What is the pathophysiology of postpartum hemorrhage (PPH)?

Updated: Jan 02, 2018
  • Author: Maame Yaa A B Yiadom, MD, MPH; Chief Editor: Bruce M Lo, MD, MBA, CPE, RDMS, FACEP, FAAEM, FACHE  more...
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At term, the uterus and placenta receive 500-800 mL of blood per minute through their low resistance network of vessels. This high flow predisposes a gravid uterus to significant bleeding if not well physiologically or medically controlled. By the third trimester, maternal blood volume increases by 50%, which increases the body's tolerance of blood loss during delivery.

Following delivery of the fetus, the gravid uterus is able to contract down significantly given the reduction in volume. This allows the placenta to separate from the uterine interface, exposing maternal blood vessels that interface with the placental surface. After separation and delivery of the placenta, the uterus initiates a process of contraction and retraction, shortening its fiber and kinking the supplying blood vessels, like physiologic sutures or "living ligatures."

If the uterus fails to contract, or the placenta fails to separate or deliver, then significant hemorrhage may ensue. Uterine atony, or diminished myometrial contractility, accounts for 80% of postpartum hemorrhage. The other major causes include abnormal placental attachment or retained placental tissue, laceration of tissues or blood vessels in the pelvis and genital tract, and maternal coagulopathies. An additional, though uncommon, cause is inversion of the uterus during placental delivery.

The traditional pneumonic "4Ts: tone, tissue, trauma, and thrombosis" can be used to remember the potential causes. Here, a 5th is added; “T” for uterine inversion that will be called “traction.”

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