Vagina and Vaginal Outlet
Early in the puerperium, the vagina and its outlet form a capacious, smooth-walled passage that gradually diminishes in size but rarely returns to nulliparous dimensions. Rugae begin to reappear by the third week but are not as prominent as before. The hymen is represented by several small tags of tissue, which scar to form the myrtiform caruncles. Vaginal epithelium begins to proliferate by 4 to 6 weeks, usually coincidental with resumed ovarian estrogen production. Lacerations or stretching of the perineum during delivery may result in relaxation of the vaginal outlet. Some damage to the pelvic floor may be inevitable, and parturition predisposes to uterine prolapse as well as urinary and anal incontinence. This is a matter of great contemporaneous concern and is discussed in detail in Chapter 17, Laceration Risks and Morbidity.
The massively increased uterine blood flow necessary to maintain pregnancy is made possible by significant hypertrophy and remodeling of all pelvic vessels. After delivery, their caliber diminishes to approximately the size of the prepregnant state. Within the puerperal uterus, larger blood vessels become obliterated by hyaline changes, gradually resorbed, and replaced by smaller ones. Minor vestiges of the larger vessels, however, may persist for years.
Cervix and Lower Uterine Segment
During labor, the outer cervical margin, which corresponds to the external os, is usually lacerated, especially laterally. The cervical opening contracts slowly and for a few days immediately after labor readily admits two fingers. By the end of the first week, this opening narrows, the cervix thickens, and the endocervical canal reforms. The external os does not completely resume its pregravid appearance. It remains somewhat wider, and typically, bilateral depressions at the site of lacerations become permanent. These changes are characteristic of a parous cervix. The markedly thinned-out lower uterine segment contracts and retracts, but not as forcefully as the uterine corpus. During the next few weeks, the lower segment is converted from a clearly distinct substructure large enough to accommodate the fetal head, to a barely discernible uterine isthmus located between the corpus and internal os.
Cervical epithelium also undergoes considerable remodeling, and this actually may be salutary. For example, Ahdoot and colleagues (1998) found that about half of women showed regression of high-grade dysplasia following vaginal delivery.
Immediately after placental expulsion, the fundus of the contracted uterus lies slightly below the umbilicus. It consists mostly of myometrium covered by serosa and lined by basal decidua. The anterior and posterior walls, in close apposition, each measure 4 to 5 cm thick (Buhimschi and colleagues, 2003). Immediately postpartum, the uterus weighs approximately 1000 g. Because the blood vessels are compressed by the contracted myometrium, the uterus on section appears ischemic compared with the reddish-purple hyperemic pregnant organ.
During the puerperium, a truly remarkable tour de force of destruction or deconstruction begins. Two days after delivery, the uterus begins to involute, as shown in Figure 30-1, and at 1 week, it weighs about 500 g. By 2 weeks, it weighs about 300 g and has descended into the true pelvis. Around 4 weeks after delivery, it regains its previous nonpregnant size of 100 g or less. The total number of muscle cells probably does not decrease appreciably. Instead, the individual cells decrease markedly in size—from 500-800 μm by 5 to 10 μm at term to 50-90 μm by 2.5-5 μm postpartum. Involution of the connective tissue framework occurs equally rapidly.
Cross sections of uteri made at the level of the involuting placental site at varying times after delivery. p.p. = postpartum. (Redrawn from Williams, 1931.)
Because separation of the placenta and membranes involves the spongy layer, the decidua basalis is not sloughed. The decidua that remains has striking variations in thickness, has an irregular jagged appearance, and is infiltrated with blood, especially at the placental site (see Fig. 30-1).
It takes up to 5 weeks for the uterine cavity to regress to its nonpregnant state of a potential space. Tekay and Jouppila (1993) studied 42 normal women postpartum and identified fluid in the endometrial cavity in 78 percent at 2 weeks, 52 percent at 3 weeks, 30 percent at 4 weeks, and 10 percent at 5 weeks. Wachsberg and Kurtz (1992) followed 72 women and identified gas in the endometrial cavity in 19 percent within 3 days after delivery. In 7 percent, it was seen at 3 weeks. Finally, using Doppler ultrasound, Sohn and colleagues (1988) described continuously increasing uterine artery vascular resistance during the first 5 postpartum days.
In primiparas, the uterus tends to remain tonically contracted following delivery. However, in multiparas, it often contracts vigorously at intervals and gives rise to afterpains, which are similar to but milder than the pain of labor contractions. They are more pronounced as parity increases and worsen when the infant suckles, likely because of oxytocin release (Holdcroft and colleagues, 2003). Usually, afterpains decrease in intensity and become mild by the third day.
Early in the puerperium, sloughing of decidual tissue results in a vaginal discharge of variable quantity. The discharge is termed lochia and consists of erythrocytes, shredded decidua, epithelial cells, and bacteria. For the first few days after delivery, there is blood sufficient to color it red—lochia rubra. After 3 or 4 days, lochia becomes progressively pale in color—lochia serosa. After about the 10th day, because of an admixture of leukocytes and reduced fluid content, lochia assumes a white or yellowish-white color—lochia alba. Lochia persists for up to 4 to 8 weeks after delivery (Visness and co-workers, 1997).
Within 2 or 3 days after delivery, the remaining decidua becomes differentiated into two layers. The superficial layer becomes necrotic and is sloughed in the lochia. The basal layer adjacent to the myometrium remains intact and is the source of new endometrium. The endometrium arises from proliferation of the endometrial glandular remnants and the stroma of the interglandular connective tissue.
Endometrial regeneration is rapid, except at the placental site. Within a week or so, the free surface becomes covered by epithelium, and Sharman (1953) identified fully restored endometrium in all biopsy specimens obtained from the 16th day onward. Histological endometritis is part of the normal reparative process. Moreover, microscopic inflammatory changes characteristic of acute salpingitis are seen in almost half of postpartum women between 5 and 15 days. However, these do not reflect infection (Andrews, 1951).
This term describes an arrest or a retardation of involution. It is accompanied by prolongation of lochial discharge and irregular or excessive uterine bleeding, which sometimes may be profuse. On bimanual examination, the uterus is larger and softer than would be expected. Both retention of placental fragments and pelvic infection may cause subinvolution. Ergonovine or methylergonovine (Methergine), 0.2 mg every 3 to 4 hours for 24 to 48 hours, is recommended by some for subinvolution, but its efficacy is questionable. On the other hand, bacterial metritis responds to oral antimicrobial therapy. Wager and colleagues (1980) reported that almost a third of cases of late postpartum uterine infection are caused by Chlamydia trachomatis. Thus, azithromycin or doxycycline therapy is appropriate empirical therapy.
Andrew and colleagues (1989) described 25 cases of hemorrhage between 7 and 40 days postpartum associated with noninvoluted uteroplacental arteries. These abnormal arteries were filled with thrombi and lacked an endothelial lining. Perivascular trophoblasts were also identified in the vessel walls. They postulated that subinvolution, at least with regard to placental vessels, may represent an aberrant interaction between uterine cells and trophoblast.
Placental Site Involution
Complete extrusion of the placental site takes up to 6 weeks (Williams, 1931). When this process is defective, late-onset puerperal hemorrhage may ensue. Immediately after delivery, the placental site is approximately the size of the palm, but it rapidly decreases thereafter. Within hours of delivery, the placental site normally consists of many thrombosed vessels that ultimately undergo organization (see Fig. 30-1). By the end of the second week, it is 3 to 4 cm in diameter.
Williams (1931) described placental site involution as a process of exfoliation, which is in great part brought about by the undermining of the implantation site by growth of endometrial tissue. Thus, involution is not simply absorption in situ. Exfoliation consists of both extension and “downgrowth” of endometrium from the margins of the placental site, as well as development of endometrial tissue from the glands and stroma left deep in the decidua basalis after placental separation. Anderson and Davis (1968) concluded that placental site exfoliation results from sloughing of infarcted and necrotic superficial tissues followed by a remodeling process.
Late Postpartum Hemorrhage
The American College of Obstetricians and Gynecologists (2006) defines secondary postpartum hemorrhage as bleeding 24 hours to 12 weeks after delivery. Clinically worrisome uterine hemorrhage develops within 1 to 2 weeks in perhaps 1 percent of women. Such bleeding most often is the result of abnormal involution of the placental site. It occasionally is caused by retention of a placental fragment. Usually the retained piece undergoes necrosis with deposition of fibrin and may eventually form a so-called placental polyp. As the eschar of the polyp detaches from the myometrium, hemorrhage may be brisk. Demers (2005) and Salman (2008) and their associates have described delayed postpartum hemorrhage caused by von Willebrand disease (see Chap. 51, von Willebrand Disease).
Because few women with delayed hemorrhage have retained placental fragments, we do not routinely perform curettage. Lee and associates (1981) studied 27 women with significant bleeding after the first postpartum day. In 20, sonographic evaluation revealed an empty uterus, and only one woman of the 27 had retained placental tissue. Importantly, in some with delayed hemorrhage, curettage will worsen bleeding by avulsing part of the implantation site. Thus, in a stable patient, if sonographic examination shows an empty cavity, then oxytocin, ergonovine, methylergonovine, or a prostaglandin analog is given. Antimicrobials are added if uterine infection is suspected. If large clots are seen in the uterine cavity with sonography, then gentle suction curettage is considered. Otherwise curettage is carried out only if appreciable bleeding persists or recurs after medical management.
Bladder trauma is associated most closely with the length of labor and thus to some degree is a normal accompaniment of vaginal delivery. Funnell and associates (1954) used cystoscopy immediately postpartum and described varying degrees of submucosal hemorrhage and edema. Postpartum, the bladder has an increased capacity and a relative insensitivity to intravesical pressure. Thus, overdistension, incomplete emptying, and excessive residual urine are common. Their management is discussed in Bladder Function.
The dilated ureters and renal pelves return to their prepregnant state over the course of 2 to 8 weeks after delivery (see Chap. 5, Urinary System). Urinary tract infection is of concern because residual urine and bacteriuria in a traumatized bladder, coupled with a dilated collecting system, are conducive to infection.
Urinary incontinence in the first few days postpartum is uncommon. That said, there is increasing attention to the potential for the development of urinary incontinence subsequent to pregnancy. Recent and ongoing evaluations have focused on the effect of delivery on urinary and anal incontinence as well as pelvic organ prolapse. These long-term effects are complex in origin and are related to numerous factors that may cause neuromuscular damage. For example, MacArthur and colleagues (2006) found that 14 percent of parous women who had delivered exclusively by cesarean reported incontinence when monitored long-term. Risks of incontinence from vaginal, perineal, and anal sphincter lacerations and from episiotomy are considered in detail in Chapter 17, Episiotomy. Importantly, the debate concerning avoidance of such injuries by elective primary cesarean delivery was addressed in detail by a National Institutes of Health (NIH) sponsored State-of-the-Science Conference in March 2006 (see Chap. 25, Patient Choice in Cesarean Delivery). Chiarelli and Cockburn (2002) reported on a randomized trial to reduce the prevalence and severity of urinary incontinence. They found that multifaceted intervention that included pelvic floor exercises was effective.
Peritoneum and Abdominal Wall
The broad and round ligaments require considerable time to recover from the stretching and loosening that occur during pregnancy. As a result of ruptured elastic fibers in the skin and prolonged distension caused by the pregnant uterus, the abdominal wall remains soft and flaccid. Several weeks are required for these structures to return to normal. Recovery is aided by exercise. Except for silvery striae, the abdominal wall usually resumes its prepregnancy appearance. When muscles remain atonic, however, the abdominal wall also remains lax. Marked separation of the rectus muscles—diastasis recti—may result.
Marked leukocytosis and thrombocytosis may occur during and after labor. The white blood cell count sometimes reaches 30,000/μL, with the increase predominantly due to granulocytes. There is a relative lymphopenia and an absolute eosinopenia. Normally, during the first few postpartum days, hemoglobin concentration and hematocrit fluctuate moderately. If they fall much below the levels present just prior to labor, a considerable amount of blood has been lost (see Chap. 35, Causes of Obstetrical Hemorrhage).
Although not extensively studied, in most women, blood volume has nearly returned to its nonpregnant level by 1 week after delivery. Cardiac output usually remains elevated for 24 to 48 hours postpartum and declines to nonpregnant values by 10 days (Robson and colleagues, 1987). Heart rate changes follow this pattern. Systemic vascular resistance follows inversely. It remains in the lower range characteristic of pregnancy for 2 days postpartum and then begins to steadily increase to normal nonpregnant values.
Pregnancy-induced changes in blood coagulation factors persist for variable periods during the puerperium. Elevation of plasma fibrinogen is maintained at least through the first week, and hence, so is the sedimentation rate.
Normal pregnancy is associated with an appreciable increase in extracellular water, and postpartum diuresis is a physiological reversal of this process. This regularly occurs between the second and fifth days and corresponds with loss of residual pregnancy hypervolemia. In preeclampsia, both retention of fluid antepartum and diuresis postpartum may be greatly increased (see Chap. 34, Fluid and Electrolyte Changes).
In addition to the loss of 5 to 6 kg due to uterine evacuation and normal blood loss, there is usually a further decrease of 2 to 3 kg through diuresis. Chesley and co-workers (1959) demonstrated a decrease in sodium space of about 2 L during the first week postpartum. According to Schauberger and co-investigators (1992), women approach their self-reported prepregnancy weight 6 months after delivery but still retain an average surplus of 1.4 kg (3 lb). Indigent women are more likely to retain weight gained during pregnancy (Olson and associates, 2003).