Third trimester bleeding
Tom Archer, MD, MBA
UCSD Anesthesia
Death in pregnancy:
Pulmonary thromboembolism (clotting
tendency in pregnancy)
Ante and postpartum hemorrhage (#1 cause
in poor countries)
Hypertensive disorders / pre-E / CVA
Third trimester bleeding-antepartum
• Placental abruption (1 / 100 pregnancies)
• Placenta previa (1 / 200 pregnancies)
• Uterine rupture (classical scar, VBAC with
LTCS)
• Vasa previa (1 / 2000 pregnancies)
Increased blood volume
• Normal delivery: transfusion usually
unnecessary, despite 500-1000cc blood
loss.
• Dangers of transfusion:
– Infection
– Immune modulation (CA, other bad things?)
Mechanisms of hemostasis in OB
• Uterine contraction!
• Platelet plug
• Vasoconstriction
• Fibrin formation and cross linking (Factor XIII)
• Fibrous tissue formation
Hemostasis
A: Under physiologic conditions, hemostasis is
prevented by the endothelium. This provides a
physical barrier and secretes platelet inhibitory
products, such as prostacycline (PGI2) and nitric oxide
(NO).
B: With endothelial cell injury, platelets adhere to vWf
in the subendothelium via the platelet membrane
receptor GPIb-IX.
C: This adhesion activates platelets, causing a shape
change and the release reaction (ADP is released,
which is a platelet agonist). The platelet membrane
intergrin receptor, GPIIb-IIIa, is activated. Fibrinogen
binds to this receptor, effectively crosslinking platelets
to form a platelet plug. During platelet activation,
thromboxane A2 is formed from hydrolysis of
phospholipids (especially phosphatidylcholine) in the
platelet membrane. This is an important platelet
agonist, recruiting other platelets and activating them,
thus promoting aggregation. In addition,
phosphatidylserine (a phospholipid) is moved to the
outer layer of the platelet membrane.
Phosphatidylserine (which used to be called PF3 or
platelet procoagulant activity) provides an essential
binding site for activated coagulation factors
(especially for the tenase and prothrombinase
complexes), optimizing activation of the coagulation
cascade and the formation of fibrin.
D: Fibrin is incorporated into the growing platelet plug
to form a stable thrombus.
www.diaglab.vet.cornell.edu/.../coa
gs/primim.htm
Placental abruption
• Risk factors: smoking, cocaine, hypertension,
advanced age and parity, trauma, PROM (all
cause arteriolar damage)
• Associated with IUGR / SGA (chronic placental
malfunction, like previa).
• Vaginal bleeding, uterine tenderness and pain
and uterine contractions.
Placental abruption: fetal) asphyxiation
(O2 supply is cut off).
Umbilical vein (UV)
Umbilical artery (UA)
Abruption
Uterine veins
Uterine arteries
Archer TL 2006 unpublished
Placental abruption with trauma
Placenta
shears off
Liquid placenta
Elastic myometrium
Miller’s Anesthesia chap. 58
Occult hemorrhage in abruption
Placental abruption
• Abruption is most common cause of DIC in
pregnancy.
• “10% of abruptions show DIC.”
Obstetric management
of placental abruption
• If fetus premature, FHTs OK and bleeding
minimal  expectant management in
hospital?
• Otherwise, prompt / immediate delivery.
Placenta previa
• Implantation in scarred area, frequently
lower uterine segment.
• Painless vaginal bleeding
• Ultrasound mainstay of Dx
• Avoid vaginal exam. “Double set-up.”
Placenta previa
Placenta previa
• Premature labor is common.
• IUGR is common (crummy placentation
site with poor nutrient transfer?)
• Steroid Rx for prematurity.
• Tocolysis or not?
Placenta previa
• Risks are:
– Profound hemorrhage
– Prematurity
• Goal is to delay delivery until fetus
matures.
• Expectant management in hospital (at
home, if close?).
Actively bleeding
previa or abruption
• General anesthesia
• Induce with ketamine or etomidate, not
propofol or pentothal.
• Blood in OR
Anesthesia for previa and abruption
• Spinal / epidural OK, IF patient is…
– Not actively bleeding
– Normovolemic
– Platelet count and PT / PTT are OK
• Nevertheless, increased risk of heavy bleeding
–
–
–
–
LUS doesn’t contract well
? Accreta
? Cut through placenta
DIC may accompany abruption
Vasa previa– hemorrhage is fetal blood.
Fetal death very common.
Uterine rupture
• Classical vertical uterine scar most vulnerable.
• Commonest cause is scar dehiscence
– With or without bleeding
• High index of suspicion and watch FHTs.
• Not always painful (esp. with LEA)
Third trimester bleeding-postpartum
• Uterine atony
• Genital tract trauma
• Retained placenta
• Placenta accreta
• Uterine inversion
Uterine atony
• Commonest cause of postpartum
hemorrhage.
• Contraction of uterus is primary
hemostatic mechanism to stop postpartum
bleeding.
• Overdistention of uterus is commonest
case of atony.
Uterine atony
• Overdistention
– Multiple gestation
– Polyhydramnios
– Macrosomia
– High parity
– Prolonged labor (tired uterus)
Uterine atony
• Other causes of atony:
– Chorioamnionitis
– Tocolytics
– Volatile anesthetic agents
Uterine atony-- management
• “Uterotonics”
– Oxytocin
– Ergots (Methylergonovine)
– Prostaglandins (Carboprost, “Hemabate”)
– Misoprostol (usually for cervical ripening)
Uterine atony-- oxytocin
• First-line, routine uterotonic.
• From posterior pituitary– released by nipple
stimulation (breast feeding)
• Older preparations from animals with ADH mixed
in water retention.
• Oxytocin has some ADH activity. Don’t give with
hypotonic solutions (e.g. D51/2NS).
• Oxytocin relaxes arteriolar and venous smooth
muscle  HYPOTENSION. No big boluses!
Flor P.
XXXX4756
25 yo repeat C/S
with Hx of
peripartum
cardiomyopathy
4 years before,
resolved.
Fatigued during
pregnancy, with
normal echoes.
Epidural
anesthesia for
C/S 5/30/2007.
C/S Delivery
Phenylephrine
Oxytocin
Uterine atony-- Carboprost
• Second-line drug?
• Contracts uterine smooth muscle– but also
bronchial and intestinal smooth muscle.
• Don’t use in patients with asthma / COPD.
• May cause bowel movement / diarrhea on OR
table.
• Very effective.
Uterine atony-- Methergine
• Third line drug?
• Ergot alkaloids (ergotism, LSD)
• Can cause hypertension, pulmonary
hypertension, N+V, coronary vasospasm.
• “Avoid combining pressors + Methergine?”
• Rarely if ever IV (0.02 mg slowly?)
Ergotism, caused by mycotoxins in rye, called “St.
Anthony’s Fire” in Middle Ages.
Gangrene in livestock due to
ergotism (mycotoxins in grain feed)
Postpartum hemorrhage:
genital tract trauma
• Suspect in vaginal bleeding despite firm uterus.
• Don’t confuse DIC with “suture deficit.”
• Cervical or vaginal laceration.
• More common with forceps or vacuum extraction.
• Will need exam under anesthesia.
Postpartum hemorrhage:
Retained placenta
• Uterus can’t fully contract
• Retained placenta needs to come out.
• Uterine relaxation does not = anesthesia.
– Which does OB need?
• Uterine relaxation  NTG or GA with volatiles.
• Anesthesia (SAB) may be enough.
• Beware of SAB or epidural + hypovolemia.
Postpartum hemorrhage:
Placenta accreta
An ill-defined area of the
placental/myometrial junction was seen
on the right lateral aspect of the
placenta (arrow). This was in vicinity of
prior myomectomy. At C-section, a 3 cm
region of placenta accreta was found.
Postpartum hemorrhage:
Placenta accreta
• Remember: with repeat C/S and previa, think
accreta.
• If accreta, think cesarean hysterectomy and
big blood loss.
Postpartum hemorrhage:
Uterine inversion
• Rare (1 / 5000).
• Bloody mass in vagina
• Excessive traction on umbilical cord
• Excessive fundal pressure
• Anesthesia +/- uterine relaxation. GA?
Postpartum hemorrhage:
Advanced options
• Angiographic arterial embolization
• Balloon occlusion of uterine arteries
• Balloon tamponade of uterine cavity
• Surgical artery ligation
• Hysterectomy.
Transfusion Therapy
• Evolving idea of risks of homologous transfusion:
–
–
–
–
Infection
Incompatibility reaction
Immune modulation
Patients don’t do as well?
• Autologous transfusion
– Antepartum donation
– Intraoperative blood salvage (“Cellsaver”)
– Acute Normovolemic Hemodilution
Transfusion Therapy
• Massive blood loss
– Can cause coagulopathy d/t dilution
• Dilutional coagulopathy
– Do platelets and clotting factors disappear
together? 1PRBC/1 platelet/1 FFP?
– This is the new teaching.
– Old teaching was that platelets went first.
Dilutional coagulopathy
• Old teaching:
• Dilutional thrombocytopenia is first to
develop (after 1 blood volume)
• Dilutional deficiency of clotting factors
(after more than 1 blood volume)
DIC
• Increased incidence with abruption, IUFD
(after a week?, and rare), “amniotic fluid
embolus” (rare, whatever it really is).
• Occurs “early” (before you would expect
based on dilution)
DIC
• Consumption of platelets and clotting factors.
• Diffuse oozing (venipuncture, IV sites)
• Low Plts and fibrinogen
• Prolonged PT / PTT
Cryoprecipitate
• Fibrinogen
• von Willebrand Factor
• Factor 8
• Factor 13
• Fibronectin
Universal preparations and Rx
• Do not confuse a “suture deficit”
(surgical bleeding) with DIC.
Evaluation of hemostasis
• When all else fails, talk with the patient!
• Hx best for chronic disorders.
• Examine patient and surgical field in acute
disorder.
• Is problem dilutional (gradual and late) or DIC
(earlier and fulminant)?
Universal preparations and Rx
• Communication and awareness!
– OBs need to tell you.
– You need to be proactive, helpful and vigorous.
•
•
•
•
•
•
Adequate IV access
Type and crossmatch
Might we need platelets, FFP, cryoprecipitate?
Patient volume status
Choice of anesthesia
Advanced measures?
– Hysterectomy, arterial ligation or embolization,
intracavitary balloon tamponade.
Disaster management
•
Call for help! Heroes call for help.
•
Prioritize. Think ahead. Don’t get behind. Don’t yell.
•
“Crew resource management”
•
More IVs (avoid neck?)
•
Arterial line
•
Warm fluids and blood
•
Early intubation (hypotension, nausea).
•
Blood, platelets, FFP, cryo, Novo-Seven
•
Get blood bank and hematologist involved early.
The End