RECOGNITION AND EARLY DETECTION
PPH is not a diagnosis, but a critically important sign that often occurs without warning and in the absence of risk factors.
When present, however, these factors warrant heightened awareness about the risk of PPH (Box 12.1). Maternal hemodynamic responses to blood loss should also be mon-itored, as these responses are indicators of well-being, vol-ume deficit, and prognosis. The loss of 10% to 15% (500 mL for an average patient with singleton pregnancy) of blood volume may be tolerated with no signs or symp-toms. As blood loss approaches 20%, the first signs of intravascular depletion become manifest, including tachy-cardia, tachypnea, and delayed capillary refill, followedby orthostatic changes and narrowed pulse pressure (due to elevated diastolic pressure secondary to vasoconstric-tion with maintenance of systolic pressure). Beyond approx-imately 30% volume loss, breathing and heart rate further increase, and overt hypotension develops. Finally, with profound blood loss above 40% to 50%, oliguria, shock, coma, and death may occur.
The source and etiology of bleeding should be identified as soon as possible, and targeted interventions applied in order to minimize morbidity and prevent mortality. The most commoncause of PPH is uterine atony, representing about 80% of cases. Retained placenta, genital tract trauma (lacera-tions, rupture), and coagulation disorders are other causes. Hematomas can occur anywhere in the lower genital tract. Ruptured uterus and inverted uterus are rare but serious causes of PPH.