Nancy K. Lowe Editor

The In Focus papers in this issue, guest edited by Dr. Debra Bingham, focus on the problem of postpartum hemorrhage (PPH) in the United States. Postpartum hemorrhage remains the most common cause of maternal death and a significant cause of maternal morbidity. Despite efforts to reduce the incidence of PPH through active management of the third stage of labor with prophylactic oxytocin administration, the incidence of PPH continues to increase. This increase has been linked to increased rates of induction of labor and cesarean delivery as reviewed by Bingham and Jones (2012).

Although the concern for uterine atony commonly concentrates on the time immediately surrounding the third stage of labor and the first-hour postpartum, anecdotal reports suggest there may also be an increase in PPH occurring some hours later during the first 12 to 24 hours after birth. My own observations, knowledge of uterine physiology, and logic suggest that injudicious use of prophylactic oxytocin (pitocin) may be partially to blame. A clinical story will illustrate my point.

A healthy 39-year-old, G6 PTPAL 22032 woman began labor at 39 5/7 weeks gestation with spontaneous rupture of membranes and onset of contractions. Her pregnancy had progressed normally, and on hospital admission her hemoglobin (HGB) was 12.7 g/dL and hematocrit (HCT) 35.4%. Following an unmedicated labor with a 7 hours latent phase and 2.5 hours active phase, she delivered a 3950 gm male infant with Apgar scores of 9 and 9 at 1 and 5 minutes and sustained a second-degree perineal laceration. Per unit standard practice, 30 international units (IU) of pitocin in 500 ml 0.9% NaCl was hung with delivery of the infant and run rapidly. The placenta delivered spontaneously, the laceration was repaired, and blood loss was estimated at 300 ml. Approximately 30 minutes after the birth, the attending RN noted that the pitocin was infused and asked the physician if the intravenous (IV) could be discontinued. The physician ordered another bag of pitocin “just to be sure.” As previously prepared per standard by the pharmacy, a second 500 ml with 30 IU of pitocin was infused and the IV capped by the time the family was transferred to the postpartum unit about an hour later. During this time, the infant was actively breastfeeding, the mother had voided in the bathroom with assistance from the nurse, and lochia was noted as normal.

Within the first few hours postpartum, the new mother got up to the bathroom twice, had breakfast, nursed her infant, and took a short nap. She later remembered that the toilet seemed “full of blood” when she voided, yet the nurses noted that her uterus was firm on assessment. When she got up to go to the bathroom at about 8 hours postpartum, the mother felt light-headed and was concerned that she might faint. The RN noted that she was pale and encouraged her to have help when she got out of bed.

At 24 hours postpartum, the woman's HGB and HCT were 8.5 and 24.0, and at 48 hours postpartum, 7.9 and 22.3 respectively. Clearly, a PPH had occurred. She declined the offer of a blood transfusion to treat her severe anemia. The woman was discharged with the morbidity of diminished strength and stamina following her PPH and related risks for impaired breastfeeding, difficulty independently caring for her infant, and other complications. Her first few weeks postpartum were dominated by the fatigue of anemia superimposed on the normal fatigue of the early weeks of new motherhood.

The question is why did this healthy mother with an uncomplicated pregnancy, labor, and birth have a delayed, but early PPH? The injudicious use of high-dose pitocin during the third stage and immediate postpartum period may be at least part of the etiology. This mother received 60 IU of intravenous pitocin in fewer than 90 minutes after the birth of her infant. International guidelines recommend 10 IU of oxytocin intramuscularly or intravenously as one acceptable uterotonic for active management of the third stage of labor (Begley, Gyte, Devane, McGuire, & Weeks, 2011).

As the “control” of labor has become more mainstream through induction and augmentation of labor, our appreciation and respect for the exquisite nature of normal uterine function during parturition has been lost. Pitocin has been labeled a high-alert medication by the Federal Drug Administration (FDA), and numerous quality improvement efforts are focused on identifying and promptly treating untoward effects of pitocin administration during labor, such as tachysystole. However, it seems that once the infant is born, pitocin is believed to be an innocuous drug, and if a little is good, a lot must be better. A lot may be needed with overt PPH due to uterine atony, but as prophylaxis in a woman with no signs of atony, what are the potential consequences of pitocin overdose?

Endogenous oxytocin is a neuropeptide released from the posterior pituitary and also synthesized locally by the amnion, chorion, and decidua of the pregnant uterus. The uterus is primed shortly prior to the onset of spontaneous labor with a dramatic increase in the number of oxytocin receptors on the smooth muscle cells of the myometrium. The increase in receptors makes the laboring uterus remarkably sensitive to increases in endogenous oxytocin that occur during spontaneous labor. After delivery of the placenta as placental steroid levels fall (particularly progesterone), the density of oxytocin receptors also dramatically decreases during the first 24 hours postpartum, while endogenous oxytocin levels rise with suckling of the infant at the maternal breast (Gimpl & Fahrenholz, 2001). Oxytocin, whether endogenous or exogenous, produces uterine contraction by binding with these myometrial oxytocin receptors. It is not difficult to deduce that a dramatic uterine load of exogenous oxytocin immediately following birth may occupy all available receptors and interfere with the normal cycle of receptor restoration. Simply put, if all the receptors are full and perhaps down-regulated by high oxytocin concentration, when exogenous oxytocin is no longer available, a period of receptor recovery may be needed resulting in corresponding uterine atony.

Many years ago as a young labor and delivery nurse, I remember learning that when intravenous pitocin was running postpartum, which was a relatively rare event with not more than 20 IU in a liter of fluid, the rate of infusion was gradually decreased over several hours to provide time for the woman's own physiology to take over the task of maintaining uterine tone. I was taught to respect the myometrium and the potential negative consequences of exogenous oxytocin during the early postpartum period.

There is a paucity of research on the physiology of normal postpartum adaptation and the complexity of forces that maintain uterine tone and prevent hemorrhage. Despite that void, it is imperative that we use the knowledge we do have to decrease the incidence of PPH, particularly hemorrhage that may be iatrogenic in origin. This begins with promoting health in women prior to and during pregnancy, avoiding unnecessary intervention into the normal processes of labor and birth, and remembering that pitocin is a high-alert medication before and after delivery. A little is likely all you need.


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