The placental bed

Uterine atony is responsible for the majority of primary postpartum hemorrhages originating from the placental bed. The main predisposing factors are prolonged labor followed by operative vaginal or abdominal delivery, uterine overdistension from polyhydramnios or multifetal pregnancy, and delivery following antepartum hemorrhage from either placenta praevia or abruption. Failure of the uterus to contract may also be due to retained placental fragments, either as disrupted portions or, more rarely, a succenturiate lobe. Fibroids may promote primary postpartum hemorrhage in a similar fashion. These factors should be considered if the uterus relaxes following normal uterotonic measures.

Disseminated intravascular coagulation (DIC) can aggravate any of the above etiological mechanisms. It is usually triggered by the degree of blood loss, coexisting abruption, and/or pre-eclampsia-eclampsia, and rarely by amniotic fluid embolism. When postpartum hemorrhage occurs following an antepartum hemorrhage, the scenario is particularly difficult since there have been two episodes of blood loss. The rare but serious complication of abruption is due to extravasation of blood into the myometrium, known as a Couvelaire uterus, which impairs the physiological uterine contraction-retraction hemostatic process. Persistent hemorrhage and coagulopathy in these circumstances can be fatal unless there is appropriate and rapid hematological support. DIC is a medical problem requiring rapid access to red cell concentrate, fresh frozen plasma, and platelets. With correct replacement and avoidance of hypotension, hypothermia, and volume overload, the situation should resolve. Unless there is a traumatic injury to the genital tract necessitating a surgical approach to arrest hemorrhage, attempts to arrest bleeding via a laparotomy may do more harm than good since hysterectomy and/or ligation of the internal iliac arteries incur further hemostatic insults to the patient.

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