Grand Rounds: CRITICAL CARE IN OB: PART 1 - Managing uterine atony and hemorrhagic shock


Your postpartum patient's profuse bleeding is threatening her life. When every minute counts, you'll need a well-informed, stepwise action plan.

Case Study

Maria is a 20-year-old G1 who presents at 41 weeks for induction of labor secondary to postdates. While undergoing prolonged induction, she spikes a fever of 38.8°C and is started on anti-biotics. Her labor progresses to the second stage. After 3 hours of pushing with poor progress, she consents to a primary cesarean delivery due to arrest of descent. The patient delivers a 4,300-g male infant, Apgars 8/9. After delivery, "mild" uterine atony occurs. She receives IV oxytocin (20 mU in 1,000 mL LR) and a single dose of 0.2 mg of methylergonovine IM. Improved uterine tone is noted and the surgery is completed. The estimated blood loss for the procedure is 1,000 mL.

In the immediate recovery period, the nurse notices that the patient's pulse pressure is narrow due to a rise in her diastolic blood pressure (BP 128/98). Her pulse is mildly tachycardic (HR 110). The nurse wonders if this effect could be due to the methylergonovine that the woman received after delivery. Over the next 45 minutes, the patient becomes progressively more tachycardic (HR 130), hypotensive (BP 70/40), and pale with cool extremities. Upon evaluation, the patient's fundus is 6 cm above the umbilicus. Bimanual exam reveals abundant clot from within the uterine cavity. Once the clot is removed, significant uterine bleeding persists. The uterus is now boggy, the blood is not clotting, and the patient's clinical status is deteriorating. What should you do?

Physiologic response to hemorrhage

A pregnant patient can adapt to hemorrhage more effectively than her nonpregnant counterpart due to several hemodynamic changes that accompany pregnancy. The most significant of these are increases in red cell mass, plasma volume, and cardiac output.2 In the early phases of hemorrhage, the body compensates for blood loss by raising systemic vascular resistance in order to maintain blood pressure and perfusion to vital organs. Clinically, this corresponds to a narrowing of the pulse pressure.

As bleeding continues, however, further vasoconstriction is impossible, resulting in decreased blood pressure, cardiac output, and end-organ perfusion.3 Table 1 classifies the physiologic responses that occur with various stages of hemorrhage. As an obstetrician, it's important to recognize these responses since physicians often underestimate the volume of blood lost during PPH, as Maria's case shows. Maria's estimated blood loss from surgery was reported as 1,000 mL; however, immediately after surgery in the recovery room, she was tachycardic with a narrow pulse pressure. These physiologic responses correspond to a class 2 hemorrhage with an estimated blood loss approaching 1,500 mL.

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