The uterus increases markedly in size and weight during pregnancy (approximately 10 times the nonpregnant weight, reaching a crude weight of 1000 g) but involutes rapidly after delivery to the nonpregnant weight of 50–100 g. The gross anatomic and histologic characteristics of this process have been studied through autopsy, hysterectomy, and endometrial specimens. In addition, the decrease in size of the uterus and cervix has been demonstrated by magnetic resonance imaging, sonography, and computed tomography.
Immediately after delivery, the uterus weighs approximately 1 kg, and its size approximates that of a 20-week pregnancy (at the level of the umbilicus). At the end of the first postpartum week, it normally will have decreased to the size of a 12-week gestation and is palpable at the symphysis pubis (Fig. 10–1). In case of abnormal uterine involution, infection and retained products of conception should be ruled out.
Involutional changes in the height of the fundus and the size of the uterus during the first 10 days postpartum.
Myometrial contractions, or afterpains, assist in involution. These contractions occur during the first 2–3 days of the puerperium and produce more discomfort in multiparas than in primiparas. Such pains are accentuated during nursing as a result of oxytocin release from the posterior pituitary. During the first 12 hours postpartum, uterine contractions are regular, strong, and coordinated (Fig. 10–2). The intensity, frequency, and regularity of contractions decrease after the first postpartum day as involutional changes proceed. Uterine involution is nearly complete by 6 weeks, at which time the organ weighs less than 100 g. The increase in the amount of connective tissue, elastin in the myometrium and blood vessels, and the increase in numbers of cells are permanent to some degree, so the uterus is slightly larger after pregnancy.
Uterine activity during the immediate puerperium (left) and at 20 hours postpartum (right).
Changes in the Placental Implantation Site
After delivery of the placenta, there is immediate contraction of the placental site to a size less than half the diameter of the original placenta. This contraction, as well as arterial smooth muscle contractions, leads to hemostasis. Involution occurs by means of the extension and down growth of marginal endometrium and by endometrial regeneration from the glands and stroma in the decidua basalis.
By day 16, placental site, endometrial, and superficial myometrial infiltrates of granulocytes and mononuclear cells are seen. Regeneration of endometrial glands and endometrial stroma has also begun. Endometrial regeneration at the placental site is not complete until 6 weeks postpartum. In the disorder termed subinvolution of the placental site, complete obliteration of the vessels in the placental site fails to occur. Patients with this condition have persistent lochia and are subject to brisk hemorrhagic episodes. This condition usually can be treated with uterotonics. In the rare event that uterine curettage is performed, partly obliterated hyalinized vessels can be seen on the histologic specimen.
Normal postpartum discharge begins as lochia rubra, containing blood, shreds of tissue, and decidua. The amount of discharge rapidly tapers and changes to a reddish-brown color over the next 3–4 days. It is termed lochia serosa when it becomes serous to mucopurulent, paler, and often malodorous. During the second or third postpartum week, the lochia alba becomes thicker, mucoid, and yellowish-white, coincident with a predominance of leukocytes and degenerated decidual cells. Typically during the fifth or sixth week postpartum, the lochial secretions cease as healing nears completion.
Changes in the Cervix, Vagina, & Muscular Walls of the Pelvic Organs
The cervix gradually closes during the puerperium; at the end of the first week, it is little more than 1 cm dilated. The external os is converted into a transverse slit, thus distinguishing the parous woman who delivered vaginally from the nulliparous woman or from one who delivered by caesarean section. Cervical lacerations heal in most uncomplicated cases, but the continuity of the cervix may not be restored, so the site of the tear may remain as a scarred notch.
After vaginal delivery, the overdistended and smooth-walled vagina gradually returns to its antepartum condition by about the third week. Thickening of the mucosa, cervical mucus production, and other estrogenic changes may be delayed in a lactating woman. The torn hymen heals in the form of fibrosed nodules of mucosa, the carunculae myrtiformes.
Two weeks after delivery, the fallopian tube reflects a hypoestrogenic state marked by atrophy of the epithelium. Fallopian tubes removed between postpartum days 5 and 15 demonstrate acute inflammatory changes that have not been correlated with subsequent puerperal fever or salpingitis. Normal changes in the pelvis after uncomplicated term vaginal delivery include widening of the symphysis and sacroiliac joints. Gas may be seen by ultrasonography in the endometrial cavity a few days after an uncomplicated vaginal delivery. This sonographic observation is more often seen after caesarean section and after manual evacuation of placenta, and it does not necessarily indicate the presence of endometritis. Ovulation occurs as early as 27 days after delivery, with a mean time of 70–75 days in nonlactating women and 6 months in lactating women. In lactating women the duration of anovulation ultimately depends on the frequency of breastfeeding, duration of each feed, and proportion of supplementary feeds. Ovulation suppression is due to high prolactin levels, which remain elevated until approximately 3 weeks after delivery in nonlactating women and 6 weeks in lactating women. However, estrogen levels fall immediately after delivery in all mothers and remain suppressed in lactating mothers. Menstruation returns as soon as 7 weeks in 70% and by 12 weeks in all nonlactating mothers, and as late as 36 months in 70% of breastfeeding mothers.
The voluntary muscles of the pelvic floor and the pelvic supports gradually regain their tone during the puerperium. Tearing or overstretching of the musculature or fascia at the time of delivery predisposes to genital prolapse and genital hernias (cystocele, rectocele, and enterocele). Overdistention of the abdominal wall during pregnancy may result in rupture of the elastic fibers of the cutis, persistent striae, and diastasis of the rectus muscles. Involution of the abdominal musculature may require 6–7 weeks, and vigorous exercise is not recommended until after that time.
In the immediate postpartum period, the bladder mucosa is edematous as a result of labor and delivery. In addition, bladder capacity is increased. Overdistention and incomplete emptying of the bladder with the presence of residual urine are therefore common problems. The decreased bladder sensibility induced by intrapartum regional analgesia may lead to postpartum urinary retention; however, it is reversible and usually not detrimental to later urinary function. Nearly 50% of patients have a mild proteinuria for 1–2 days after delivery. Ultrasonographic examination demonstrates resolution of collecting system dilatation by 6 weeks postpartum in most women. Urinary stasis, however, may persist in more than 50% of women at 12 weeks postpartum. The incidence of urinary tract infection is generally higher in women with persistent dilatation. Significant renal enlargement may persist for many weeks postpartum.
Pregnancy is accompanied by an estimated increase of approximately 50% in the glomerular filtration rate. These values return to normal or less than normal during the eighth week of the puerperium. Endogenous creatinine clearance similarly returns to normal by 8 weeks. Renal plasma flow, which increased during pregnancy by 25% in the first trimester, falls in the third trimester and continues to fall to below normal levels for up to 24 months. Normal levels return slowly over 50–60 weeks. The glucosuria induced by pregnancy disappears. The blood urea nitrogen rises during the puerperium; at the end of the first week postpartum, values of 20 mg/dL are reached, compared with 15 mg/dL in the late third trimester.
Fluid Balance & Electrolytes
An average decrease in maternal weight of 10–13 lb occurs intrapartum and immediately postpartum due to the loss of amniotic fluid and blood as well as delivery of the infant and placenta. The average patient may lose an additional 4 kg (9 lb) during the puerperium and over the next 6 months as a result of excretion of the fluids and electrolytes accumulated during pregnancy. Contrary to widespread belief, breastfeeding has minimal effects on hastening weight loss postpartum. The magnitude of weight gain during pregnancy has impact on the postpartum weight retention. Women who gain more weight than the recommended range during the pregnancy tend to be heavier at 3 years postpartum than women who gained weight within recommended range during pregnancy, and this applies to both obese and nonobese patients.
There is an average net fluid loss of at least 2 L during the first week postpartum and an additional loss of approximately 1.5 L during the next 5 weeks. The water loss in the first week postpartum represents a loss of extracellular fluid. A negative balance must be expected of slightly more than 100 mEq of chloride per kilogram of body weight lost in the early puerperium. This negative balance probably is attributable to the discharge of maternal extracellular fluid. The puerperal losses of salt and water are generally larger in women with preeclampsia or eclampsia.
The changes occurring in serum electrolytes during the puerperium indicate a general increase in the numbers of cations and anions compared with antepartum values. Although total exchangeable sodium decreases during the puerperium, the relative decrease in body water exceeds the sodium loss. The diminished aldosterone antagonism due to falling plasma progesterone concentrations may partially explain the rapid rise in serum sodium. Cellular breakdown due to tissue involution may contribute to the rise in plasma potassium concentration noted postpartum. The mean increase in cations, chiefly sodium, amounts to 4.7 mEq/L, with an equal increase in anions. Consequently, the plasma osmolality rises by 7 mOsm/L at the end of the first week postpartum. In keeping with the chloride shift, there is a tendency for the serum chloride concentration to decrease slightly postpartum as serum bicarbonate concentration increases.
Metabolic & Chemical Changes
Total fatty acids and nonesterified fatty acids return to nonpregnant levels on about the second day of the puerperium. Both cholesterol and triglyceride concentrations decrease significantly within 24 hours after delivery, and this change is reflected in all lipoprotein fractions. Plasma triglycerides continue to fall and approach nonpregnant values 6–7 weeks postpartum. By comparison, the decrease in plasma cholesterol levels is slower; low-density lipoprotein cholesterol remains above nonpregnant levels for at least 7 weeks postpartum. Lactation does not influence lipid levels, but, in contrast to pregnancy, the postpartum hyperlipidemia is sensitive to dietary manipulation.
During the early puerperium, blood glucose concentrations (both fasting and postprandial) tend to fall below the values seen during pregnancy and delivery. This fall is most marked on the second and third postpartum days. Accordingly, the insulin requirements of diabetic patients are lower. Reliable indications of the insulin sensitivity and the blood glucose concentrations characteristic of the nonpregnant state can be demonstrated only after the first week postpartum. Thus a glucose tolerance test performed in the early puerperium may be interpreted erroneously if nonpuerperal standards are applied to the results.
The concentration of free plasma amino acids increases postpartum. Normal nonpregnant values are regained rapidly on the second or third postpartum day and are presumably a result of reduced utilization and an elevation in the renal threshold.
The production of both prostacyclin (prostaglandin I2 [PGI2]), an inhibitor of platelet aggregation, and thromboxane A2, an inducer of platelet aggregation and a vasoconstrictor, is increased during pregnancy and the puerperium. Possibly, the balance between thromboxane A2 and PGI2 is shifted to the side of thromboxane A2 dominance during the puerperium because platelet reactivity is increased at this time. Rapid and dramatic changes in the coagulation and fibrinolytic systems occur after delivery (Table 10–1). A decrease in the fibrinogen concentration begins during labor and reaches its lowest point during the first day postpartum. Thereafter, rising plasma fibrinogen levels reach prelabor values by the third or fifth day of the puerperium. This secondary peak in fibrinogen activity is maintained until the second postpartum week, after which the level of activity slowly returns to normal nonpregnant levels during the following 7–10 days. A similar pattern occurs with respect to factor VIII and plasminogen. Circulating levels of antithrombin III are decreased in the third trimester of pregnancy. Patients with a congenital deficiency of antithrombin III (an endogenous inhibitor of factor X) have recurrent venous thromboembolic disease, and a low level of this factor has been associated with a hypercoagulable state.
Table 10–1. Changes in Blood Coagulation and Fibrinolysis during the Puerperium. ||Download (.pdf)
Table 10–1. Changes in Blood Coagulation and Fibrinolysis during the Puerperium.
|1 Hour||1 Day||3–5 Days||1st Week||2nd Week|
|Factors II, VII, X||↓||↓||↓↓||↓↓|
|Fibrin split products||↑||↑↑||↑↑|
The fibrinolytic activity of maternal plasma is greatly reduced during the last months of pregnancy but increases rapidly after delivery. In the first few hours postpartum, an increase in tissue plasminogen activator (t-PA) activity develops, together with a slight prolongation of the thrombin time, a decrease in plasminogen activator inhibitors, and a significant increase in fibrin split products. Protein C is an important coagulation inhibitor that requires the nonenzymatic cofactor protein S (which exists as a free protein and as a complex) for its activity. The level of protein S, both total and free, increases on the first day after delivery and gradually returns to normal levels after the first week postpartum.
The increased concentration of clotting factors normally seen during pregnancy can be viewed as important reserve to compensate for the rapid consumption of these factors during delivery and in promoting hemostasis after parturition. Nonetheless, extensive activation of clotting factors, together with immobility, sepsis, or trauma during delivery, may set the stage for later thromboembolic complications (see Chapter 27). The secondary increase in fibrinogen, factor VIII, or platelets (which remain well above nonpregnant values in the first week postpartum) also predisposes to thrombosis during the puerperium. The abrupt return of normal fibrinolytic activity after delivery may be a protective mechanism to combat this hazard. A small percentage of puerperal women who show a diminished ability to activate the fibrinolytic system appear to be at high risk for the development of postpartum thromboembolic complications.
The total blood volume normally decreases from the antepartum value of 5–6 L to the nonpregnant value of 4 L by the third week after delivery. One-third of this reduction occurs during delivery and soon afterward, and a similar amount is lost by the end of the first postpartum week. Additional variation occurs with lactation. The volume expansion with increased water retention in the extracellular space during pregnancy may be viewed as a protective mechanism that allows most women to tolerate considerable blood loss during parturition. Normal vaginal delivery of a single fetus entails an average blood loss of approximately 400 mL, whereas caesarean section leads to a blood loss of nearly 1 L. If total hysterectomy is performed in addition to caesarean section delivery, the mean blood loss increases to approximately 1500 mL. Delivery of twins and triplets entails blood losses similar to those of operative delivery, but a compensatory increase in maternal plasma volume and red blood cell mass may be exacerbated in mothers carrying multiple gestations.
Dramatic and rapid readjustments occur in the maternal vasculature after delivery so that the response to blood loss during the early puerperium is different from that occurring in the nonpregnant woman. Delivery leads to obliteration of the low-resistance uteroplacental circulation and results in a 10–15% reduction in the size of the maternal vascular bed. Loss of placental endocrine function also removes a stimulus to vasodilatation.
A declining blood volume with a rise in hematocrit is usually seen 3–7 days after vaginal delivery (Fig. 10–3). In contrast, serial studies of patients after caesarean section indicate a more rapid decline in blood volume and hematocrit and a tendency for the hematocrit to stabilize or even decline in the early puerperium. Hemoconcentration occurs if the loss of red cells is less than the reduction in vascular capacity. Hemodilution takes place in patients who lose 20% or more of their circulating blood volume at delivery. In patients with preeclampsia–eclampsia, resolution of peripheral vasoconstriction and mobilization of excess extracellular fluid may lead to significant expansion of vascular volume by the third postpartum day. Plasma atrial natriuretic peptide levels nearly double during the first days postpartum in response to atrial stretch caused by blood volume expansion and may have relevance for postpartum natriuresis and diuresis. Occasionally, a patient sustains minimal blood loss at delivery. In such a patient, marked hemoconcentration may occur in the puerperium, especially if there has been a preexisting polycythemia or a considerable increase in the red cell mass during pregnancy.
Postpartum changes in hematocrit and blood volume in patients delivered vaginally and by caesarean section. Values are expressed as the percentage change from the predelivery hematocrit or blood volume. (Data from Ueland K, et al. Maternal cardiovascular dynamics. 1. Cesarean section under subarachnoid block anesthesia. Am J Obstet Gynecol 1968;100:42; PMID 5634434; and Ueland K, Hansen J. Maternal cardiovascular dynamics. 3. Labor and delivery under local and caudal analgesia. Am J Obstet Gynecol 1969;103: 8;[PubMed: 5761783].)
The red cell mass increases by about 25% during pregnancy, whereas the average red cell loss at delivery is approximately 14%. Thus the mean postpartum red cell mass level should be about 15% above nonpregnant values. The sudden loss of blood at delivery, however, leads to a rapid and short-lived reticulocytosis (with a peak on the fourth postpartum day) and moderately elevated erythropoietin levels during the first week postpartum.
The bone marrow in pregnancy and in the early puerperium is hyperactive and capable of delivering a large number of young cells to the peripheral blood. Prolactin may play a minor role in bone marrow stimulation.
A striking leukocytosis occurs during labor and extends into the early puerperium. In the immediate puerperium, the white blood cell count may be as high as 25,000/mL, with an increased percentage of granulocytes. The stimulus for this leukocytosis is not known, but it probably represents a release of sequestered cells in response to the stress of labor.
The serum iron level is decreased and the plasma iron turnover is increased between the third and fifth days of the puerperium. Normal values are regained by the second week postpartum. The shorter duration of ferrokinetic changes in puerperal women compared with the duration of changes in nonpregnant women who have had phlebotomy is due to the increased erythroid marrow activity and the circulatory changes described previously.
Most women who sustain an average blood loss at delivery and who received iron supplementation during pregnancy show a relative erythrocytosis during the second week postpartum. Because there is no evidence of increased red cell destruction during the puerperium, any red cells gained during pregnancy will disappear gradually according to their normal life span. A moderate excess of red blood cells after delivery, therefore, may lead to an increase in iron stores. Iron supplementation is not necessary for normal postpartum women if the hematocrit or hemoglobin concentration 5–7 days after delivery is equal to or greater than a normal predelivery value. In the late puerperium, there is a gradual decrease in the red cell mass to nonpregnant levels as the rate of erythropoiesis returns to normal.
The hemodynamic adjustments in the puerperium depend largely on the conduct of labor and delivery (eg, maternal position, method of delivery, mode of anesthesia or analgesia, and blood loss). Cardiac output increases progressively during labor in patients who have received only local anesthesia. The increase in cardiac output peaks immediately after delivery, at which time it is approximately 80% above the prelabor value. During a uterine contraction there is a rise in central venous pressure, arterial pressure, and stroke volume—and, in the absence of pain and anxiety, a reflex decrease in the pulse rate. These changes are magnified in the supine position. Only minimal changes occur in the lateral recumbent position because of unimpaired venous return and absence of aortoiliac compression by the contracting uterus (Poseiro's effect). Epidural anesthesia can interfere with the hemodynamic change by attenuating the progressive rise in cardiac output during labor and reduces the absolute increase observed immediately after delivery, probably by limiting pain, anxiety, and oxygen consumption.
Although major hemodynamic readjustments occur during the period immediately after delivery, there is a return to nonpregnant conditions in the early puerperium. A trend for normal women to increase their blood pressure slightly in the first 5 days postpartum reflects an increased uterine vascular resistance and a temporary surplus in plasma volume. A small percentage will have diastolic blood pressures of 100 mm Hg. Cardiac output (measured by Doppler and cross-sectional echocardiography) declines 28% within 2 weeks postpartum from peak values observed at 38 weeks' gestation. This change is associated with a 20% reduction in stroke volume and a smaller decrease in myocardial contractility indices. Postpartum resolution of pregnancy-induced ventricular hypertrophy takes longer than the functional postpartum changes (Fig. 10–4). In fact, limited data support a slow return of cardiac hemodynamics to prepregnancy levels over a 1-year period. There are no hemodynamic differences between lactating and nonlactating mothers.
Changes in cardiac output, stroke volume, and heart rate during the puerperium after normal delivery. (Reproduced, with permission, from Hunter S, Robson SC. Adaptation of the maternal heart in pregnancy. Br Heart J 1992;68:540.)
The pulmonary functions that change most rapidly are those influenced by alterations in abdominal contents and thoracic cage capacity. Lung volumes change in the puerperium and gradually return to the nonpregnant states. The total lung capacity increases after delivery due to decreased intra-abdominal pressure on the diaphragm. An increase in resting ventilation and oxygen consumption and a less efficient response to exercise may persist during the early postpartum weeks. Comparisons of aerobic capacity before pregnancy and again postpartum indicate that lack of activity and weight gain contribute to a generalized detraining effect 4–8 weeks postpartum.
Changes in acid–base status generally parallel changes in respiratory function. The state of pregnancy is characterized by respiratory alkalosis and compensated metabolic acidosis, whereas labor represents a transitional period. A significant hypocapnia (<30 mm Hg), a rise in blood lactate, and a fall in pH are first noted at the end of the first stage of labor and extend into the puerperium. Within a few days, a rise toward the normal nonpregnant values of PCO2 (35–40 mm Hg) occurs. Progesterone influences the rate of ventilation by means of a central effect, and rapidly decreasing levels of this hormone are largely responsible for the increased PCO2 seen in the first week postpartum. An increase in base excess and plasma bicarbonate accompanies the relative postpartum hypercapnia. A gradual increase in pH and base excess occurs until normal levels are reached at approximately 3 weeks postpartum.
The resting arterial PO2 and oxygen saturation during pregnancy are higher than those in nonpregnant women. During labor, the oxygen saturation may be depressed, especially in the supine position, probably as a result of a decrease in cardiac output and a relative increase in the amount of intrapulmonary shunting. However, a rise in the arterial oxygen saturation to 95% is noted during the first postpartum day. An apparent oxygen debt incurred during labor extends into the immediate puerperium and appears to depend on the length and severity of the second stage of labor. Many investigators have commented on the continued elevation of the basal metabolic rate for a period of 7–14 days after delivery. The increased resting oxygen consumption in the early puerperium has been attributed to mild anemia, lactation, and psychologic factors.
The plasma levels of placental hormones decline rapidly after delivery. Human placental lactogen has a half-life of 20 minutes and reaches undetectable levels in maternal plasma during the first day after delivery. Human chorionic gonadotropin (hCG) has a mean half-life of approximately 9 hours. The concentration of hCG in maternal plasma falls below 1000 mU/mL within 48–96 hours postpartum and falls below 100 mU/mL by the seventh day. Highly specific and sensitive radioimmunoassay for the subunit of hCG indicates virtual disappearance of hCG from maternal plasma between the 11th and 16th days after normal delivery. The regressive pattern of hCG activity is slower after first-trimester abortion than it is after term delivery and even more prolonged in patients who have undergone suction curettage for molar pregnancy.
Within 3 hours after removal of the placenta, the plasma concentration of 17β-estradiol falls to 10% of the antepartum value. The lowest levels are reached by the seventh postpartum day. Plasma estrogens do not reach follicular phase levels (>50 pg/mL) until 19–21 days postpartum in nonlactating women. The return to normal plasma levels of estrogens is delayed in lactating women. Lactating women who resume spontaneous menses achieve follicular-phase estradiol levels (>50 pg/mL) during the first 60–80 days postpartum. Lactating amenorrheic persons are markedly hypoestrogenic (plasma estradiol <10 pg/mL) during the first 180 days postpartum. The onset of breast engorgement on days 3–4 of the puerperium coincides with a significant fall in estrogen levels and supports the view that high estrogen levels suppress lactation.
The metabolic clearance rate of progesterone is high, and, as with estradiol, the half-life is calculated in minutes. By the third day of the puerperium, the plasma progesterone concentrations are below luteal phase levels (<1 ng/mL).
Prolactin levels in maternal blood rise throughout pregnancy to reach concentrations of 200 ng/mL or more. After delivery, prolactin declines in erratic fashion over a period of 2 weeks to the nongravid range in nonlactating women (Fig. 10–5). In women who are breastfeeding, basal concentrations of prolactin remain above the nongravid range and increase dramatically in response to suckling. As lactation progresses, the amount of prolactin released with each suckling episode declines. If breastfeeding occurs only 1–3 times each day, serum prolactin levels return to normal basal values within 6 months postpartum; if suckling takes place more than 6 times each day, high basal concentrations of prolactin will persist for more than 1 year. The diurnal rhythm of peripheral prolactin concentrations (a daytime nadir followed by a nighttime peak) is abolished during late pregnancy but is re-established within 1 week postpartum in non-nursing women.
Serum concentrations of prolactin, follicle-stimulating hormone (FSH), luteinizing hormone (LH), estradiol, and progesterone in a lactating and nonlactating woman during the puerperium. The hatched bars for the prolactin data represent the normal nongravid range. To convert the FSH and LH to milli-international units per milliliter, divide the FSH values by 2 and multiply the LH values by 4.5. (Reproduced, with permission, from Reyes FI, Winter JS, Faiman C. Pituitary-ovarian interrelationships during the puerperium. Am J Obstet Gynecol 1972;114:589.)
Serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) concentrations are very low in all women during the first 10–12 days postpartum, whether or not they lactate. The levels increase over the subsequent days and reach follicular-phase concentrations during the third week postpartum (Fig. 10–5). At this time, marked LH pulse amplification occurs during sleep but disappears as normal ovulatory cycles are established. In this respect, the transition from postpartum amenorrhea to cyclic ovulation is reminiscent of puberty, when gonadotropin secretion increases during sleep. There is a preferential release of FSH over LH postpartum during spontaneous recovery or after stimulation by exogenous gonadotropin-releasing hormone (GnRH). In the early puerperium, the pituitary is relatively refractory to GnRH, but 4–8 weeks postpartum, the response to GnRH is exaggerated. The low levels of FSH and LH postpartum are most likely related to insufficient endogenous GnRH secretion during pregnancy and the early puerperium, resulting in depletion of pituitary gonadotropin stores. The high estrogen and progesterone milieu of late pregnancy is associated with increased endogenous opioid activity, which may be responsible for suppression of GnRH activity in the puerperium. Resumption of FSH and LH secretion can be accelerated by administering a long-acting GnRH agonist during the first 10 days postpartum.
Because ovarian activity normally resumes upon weaning, either the suckling stimulus itself or the raised level of prolactin is responsible for suppression of pulsatile gonadotropin secretion. Hyperprolactinemia may not entirely account for the inhibition of gonadotropin secretion during lactation, as bromocriptine treatment abolishes the hyperprolactinemia of suckling but not the inhibition of gonadotropin secretion. Sensory inputs associated with suckling (if sufficiently intense), as well as oxytocin and endogenous opioids that are released during suckling, may affect the hypothalamic control of gonadotropin secretion, possibly by inhibiting the pulsatile secretion of GnRH. It appears that by 8 weeks after delivery, although ovarian activity still remains suppressed in fully breastfeeding women, pulsatile secretion of LH has resumed at a low and variable frequency in most women. However, the presence or absence of GnRH or LH pulses at 8 weeks does not predict the time of resumption of ovarian activity.
The time of appearance of the first ovulation is variable, and it is delayed by breastfeeding. Approximately 10–15% of non-nursing mothers ovulate by the time of the 6-week postpartum examination, and approximately 30% ovulate within 90 days postpartum. An abnormally short luteal phase is noted in 35% of first ovulatory cycles. The earliest reported time of ovulation as determined by endometrial biopsy is 33 days postpartum. Patients who have had a first-trimester abortion or ectopic pregnancy generally ovulate sooner after termination of pregnancy (as early as 14 days) than do women who deliver at term. Moreover, the majority of these women do ovulate before the first episode of postabortal bleeding—in contrast to women who have had a term pregnancy.
Endometrial biopsies in lactating women do not show a secretory pattern before the seventh postpartum week. Provided that nursing is in progress and that menstruation has not returned, ovulation before the tenth week postpartum is rare. In well-nourished women who breastfed for an extended period of time, fewer than 20% had ovulated by 6 months postpartum. Much of the variability in the resumption of menstruation and ovulation observed in lactating women may be due to individual differences in the strength of the suckling stimulus and to partial weaning (formula supplementation). This emphasizes the fact that suckling is not a reliable form of birth control. Because the period of lactational infertility is relatively short in Western societies, some form of contraception must be used if pregnancy is to be prevented. Among women who have unprotected intercourse only during lactational amenorrhea but adopt other contraceptive measures when they resume menstruation, only 2% will become pregnant during the first 6 months of amenorrhea. In underdeveloped countries, lactational amenorrhea and infertility may persist for 1–2 years owing to frequent suckling and poor maternal nutrition. When maternal dietary intake is improved, menstruation resumes at least 6 months earlier.
Progressive enlargement of the pituitary gland occurs during pregnancy, with a 30–100% increase in weight achieved at term. Magnetic resonance imaging shows a linear gain in pituitary gland height of approximately 0.08 mm/wk during pregnancy. An additional increase in size occurs during the first week postpartum. Beyond the first week postpartum, however, the pituitary gland returns rapidly to its normal size in both lactating and nonlactating women.
The physiologic hypertrophy of the pituitary gland is associated with an increase in the number of pituitary lactotroph cells at the expense of the somatotropic cell types. Thus growth hormone secretion is depressed during the second half of pregnancy and the early puerperium. Because levels of circulating insulin-like growth factor (IGF)-1 increase throughout pregnancy, a placental growth hormone has been postulated and recently identified. Maternal levels of IGF-1 correlate highly with this distinct placental growth hormone variant, but not with placental lactogen during pregnancy and in the immediate puerperium.
Late pregnancy and the early puerperium are also characterized by pituitary somatotroph hyporesponsiveness to growth hormone-releasing hormone and to insulin stimulation. Whatever the inhibitory mechanism may be (possibly increased somatostatin secretion), it persists during the early postpartum period.
The rapid disappearance of placental lactogen and the low levels of growth hormone after delivery lead to a relative deficiency of anti-insulin factors in the early puerperium. It is not surprising, therefore, that low fasting plasma glucose levels are noted at this time and that the insulin requirements of diabetic patients usually drop after delivery. Glucose tolerance tests performed in women with gestational diabetes demonstrate that only 30% have abnormal test results 3–5 days after delivery, and 20% have abnormal glucose tolerance at 6 weeks postpartum. Because the early puerperium represents a transitional period in carbohydrate metabolism, the results of glucose tolerance tests may be difficult to interpret.
Evaluation of thyroid function is also difficult in the period immediately after birth because of rapid fluctuations in many indices. Characteristically, the plasma thyroxine level and other indices of thyroid function are highest at delivery and in the first 12 hours thereafter. A decrease to antepartum values is seen on the third or fourth day after delivery. Reduced available estrogens postpartum lead to a subsequent decrease in circulating thyroxine-binding globulin and a gradual diminution in bound thyroid hormones in serum. Serum concentrations of thyroid-stimulating hormone (TSH) are not significantly different postpartum from those of the pregnant or nonpregnant state. Administration of thyroid-releasing hormone in the puerperium results in a normal increase in both TSH and prolactin, and the response is similar in lactating and nonlactating patients. Because pregnancy is associated with some immunosuppressive effects, hyperthyroidism or hypothyroidism may recur postpartum in autoimmune thyroid disease. Failure of lactation and prolonged disability may be the result of hypothyroidism postpartum. In Sheehan's syndrome of pituitary infarction, postpartum cachexia and myxedema are seen secondary to anterior hypophyseal insufficiency.
Maternal concentrations of total and unbound (free) plasma cortisol, adrenocorticotropic hormone (ACTH), immunoreactive corticotropin-releasing hormone (CRH), and β-endorphin rise progressively during pregnancy and increase further during labor. Plasma 17-hydroxycorticosteroid levels increase from a concentration of 4–14 μg/dL at 40 weeks' gestation. A 2- to 3-fold increase is seen during labor. ACTH, CRH, and β-endorphin decrease rapidly after delivery and return to nonpregnant levels within 24 hours. Prelabor cortisol values are regained on the first day postpartum, but a return to normal, nonpregnant cortisol and 17-hydroxycorticosteroid levels is not reached until the end of the first week postpartum.
Much of the rise in total cortisol (but not in the unbound fraction) can be explained by the parallel increase in corticosteroid-binding globulin (CBG) during pregnancy. Displacement of cortisol from CBG by high concentrations of progesterone cannot account for the increased free cortisol levels because saliva progesterone levels (a measure of the unbound hormone) do not fluctuate, whereas a normal diurnal rhythm of saliva cortisol is maintained during pregnancy and postpartum. An extrapituitary source of ACTH, a progesterone-modulated decrease in the hypothalamic–pituitary sensitivity to glucocorticoid feedback inhibition, and an extrahypothalamic (eg, placental) source of CRH have been suggested as explanations for elevated plasma ACTH levels and the inability of dexamethasone to completely suppress ACTH in pregnant women.
In the third trimester, the placenta produces large amounts of CRH, which is released into the maternal circulation and may contribute to the hypercortisolemia of pregnancy. Present evidence suggests that it stimulates the maternal pituitary to produce ACTH while desensitizing the pituitary to further acute stimulation with CRH. Maternal hypothalamic control of ACTH production is retained (perhaps mediated by vasopressin secretion); this permits a normal response to stress and a persistent diurnal rhythm.
Overall, it is most likely that under the influence of rising estrogens and progesterone, there is a resetting of the hypothalamic–pituitary sensitivity to cortisol feedback during pregnancy, which persists for several days postpartum. Several studies have suggested a relationship between peripartum alterations in maternal levels of cortisol and β-endorphin and the development of postnatal mood disturbances.
The excretion of urinary 17-ketosteroids is elevated in late pregnancy as a result of an increase in androgenic precursors from the fetoplacental unit and the ovary. An additional increase of 50% in excretion occurs during labor. Excretion of 17-ketosteroids returns to antepartum levels on the first day after delivery and to the nonpregnant range by the end of the first week. The mean levels of testosterone during the third trimester of pregnancy range from 3 to 7 times the mean values for nonpregnant women. The elevated levels of testosterone decrease after parturition parallel with the gradual fall in sex hormone-binding globulin (SHBG). Androstenedione, which is poorly bound to SHBG, falls rapidly to nonpregnant values by the third day postpartum. Conversely, the postpartum plasma concentration of dehydroepiandrosterone sulfate remains lower than that of nonpregnant women, because its metabolic clearance rate continues to be elevated in the early puerperium. Persistently elevated levels of 17-ketosteroids or androgens during the puerperium are an indication for investigation of ovarian abnormalities. Plasma renin and angiotensin II levels fall during the first 2 hours postpartum to levels within the normal nonpregnant range. This suggests that an extrarenal source of renin has been lost with the expulsion of the fetus and placenta.
There is little direct information about the puerperal changes in numerous other hormones, including aldosterone, parathyroid hormone, and calcitonin. More research should be done on these important endocrine relationships in the puerperium.
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