Third trimester bleeding

Tom Archer, MD, MBAUCSD 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

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.

Hemostasis

www.diaglab.vet.cornell.edu/.../coags/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.

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Umbilical artery (UA)Umbilical vein (UV)

Uterine arteriesUterine veins

Placental abruption: fetal asphyxiation (O2 supply is cut off).

Abruption

Archer TL 2006 unpublished

Placental abruption with trauma

Elastic myometrium

Liquid placenta

Placenta shears off

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!

Phenylephrine C/S Delivery

Oxytocin

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.

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