Aetiology

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Primary PPH accounts for the vast majority of cases of PPH. The most common aetiologies of primary PPH include uterine atony, genital tract lacerations, retained or invasive placentation, uterine rupture, uterine inversion, or coagulopathy.[3]

The causes of primary PPH can be classified by the 'four Ts' mnemonic: tone, trauma, tissue, and thrombin. In descending order, the most common causes are:[3][20]

  • Tone (uterine atony), accounting for approximately 70% to 80% of cases

  • Trauma (obstetric lacerations, expanding haematomas, or uterine rupture), present in around 20% to 30% of cases

  • Tissue (retained placental tissue or other products of conception), present in approximately 10% of cases

  • Thrombin, or clotting factor deficiencies, accounting for <1% of cases.

Note that more than one cause of bleeding can be present in any individual case of PPH.

Obstetric lacerations leading to PPH may be associated with operative vaginal delivery, rapid delivery, or episiotomy. Retained placental tissue as a cause of PPH may be linked to placenta accreta spectrum disorder in women with a history of prior uterine surgery. Maternal coagulopathy as a cause of PPH may be triggered by pre-eclampsia, HELLP syndrome, intrauterine fetal demise, placental abruption, the use of therapeutic anticoagulation, or acquired and inherited coagulopathies (e.g., amniotic fluid embolism).

Secondary PPH is rare, comprising approximately 1% to 2% of cases.[21] The most common aetiologies include placental site subinvolution, retained products of conception, infection (e.g., endometritis), uterine vascular disorders such as arteriovenous malformations, and coagulopathies such as von Willebrand disease.[3]

Pathophysiology

The pathophysiology of PPH involves a disruption in the normal mechanisms of uterine contraction, placental separation, and haemostasis, leading to uncontrolled bleeding. The specific mechanism of PPH varies depending on the underlying cause.

The most common cause of PPH is uterine atony, which refers to the inability of the uterus to contract adequately after delivery, leading to excessive bleeding. Due to the increase in uterine blood flow at term, uterine atony following placental delivery results in rapid haemorrhage from the placental bed.[22] Normally following delivery, the contraction of the myometrium compresses the spiral arteries supplying the placental bed, which reduces bleeding from the placental site. In cases of uterine atony, the uterus fails to contract effectively, resulting in inadequate compression of the spiral arteries and persistent bleeding.[22]

Other less common causes of PPH include retained placental tissue, genital tract trauma (such as lacerations or uterine rupture), coagulation disorders, and abnormalities of the placenta (such as placenta accreta or placenta previa). These conditions also disrupt normal haemostatic mechanisms and lead to excessive bleeding.

Classification

Classification by timing of presentation

PPH can be classified according to its timing relative to delivery.[3][4]

  • Primary PPH - occurs within 24 hours of delivery.

  • Secondary PPH - excessive bleeding that occurs >24 hours after delivery and up to 12 weeks postpartum.

Safe Motherhood Initiative (SMI): obstetric haemorrhage stages

The SMI obstetric haemorrhage checklist produced by the American College of Obstetricians and Gynecologists provides a practical staging system for the identification and treatment of PPH:[7][8] Safe Motherhood Initiative: Obstetric hemorrhage checklist Opens in new window

  • Stage 1 definition: estimated blood loss (EBL) >1000 mL after delivery with normal vital signs and laboratory values. Vaginal delivery with EBL 500-999 mL should be treated as stage 1

  • Stage 2 definition: continued bleeding (EBL up to 1500 mL OR >2 uterotonics*) with normal vital signs and laboratory values (*two or more uterotonics in addition to routine oxytocin administration, or >2 administrations of the same uterotonic)

  • Stage 3 definition: continued bleeding (EBL >1500 mL OR >2 RBCs given OR at risk for occult bleeding/coagulopathy OR any patient with abnormal vital signs/labs/oliguria)

  • Stage 4 definition: cardiovascular collapse (massive haemorrhage, profound hypovolaemic shock, or amniotic fluid embolism).

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