Post-partum Hemorrhage
Introduction
- Post partum hemorrhage (PPH) is the leading cause of maternal mortality (60% of all maternal dealths in the developing world). The rate has been increasing in recent years
- Risk factors: previous PPH, chorioamnionitis, placental abnormalities, newborn who is large for gestational age (LGA), maternal obesity, failure to progress in labor, hypertension
- Definition: >500cc blood loss in vaginal delivery or >1000cc in c-section; or any amount of blood loss with hemodynamic instability
- Early/primary PPH is within 24 hrs; late/secondary PPH is after 24 hours
- Typically occurs after 20 weeks gestational age
Causes
- Differential Diagnosis: (A useful mnemonic is the 4 Ts- tone, tissue, trauma, thrombosis)
- Tone: Uterine atony is the most common cause by far
- Commonly due to overdistention of the uterus (from multiple gestations, polyhydramnios, large fetus, etc.) and subsequent failure of the uterus to contract, structural abnormalities of the uterus, retained blood clots or products of conception preventing contraction of uterus.
- Other contributing factors include prolonged labor (resulting in muscle fatigue); infections; medications that inhibit contractions (such as NSAIDs, certain anesthetics, and magnesium sulfate)
- Tissue: Retained products of conception
- Retained placental tissue is more common in preterm deliveries, prior c-sections (or other reasons for uterine scarring), and in placental previa/accreta
- Trauma: Lacerations to vagina, perineum; Uterine rupture
- Lacerations to the genital tract commonly occur in vaginal deliveries
- Uterine rupture more common in women with prior C-sections other uterine surgeries, dilation and curettage (D&C), and IUD placement
- Arterial aneurysm rupture (rare)
- Commonly reported arteries to have aneurysmal rupture in pregnancy include splenic, cerebral, renal, ovarian, coronary, and the aorta
- More common in multiparous women
- Estrogen/progesterone facilitate arterial wall degeneration due to sub-endothelial thickening and accumulation of glycosaminoglycans, which leads to aneurysmal dilatation
- Increased cardiac output and blood volume also stresses the arterial wall
- Thrombosis: Less relevant in acute hemorrhage, but can lead to bleeding-related problems later
- Pregnancy in itself is a hypercoagulable state; previously undiagnosed coagulation defects may become clinically significant in pregnancy as well
- Acquired coagulopathies can also occur
- DIC
- HELLP
- sepsis
- amniotic fluid embolism
- Tone: Uterine atony is the most common cause by far
Management, Workup, and Treatment
- Initial stabilization and resuscitation as with any hemodynamically unstable patient: assess ABCs, place 2 large bore IVs, start with rapid infusion of IV fluid, give pRBC and platelet transfusions if needed
- Fundal massage can be attempted to help with uterine atony and to assess for retained POC
- Exam should include a FAST (ultrasound to look for intra-abdominal free fluid), pelvic/perineal exam for lacerations, bimanual exam to remove easily accessible clots or retained POC
- Consider upright chest x-ray in a stable patient to evaluate for free air (indicating possible uterine rupture)
- Ob/gyn consult if evidence of intra-abdominal bleeding (positive FAST, hemodynamic instability, etc.)
- Operative management includes hysterectomy or arterial embolization (typically uterine artery if bleeding is from uterine source)
- Consider foley or Blakemore placement in the uterus if there is uncontrolled uterine bleeding
- Medications
- Oxytocin-facilitates contractions and has vasopressive effect; prophylactic use in labor reduces the rate of subsequent post partum hemorrhage
- Methergine- causes contraction of uterine smooth muscle
- Misoprostol (less effective)
- Tranexamic acid/antifibrinolytic