary:
Placental abruption is an important cause of antepartum hemorrhage and is an obstetric emergency
It results in morbidity and mortality in mother and child
Smoking and cocaine use are modifiable risk factors
A high index of suspicion is sometimes required to make a diagnosis. The classic clinical triad for diagnosis is vaginal bleeding, a tender uterus, and decreased fetal movements. The patient does not always present with this triad.
Appropriate investigations are essential. This may include: ultrasound and blood investigations. Be aware of CTG changes associated with abruption.
Resuscitation is required and must be ongoing. Patients may require admission to ICU.
Vaginal delivery is the preferable route of delivery when the fetus has demised unless there is an obstetric contraindication to vaginal birth.
Cesarean section (C-section) is the preferable route of delivery in placental abruption with a live fetus, unless the patient is fully dilated with a low fetal presenting part.
Notable, serious complications include coagulopathy and renal failure.
Patients may require ICU admission.
Postpartum hemorrhage may also occur. The doctor in charge of the patient must be prepared for this and know how to perform cesarean-hysterectomy if required.
Multi-disciplinary intervention is sometimes required.
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