obstetric and gynecology

1. Antepartum bleeding
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INCIDENCE
Occurs in 2 to 5% of pregnancies
WORKUP
_ History and physical
_ Vitals signs
_ Labs: CBC, coagulation profile, type and cross, urine analysis
DIFFERENTIAL
A. Obstetric Causes
1. Placental abruption
2. Placenta previa
3. Vasa previa/velamentous insertion
4. Uterine rupture
5. Extrusion of cervical mucus (“bloody show”)
B. Nonobstetric Causes
1. Cervicitis
2. Polyp
3. Neoplasm
I. Placental Abruption (Abruptio Placentae)
Premature separation of normally implanted of placenta from uterine wall before the
delivery of baby, usually after 20 weeks, initiated by bleeding into decidua basalis.
INCIDENCE
0.5 to 4%
MORTALITY
 Maternal: 1 to 5%
 Fetal: 50 to 80%

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RISK FACTORS
 Trauma (such as a car accident),
 Preeclampsia,
 Smoking, cocaine abuse,
 high parity,
 Previous history of abruption.
CLINICAL MANIFESTATION
1. Painful vaginal bleeding common presenting sign 78–84% (maternal and fetal blood
present)
2. Darker blood.
3. Constant and severe back pain.
4. Increased uterine tenderness.
5. Evidence of fetal distress.
6. Maternal shock.
7. Severe sharp abdominal pain.
8. Uterine hypertonic.
DIAGNOSIS
1. Ultrasound will show retroplacental hematoma only part of the time.
2. Clinical and pathological findings
MANAGEMENT
1. Correct shock (packed RBCs, fresh frozen plasma, platelets).
2. Insert two large-bore i.v. cannulae and infusion of normal saline.
3. Send 20ml blood for cross-match of 4 units, haemoglobin and coagulation studies.
4. Perform an immediate Caesarean section if necessary to save the baby’s life (high
risk of postpartum haemorrhage).
5. Ensure adequate fluid replacement following the Caesarean section.
6. Leave an indwelling urinary catheter in to monitor urinary output.

3. 7. If the fetus is dead, then the woman should be allowed to deliver vaginally. This
usually happens rapidly (within 4–6 hours) as the abruption stimulates labour. If not
in labour, rupture of membranes usually leads to a swift delivery.
8. The relevant points of the management of labour are:
 Epidural analgesia is contraindicated because of the risk of coagulopathy, but
a patient-controlled opiate infusion can be used.
 If a coagulopathy has developed (prolonged APTT, PTT, increased fibrin
degradation products, low platelets) or the woman starts to bleed, she should
be managed in the following manner in conjunction with a consultant
haematologist:
a. Give 4 units of fresh frozen plasma.
b. Ask the blood bank to get 6 units of platelets ready.
 The consumptive coagulopathy begins to improve immediately after the uterus has been
evacuated of its contents. Marked abnormalities of the coagulation tests usually resolve
within 4–6 hours of delivery of the placenta.
II. Placenta Previa
A placenta previa is a placenta implanted on the lower uterine segment that prevents descent
of the fetus.
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Types of placenta previa:
1. Complete placenta previa: The placenta covers the entire internal cervical os.
2. Partial placenta previa (incomplete): The placenta partially covers the
internal cervical os.
3. Marginal placenta previa: One edge of the placenta extends to the edge of
the internal cervical os.
INCIDENCE
0.5 to 1%

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ETIOLOGY
Unknown, but associated with:
1. Increased parity
2. Older mothers
3. Previous abortions
4. Previous history of placenta previa
5. Fetal anomalies
CLINICAL MANIFESTATION:
1. Painless, profuse bleeding in T3
2. Postcoital bleeding
3. Spotting during T1 and T2
4. Cramping (10% of cases)
DIAGNOSIS
1. Transabdominal ultrasound (95% accurate)
MANAGEMENT
Cesarean section is always the delivery method of choice for placenta previa. The
specific management is geared toward different situations.
For Preterm
 If there is no pressing need for delivery, monitor in hospital or send home after
bleeding has ceased.
A. If a placenta previa is diagnosed in second trimester, the following steps should be
taken:
1. Do not perform a pelvic examination.
2. Start intravenous infusion of fluid with 18-gauge needle
3. Obtain a coagulation profile.
4. Evaluate fetal viability, advanced labor or uncontrollable hemorrhage

5.  If ultrasound examination shows no heart activity, consider termination. If
fetus is alive, manage conservatively (if bleeding is mild to moderate)
 If advanced labor or uncontrollable bleeding is present, proceed with C-section
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5. Use of tocolytic agents:
a) Use only when the uterus is contracting and/or vaginal bleeding is not
sufficient to cause maternal hypotension
b) Do not use if blood replacement would be unable to keep up with blood loss
or the patient is in active labor
6. Provide patient with risk, benefits and alternatives regarding increased incidence of
intrauterine growth restriction, need for adequate nutrition and cessation of smoking
7. Repeat ultrasound examination at 35–36 weeks
B. If placenta previa is diagnosed at 35–36 weeks, the following steps should be taken:
1. Complete previa
a) Determine fetal lung maturity via ultrasound-guided amniocentesis
b) If fetal lungs mature, delivery by C-section
c) If fetal lungs immature, monitor weekly for maturity, then do C-section
2. Marginal or partial previa
a) Do amniocentesis.
b) If fetal lungs mature, consider two possible causes:
 Double set-up when ready to commit to delivery
 Follow with serial ultrasound to see whether placenta moves upward,
as long as there is no further bleeding
c) If no longer a placenta previa on ultrasound, treat as a normal pregnancy
Even after the bleeding has stopped, repeated small hemorrhages may cause IUGR.
For Mature Fetus
 C-section
For a Patient in Labor

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 C-section
If Severe Hemorrhage
 C-section regardless of fetal maturity
III. Fetal Vessel Rupture
Two conditions cause third-trimester bleeding resulting from fetal vessel rupture:
(1) Vasa previa and (2) velamentous cord insertion. These two conditions often occur
together.
1. VASA PREVIA
A condition in which the fetal cord vessels unprotectedly pass over the internal os, making
them susceptible to rupture and bleeding
Incidence
0.03 to 0.05%
Manifestation
 Rapid vaginal bleeding and fetal distress.
Management
 Correction of shock and immediate C-section
2. VELAMENTOUS CORD INSERTION
The velamentous insertion of the umbilical cord into the fetal membranes: In other words,
the fetal vessels insert between amnion and chorion. This leaves them susceptible to ripping
when the amniotic sac ruptures.
Clinical Presentation
 Vaginal bleeding with fetal distress.
Management
 Correction of shock and immediate C-section

7. IV. Uterine Rupture
The ripping of the uterine musculature through all of its layers, usually with part of the fetus
protruding through the opening
Incidence
0.5%
Risk Factors
Prior uterine scar is associated with 40% of cases:
_ Vertical scar: 5% risk
_ Transverse scar: 0.5% risk
Presentation and Diagnosis
1. Sudden cessation of uterine contractions with a “tearing” sensation
2. Recession of the fetal presenting part
3. Increased suprapubic pain and tenderness with labor (may not be readily apparent if
analgesia/narcotics are administered)
4. Vaginal bleeding (or bloody urine)
5. Sudden, severe fetal heart rate decelerations
6. Sudden disappearance of fetal heart tones
7. Maternal hypovolemia from concealed hemorrhage
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Management
1. Total abdominal hysterectomy is treatment of choice (after delivery).
2. If childbearing is important to the patient, rupture repair is possible but risky.

8. Disseminated Intravascular Coagulation (DIC)
Definition: DIC is an acquired disorder of blood clotting in which the fibrinogen level falls
to below effective limits.
Manifestation:
Bruising or bleeding from an intravenous site
Risk factors:
1. premature separation of the placenta,
2. pregnancy-induced hypertension,
3. amniotic fluid embolism,
4. placental retention,
5. septic abortion,
6. Retention of a dead fetus.
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Pathophysiology
 Normally, platelets quickly form a seal over a point of bleeding to prevent further
loss of blood.
 Intrinsic and extrinsic clotting pathways then activate and strengthen this plug by
fibrin threads to produce a firm, fixed structure.
 To prevent too much clotting from occurring, at the same time the clot is being
formed, thrombin activates fibrinolysin, a proteolytic enzyme, to begin to digest
excess fibrin threads (anticoagulation).
 This lysis results in the release of fibrin degradation إنحلال products.
 DIC occurs when there is such extreme bleeding and so many platelets and
fibrin from the general circulation rush to the site that not enough are left in the
rest of the body for further clotting.
 The high thrombin level continues to encourage anticoagulation.
 This result in a paradox: at one point, the person has increased coagulation, but
throughout the rest of the system, a bleeding defect exists.

9.  DIC is an emergency because it can result in extreme blood loss from lack of
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fibrinogen.
Diagnosis
1. Physical exam may reveal multiple bleeding points associated with purpura
and petechiae.
2. Lab evaluation reveals thrombocytopenia, hypofibrinogenemia, an elevated
prothrombin time, and increased fibrin split products.
Management:
1. Supportive therapy to correct/prevent shock
2. Correct the underlying cause
3. When the DIC was a complication of pregnancy such as premature separation of the
placenta, ending the pregnancy by delivering the fetus and placenta.
4. Blood or platelet transfusion may be necessary to replace blood or platelet loss. This
administration may be delayed, however, until after heparin therapy so the new blood
factors are also not consumed by the coagulation process.
5. Intravenous administration of heparin to halt توقف the clotting cascade .شلال
6. fresh-frozen plasma or platelets can also aid in restoring clotting function

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Abruptio Placentae
Placenta Previa
VASA PREVIA
VELAMENTOUS CORD INSERTION