If the nurse suspects a uterine infection in the postpartum patient, she should assess the

Key Points

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Obstetric hemorrhage is the most common cause of maternal mortality worldwide and a leading contributor to maternal mortality in developed nations.

Most severe morbidity and mortality that occurs secondary to obstetric hemorrhage is considered preventable and is caused by delays in recognition and treatment.

The visual estimate of vaginal bleeding often underestimates true blood loss; training clinicians, separation of amniotic fluid, use of calibrated drapes, and weighing pads and bedding improves estimation accuracy.

Hypotension and tachycardia are late signs in hypovolemic shock.

Antepartum hemorrhage usually represents a greater threat to the fetus than to the mother.

Postpartum hemorrhage is increasing in both rate and severity in the developed world, mostly resulting from an increase in the incidence of uterine atony.

Uterine atony is the most common cause of postpartum hemorrhage.

The incidence of placenta accreta is increasing because of the higher cesarean delivery rate.

Peripartum hysterectomy is increasing in frequency because of an increase in the incidence of both uterine atony and placenta accreta.

Patients with placenta accreta are at high risk for massive hemorrhage and should be managed only in facilities with multidisciplinary specialists, including interventional radiologists and a well-staffed blood bank.

Multidisciplinary team responses that emphasize the accurate estimation of blood loss, early warning signs of shock, and rapid response to blood loss and coagulopathy are associated with less maternal morbidity.

Coagulopathy develops quickly during bleeding from the placental bed, and may be out of proportion to blood loss or dilution because of the rapid consumption of fibrinogen.

Intraoperative blood salvage may be lifesaving in cases of intractable hemorrhage if allogeneic blood is not available, or if the patient refuses allogeneic blood.

Administration of tranexamic acid during postpartum hemorrhage decreases deaths caused by bleeding in low-resource settings. Its effect in high-resource settings is unknown, but it may decrease blood loss and transfusion risk.

Risk Assessment

Causes of postpartum hemorrhage and predisposing factors are listed in Table 194-1. The most common cause is uterine atony. At term, blood flow through the placental vasculature is approximately 600 mL/minute. After delivery, the primary mechanism by which blood loss is controlled is contraction of the uterine myometrium to constrict severed vessels at the former placental site. Failure of this mechanism can result in massive and rapid blood loss. Predisposing factors are any that result in overdistention of the uterus or reduce the ability of the myometrium to contract, including

Multiple gestation

Macrosomia

Polyhydramnios

Chorioamnionitis

Prolonged labor

Precipitous labor

Augmented labor

High parity

Tocolytic agents

Inhalational anesthetics at high concentrations

History of uterine atony (increased likelihood of recurrence)

Retained placenta is also a common cause of both early and delayed postpartum hemorrhage, although not all cases result in significant blood loss. Retained placental fragments may be unrecognized; thus, bleeding might be insidious and cause delayed postpartum hemorrhage. Patients who have had a prior retained placenta or who deliver well before term are predisposed to retained placenta.

Trauma associated with delivery represents another cause of postpartum hemorrhage and should be considered in all postpartum patients with continued blood loss despite a firm, contracted uterus. Traumatic postpartum hemorrhage can be categorized as follows:

Vaginal

Cervical

Perineal laceration

Episiotomy

Traumatic laceration of blood vessels, whether occurring during vaginal or cesarean delivery, can result in pelvic hematoma. Uterine rupture, especially in patients who give birth vaginally after a previous cesarean delivery, is another potential cause of postpartum bleeding. In addition to the use of instrumentation for delivery, many cases of postpartum hemorrhage occur with precipitous delivery or delivery of macrosomic infants.

Uterine inversion is a rare cause of postpartum hemorrhage but can be catastrophic. It should be suspected in any case of postpartum hemorrhage when significant hypotension coexists. Most cases of uterine inversion are obvious owing to the associated vaginal mass. Risk factors for uterine inversion include uterine atony, inappropriately applied fundal pressure or umbilical cord traction, uterine anomalies, and abnormal placentation.

Uterotonic therapy

Uterotonic medications represent the mainstay of drug therapy for postpartum hemorrhage secondary to uterine atony.Table 18.4 lists available uterotonic agents (within the United States) with their dosages, side effects, response times, and contraindications.Oxytocin is usually given as a first-line agent. IV therapy is the preferred route of administration, but either intramuscular or intrauterine dosing is possible. Initial treatment starts with 10 to 30 U of oxytocin in 500 to 1000 mL of crystalloid solution. Short durations of higher doses are safe, efficacious, and associated with a reduced need for additional uterotonic therapy and composite hemorrhage treatment (uterotonic drugs, transfusion, tamponade, embolization, surgery).85

When oxytocin fails to produce adequate uterine tone, second-line therapy must be initiated. Currently a variety of additional uterotonic agents are available. The choice of a second-line agent depends on its side-effect profile as well as its contraindications.Misoprostol, a synthetic prostaglandin E1 analogue, is a safe, inexpensive, and efficacious uterotonic medication that does not require refrigeration. It has been used for both the prevention and treatment of postpartum hemorrhage. Sublingual misoprostol allows for lower dosing (200 to 400 µg) and higher bioavailability than rectal dosing (600 to 1000 µg). The advantages ofmethylergonovine for uterine atony are its rapid bioavailability and long half-life; however, disadvantages include its instability at room temperature, side-effect profile, and contraindication for hypertensive women. Natural and syntheticprostaglandins are highly effective uterotonic agents. Recurrent doses of intramuscular and intrauterineprostaglandin F2α can be used to control atony. It is important to note that asthma is astrong contraindication to the use of prostaglandin F2α because of its bronchoconstrictive properties.Prostaglandin E2 is a naturally occurring oxytocic that can dramatically improve uterine tone; however, its unfavorable side-effect profile often precludes its use (fever, chills, nausea, emesis, diarrhea, and headaches). Lastly, oxytocin analogues and combined ergometrine-oxytocin preparations are available outside the United States for the control of uterine atony.

When atony is due to tocolytic drugs that have impaired calcium entry into the cell (magnesium sulfate, nifedipine), calcium chloride or calcium gluconate should be considered as an adjuvant therapy. Given intravenously, one ampule (1 g in 10 mL) can effectively improve uterine tone and resolve bleeding due to atony.

Discharge of lochia

Lochia is the name given to the discharge coming from the placental site. The normal pattern is for red discharge in the first 3 or 4 days: lochia rubra or red lochia. It consists mainly of blood mixed with shreds of decidua. This becomes lighter (more brownish) and eventually serous after about 5 or 6 days: lochia serosa or serous lochia. This is altered blood and serum and contains leucocytes and organisms. The final discharge is known as lochia alba, yellowish-white lochia, in which there is little blood. It is mostly white blood cells, cervical mucous and organisms. Discharge decreases in amount as the site heals. The average time for lochia to become colourless is about 3–4 weeks.

Lochia that remain red and abundant for longer than usual may indicate delayed involution of the uterus, which may be due to retention of a piece of placenta within the uterus and/or to infection. If placental tissue is retained the uterus remains enlarged and this may show on an ultrasound scan. Lochia with offensive odour may indicate infection. It is possible for red lochial discharge to still be present at 6–8 weeks. It is more common also after instrumental delivery. Seek medical help if concerned.

Postpartum Hemorrhage

A leading cause of maternal and fetal morbidity and mortality worldwide, mild to moderate obstetric hemorrhage can be masked by pregnancy-related physiologic changes. Under­estimation of blood loss and inadequacy of resuscitation are common problems (seeChapter 37).

Failure of the uterus to contract (uterine atony) after delivery accounts for most cases of postpartum hemorrhage and remains a leading cause of postpartum hysterectomy and blood transfusion. Each minute, 600 to 700 mL of blood flows through the placental intervillous spaces; thus, obstetric hemorrhage can rapidly result in maternal shock. Uterine atony occurs more commonly after cesarean delivery than after vaginal delivery, perhaps as a reflection of the condition(s) that prompted the cesarean delivery or possibly because surgery disrupts the normal postpartum response to uterotonic hormones and pharmacologic agents. Risk factors for uterine atony include (1) high parity, (2) an overdistended uterus (multiple gestation, macrosomia, polyhydramnios), (3) prolonged labor (augmented by oxytocin), (4) chorioamnionitis, (5) abnormalities in placentation (placenta accreta, increta, or percreta), (6) retained placental tissue, (7) mechanical barriers to effective contraction (e.g., fibroids, uterine anomalies), and (8) poor perfusion of the uterine myometrium (e.g., hypotension).

Initial efforts to control uterine atony include uterine massage and exogenousoxytocin administration. Postpartum oxytocin is administered in a wide range of doses, methods, and timing patterns (e.g., before or after delivery of the placenta),429 although small doses of oxytocin are sufficient to produce adequate uterine contraction after cesarean delivery in most women.429 The effective bolus dose necessary for adequate uterine tone in 90% (ED90) of nonlaboring women undergoing cesarean delivery oxytocin is 0.35 unit430; in laboring women who have received approximately 10 hours of oxytocin augmentation, the ED90 is 2.99 units.431 The ED90 of an oxytocininfusion in elective cesarean delivery patients is estimated to be 0.29 unit/min (95% CI, 0.15 to 0.43).432 Women undergoing intrapartum cesarean delivery after exposure to exogenous oxytocin during labor require higher infusion rates (ED90 0.74 units/min, 95% CI, 0.56 to 0.93).433

Women receiving oxytocin augmentation for labor have greater blood loss despite higher oxytocin doses; this appears to originate from signal attenuation and desensitization of the oxytocin receptors in a time- and concentration-dependent manner.434–437 Continued high-dose oxytocin exposure in the postpartum period can lead to acute receptor desensitization and render the myometrium less responsive to additional oxytocin but not to other uterotonic agents.437 Pregnancy causes a 180-fold increase in the concentration of oxytocin receptors, with a significant proportion of this increase occurring just before the onset of labor438; this change in receptor number may have relevance to parturients who are delivering preterm infants.

Postpartum Hemorrhage

Postpartum hemorrhage (PPH) is a major cause of maternal mortality, causing an estimated 140,000 deaths worldwide annually.14 Studies have reported recent increases in the incidence of PPH in developed countries, including an increase of 27.5% between 1995–2004 to 2.9% of all deliveries in the US, and an increase from 4.1% in 1991 to 5.1% in 2004 in Canada, a 23% increase.15,16 PPH is generally defined as blood loss >500 ml for vaginal delivery and >1,000 ml for cesarean delivery, although accurate estimation of blood loss at delivery and subsequent ascertainment of PPH can be challenging.13 The majority of cases of PPH can be prevented through the routine application of ‘active management of the third stage’ (AMTS). This approach consists of a package of interventions including administration of prophylactic uterotonic agents with or immediately after delivery of the baby, early clamping and cutting of the umbilical cord, controlled traction to deliver the placenta, and uterine massage after delivery of the placenta (where appropriate).17 AMTS has been compared with expectant management in several randomized, controlled trials, and the results have been summarized in a meta-analysis.18 AMTS is associated with statistically and clinically significant reductions in a number of indicators of blood loss including PPH >500 ml, PPH >1,000 ml, maternal hemoglobin <90 g/l, and blood transfusion. Benefits were observed both among unselected populations and populations at low risk of PPH. Despite the evidence in favor of AMTS for reduction of postpartum hemorrhage, its adoption varies worldwide.19

I. EPIDEMIOLOGY AND RISK FACTORS: GENERAL

PPH has been defined as more than 500 ml of blood loss in the first 24 hours after vaginal delivery, with more after cesarean delivery. A loss of 1000 ml, often described as severe, is recognized as clinically relevant. Definitions of PPH useful for research include a 10% decline in hematocrit, change in vital signs, or need for transfusion, though these all reflect recognition after the fact.6 Estimating blood loss has been shown to be inaccurate, especially when there is a high-volume loss.7 Depending on the definition used and the population studied, the incidence of PPH ranges from 3% to 18%.8 According to expert consensus from the World Health Organization, PPH occurs in 10.5% of live births globally, with a case fatality rate of 1%.1 The incidence of severe blood loss in developed nations remains at 3%, even with most effective management strategies.4,5 Risk factors for PPH include, but are not limited to, prolonged third stage, prior PPH, multiple pregnancy, episiotomies, and fetal macrosomia.9–11 It is important to remember that this is not always a predictable event, so one must be prepared to treat it at every delivery.3

Post-partum Care

PPH is increased in women with obesity, even after accounting for the increased incidence of Caesarean section [26,29]. This may be due to the association with macrosomia, or the large volume of distribution in obese women, which may reduce the efficacy of standard doses of uterotonic drugs [29]. The CMACE report showed that [4] the incidence of PPH was almost four times higher in obese women than in the general obstetric population. After controlling for significant risk factors (Caesarean section, pre-eclampsia and birth weight over 4000 g), each BMI unit increment in women with a BMI over 35 kg/m2 saw a 2.6% increase in the risk of PPH. Major PPH (>1000 ml) was seen in 5% [10]. Blomberg [61] reported an association between Class III obesity and atonic uterine haemorrhage over 1000 ml, following spontaneous vaginal delivery (AOR 1.23, 95% CI 1.04–1.45). This association was even more pronounced after operative vaginal delivery.

I. DEFINITION

Late postpartum bleeding (secondary postpartum hemorrhage) is defined as abnormal or excessive vaginal bleeding occurring anywhere from 24 hours until 12 weeks after delivery.1 This postpartum complication occurs most commonly as a result of uterine subinvolution, that is, failure of vessels at the former placental site to return to normal size or obliterate, or both.2 This may result from partial retention of placental tissue or blood clots or infection. Retained placental fragments that do not cause immediate postpartum hemorrhage undergo necrosis and fibrin deposition, leading to formation of a placental polyp. As the polyp eschar detaches from the myometrium, a brisk late postpartum hemorrhage may occur. Other less common causes include a ruptured varix, submucosal leiomyomata, genital tract hematomas, and clotting disorders.3

Definition

Postpartum hemorrhage can threaten the life of a healthy woman undergoing an otherwise uncomplicated vaginal delivery. It is the ultimate test of the obstetrical, anesthesia, nursing, and transfusion services. Processes should be in place in every obstetrical unit to clearly delineate the management of these women. Primary hemorrhage in the obstetric patient can be defined as any of the following within 24 hours of delivery: estimated blood loss greater than 1500 mL, 40 g/L or greater drop in the hemoglobin level, or the transfusion of 4 or more units of red blood cells.1 Other definitions for postpartum hemorrhage have been proposed. A common definition is blood loss in excess of 500 mL after vaginal birth or greater than 1000 mL after cesarean section. The difficulty with the latter definition is illustrated by studies assessing blood loss in the postpartum period, showing that mean blood loss after vaginal and cesarean deliveries is approximately 500 mL and 1000 mL, respectively.2,3 Clearly, the first definition more accurately identifies patients with a significant postpartum hemorrhage who are at risk for transfusion.