3. Definition
■ blood loss in excess of 500 mL at the time of vaginal delivery or blood loss
in excess of 1000 mL following cesarean delivery.
■ the leading cause of maternal mortality.
■ Could be immediate or delayed.
5. UTERINE ATONY
■ This is the most common cause of excessive postpartum bleeding. (75-80%)
■ Risk Factors. Rapid or protracted labor, chorioamnionitis, medications and
overdistended uterus.
■ Clinical Findings. A soft uterus (feels like dough) palpable above the umbilicus
■ Management. Uterine massage and uterotonic agents (e.g., oxytocin,
methylergonovine, or carboprost).
6. ■ Lacerations (15%) Risk Factors. Uncontrolled vaginal delivery, difficult delivery, and
operative vaginal delivery.
■ Clinical Findings. Identifiable lacerations (cervix, vagina, perineum) in the presence of
a contracted uterus.
■ Management. Surgical repair
■ Retained Placenta (5%)
■ Risk Factors. Accessory placental lobe and abnormal trophoblastic uterine invasion
(e.g., cervix, vagina, perineum).
■ Clinical Findings. Missing placental cotyledons in the presence of a contracted uterus.
■ Management. Manual removal or uterine curettage under ultrasound guidance.
7. approach
■ 1. All women in early labor who have risk factors for PPH should be identified and
their hemoglobin checked. For medium-risk women, their blood should be typed
and screened for irregular antibodies such as Rh and Kell. For high-risk women, 2
units of blood should be typed and crossmatched.
■ 2. As soon as the fetus has been delivered, an infusion of oxytocin (Pitocin) 10 to 40
U/L IV should be started and maintained during the first 6 hours postpartum.
■ 3. The vagina and perineum should be inspected to rule out any lacerations that
could cause excessive bleeding.
■ 4. The placenta should be carefully assessed at delivery to make certain there are
no missing cotyledons (lobules of placenta).
■ 5. The uterus should be evaluated by abdominal palpation during the first 1 to 2
hours before transfer to the postpartum unit.
11. Definition
■ Descent of the cord to a level adjacent to or below the presenting part, causing
cord compression between cord and pelvis.
■ It is an obstetrical emergency because the prolapsed cord is vulnerable to
compression, which can compromise fetal oxygenation.
■ Incidence: 0.16-0.18%.
13. Classification
■ overt umbilical cord prolapse:
■ descent of the umbilical cord below the presenting fetal part through the cervix and into
or beyond the vagina, This is the most common type of cord prolapse.
■ occult umbilical prolapse:
■ descent of the umbilical cord alongside the presenting fetal part, but has not advanced
past the presenting fetal part.
14.
15. Clinical features
■ sudden decrease in fetal heart rate with variable decelerations.
■ the cord can be seen or felt on vaginal examination, particularly with overt cord
prolapse.
16. Management
■ Do not hold the cord or try to push it back into the uterus, elevate the presenting
part, avoid palpating the cord, Place the patient in knee-chest position, and
perform immediate cesarean delivery.
■ If fetal demise or too premature (<22 weeks), allow labor and delivery.
18. Definition
■ Occurs when the fetal head is delivered but the shoulders cannot be
spontaneously delivered with gentle downward traction
■ Due to impaction of the fetal shoulder behind the symphysis
■ Occurs in 0.6 to 1.4%
of deliveries
21. Shoulder Dystocia
■ Diagnosis is made during the 2nd stage of labor
■ Turtle sign : The fetal head recoils back against
the perineum after it comes out of the vagina.
■ The shoulders fail to deliver with maternal pushing and gentle
downward traction.
22. ■ unilateral shoulder dystocia
the anterior shoulder that becomes impacted
behind the pubic symphysis
■ bilateral shoulder dystocia
very rare the posterior shoulder fails to descend below
the sacral promontory, so that both the anterior and posterior
shoulders are arrested .
23. How much time does one have to resolve a shoulder
dystocia before hypoxic brain happend ?
■ In general, the operator has up to five minutes to deliver a
previously well-oxygenated term infant before an increased risk of
asphyxial injury occurs.
■ After 5 minuet we have to do argent c/s
25. episiotomy
■ episiotomy does not decrease risk of brachial plexus
injury and increases the risk of perineal trauma.
■ The only reason to perform an episiotomy is to eliminate soft
tissue resistance that is interfering with the ability to insert the
whole hand into the hollow of the sacrum posteriorly to
perform fetal maneuvers.
27. Suprapubic pressure
Apply oblique pressure above the pubic bone with the heel of the
hands against the posterior aspect of the fetal shoulder
Fundal pressure and Maternal pushing
should not be employed.
It is may lead to further impaction
of the shoulders.
28. Rotational manavure
Woods' corkscrew maneuver
Apply pressure on anterior surface
of the posterior shoulder
rotating it 180 degrees
Done only if the posterior
Shoulder is accessible
29. Rotational manavure
■ Rubin maneuver :
■ Reverse Woods' corkscrew maneuver
The pressure is applied on the posterior
surface of the posterior shoulder
30. removal of the
posterior arm and shoulder
antecubital fossa is located and pressure of a
finger is applied in order to flex the arm.
The forearm is swept across the chest and face.
The hand is then grasped, to extend
along the fetal face, and delivered.
Major risk for humeral
fracture
31. Other manuevers
■ – Fetal clavicle fracture
■ – Rolling to “all fours” position
■ – Zavanelli
■ – Symphysiotomy
32. Fetal clavicle fracture
■ Often described but rarely performed
■ Fracture decreases the bisacromial diameter to effect
delivery of the shoulder
■ it Causes major damage to lungs ang major blood vessels
33. Rolling over to 'all fours' position
■ Gaskin maneuver
■ Increases pelvic dimensions , freeing the posterior shoulder easly
34. Zavanelli maneuver
reversing cardinal movements of labor
Fetal head is rotated to occiputanterior position, flexed,
rotated and pushed back up to the uterus
35. Symphysiotiomy
Involves dividing the ligaments between the
right and left pubic symphyseal bones
Increase of the transverse diameter of the
pubis adds 3 cms to the pelvic circumference
Complications
Injury to the urethra or bladder.
Vesico-vaginal or urethro-vaginal fistula
Difficulty of walking and unstable
pelvis usually improved by time.
36. Complication
Maternal Complications
Lower genital tract lacerations
Post-partum haemorrhage
Rectovaginal fistula
Fetal Complications :
Brachial plexus palsy
Clavicle fracture - Fracture of the humerus
Fetal hypoxia, with or without permanent neurological damage
Fetal death
Editor's Notes
usually due to subinvolution of the uterus and disruption of the placental site “scab” several weeks postpartum or to the retention of placental fragments that separate several days after delivery.
(e.g., MgSO4, β-adrenergic agonists, halothane)
including vitamin D deficiency and maternal and fetal genetic factors. Vitamin D is known to play an important role in muscle function, and muscle is a component of both the uterine and vascular system. Studies have suggested that among patients having a vaginal delivery, 18% of the variation in excessive postpartum bleeding may be attributable to maternal genetic factors, 11% to maternal environmental factors, and 11% to fetal genetic effects.
Most of the blood loss due to uterine atony occurs from the myometrial spiral arterioles and decidual veins that previously supplied and drained the intervillous spaces of the placenta. As the contractions of the partially empty uterus cause placental separation, bleeding occurs and continues until the uterine musculature contracts around the blood vessels and acts as a physiologic-anatomic ligature. Failure of the uterus to contract after placental separation (uterine atony) leads to excessive placental site bleeding.
During pregnancy, uterine relaxation is facilitated by progesterone and parathyroid hormone–related peptide (PTHrP). The latter plays an important role in maintaining uterine relaxation during pregnancy (see Chapter 5); however, as soon as the uterus is emptied (delivery of the fetus and placenta), the gene controlling this hormone is turned off and the uterus is allowed to contract more completely. If there is a failure of complete expulsion of the placenta or poor uterine contractility leading to excessive bleeding, the uterus will fill with blood. The distention is thought to reactivate the expression of PTHrP and cause uterine relaxation, thereby leading to excessive hemorrhage.
Disseminated Intravascular Coagulation (rare)
Risk Factors. Abruptio placentae (most common), severe preeclampsia, amniotic fluid embolism,
and prolonged retention of a dead fetus.
Clinical Findings. Generalized oozing or bleeding from IV sites or lacerations in the presence
of a contracted uterus.
Management. Removal of pregnancy tissues from the uterus, intensive care unit (ICU) support,
and selective blood-product replacement.
Uterine Inversion (rare)
Risk Factors. Myometrial weakness (most common) and previous uterine inversion.
Clinical Findings. Beefy-appearing bleeding mass in the vagina and failure to palpate the
uterus abdominally.
Management. Uterine replacement by elevating the vaginal fornices and lifting the uterus
back into its normal anatomic position, followed by IV oxytocin.
Unexplained
If despite careful searching, no correctible cause of continuing hemorrhage is found, it may be
necessary to perform a laparotomy and bilaterally surgically ligate the uterine or internal iliac
arteries. Hysterectomy would be a last resort.