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The puerperium is defined as the period from birth to the first 6 weeks postpartum. Multiple anatomic and physiologic changes occur during this time, and there is the potential for significant complications such as infection or hemorrhage.
The uterus usually undergoes complete involution by 6 weeks postpartum, going from a weight of 1,000 g to a weight of 100 g or less. The endometrium begins to regenerate early in the postpartum period, essentially completing the regeneration by the third week. The last part of the uterus to return to normal is the placental attachment site, which may take up to 6 weeks to regenerate. The sloughed tissue becomes part of the 1ochia. Initially, the lochia contains blood mixed with decidua and is called the lochia rubra. By the 3rd or 4th day, the lochia becomes pale and watery, although it is still tinged with blood; at this stage, it is termed the 1ochia serosa. After the 10th day, the 1ochia becomes yellowish-white (the 1ochia alba). The vagina, which is dusky, engorged, spacious, and smooth after delivery, diminishes in size and regains its normal ragouted, pink appearance by approximately 3 weeks postpartum.
Anatomically, the dilatation of the calyces, renal pelvis, and ureters that is characteristic of pregnancy may persist as long as 8 weeks postpartum. Functionally, the increased renal plasma flow, glomerular filtration rate, and creatinine clearance rate associated with pregnancy return to normal by 6 weeks after delivery.
The changes in the cardiovascular system that occurred during pregnancy (ie, increase in heart rate, cardiac output, and blood volume) generally return to baseline by approximately 6 weeks postpartum. Peripheral vascular resistance also returns to the prepregnancy level by this time. Most of these parameters return to normal pueperium, lactation , breast-feeding, breast feeding, breastfeeding, postpartum, postpartum depression, postpartum hemorrhage, uterine infection, mastitis, episiotomy infection within the first 2 weeks postpartum.
After delivery, ovulation occurs at an average of 10 weeks but may occur as early as 27 days after delivery in non-lactating women. In women who breast-feed for at least 3 months, the average time to ovulation is 17 weeks. In non-lactating women, the mean time to menstruation is 6-8 weeks after delivery, and 70% menstruate by 12 weeks after delivery. In lactating women, the return to menstruation is more gradual, so that one half to three fourths have menstruated by 36 weeks. For obvious reasons, lactation is not an ideal or necessarily effective method of birth control.
Breast-feeding should be encouraged for several reasons. First and foremost, breast milk is the ideal source of nutrients for the neonate. Breast milk also provides some degree of immunologic protection for the neonate. Nursing is contraindicated in patients with certain viral infections such as CMV, hepatitis B, and HIV infection.
The breast and nipples of a woman who is nursing her infant require little attention in the puerperium other than attention to cleanliness and fissures. Some parturients may request lactation suppression during the postpartum period. Lactation is suppressed in 60-70% of women who wear a fight brassiere and avoid stimulation of the nipples. Althoughbreast engorgement may occasionally cause a temperature elevation of short duration, any rise in temperature during the puerperium might be a sign of infection.
One distinguishing characteristic of mammals is their capacity to nourish their young with secretions from the mammary glands. On the basis of studies in animals, lactogenesis can be arbitrarily divided into two stages. During the first stage, which occurs during the third trimester of pregnancy, the lobular-alveolar complex is stimulated to differentiate such that there are increases in synthesis of enzymes necessary for the production of milk components. These special constituents of human milk include major proteins such as a-lactalbumin, [3-1actoglobulin, and casein, as well as triglycerides and lactose. The second stage is characterized by secretion of colostrum, followed by significant milk secretion approximately 5 days after delivery.
In concert with cortisol, insulin, estrogen, progesterone, and placental lactogen, prolactin stimulates growth and de velopment of the milk-secreting apparatus of the mammary gland. Prolactin is the principal hormone that stimulates lactogenesis, and levels increase progressively throughout pregnancy from a mean of less than 20 ng/mL in a nonpregnant woman to an average of 250-300 ng/mL during the third trimester. Prolactin exerts its principal action by binding to specific membrane receptors on mammary tissue to stimulate gene transcription of messenger RNA and subsequent synthesis of lactose, casein, milk fat, and a-lactalbumin. During pregnancy, the high estrogen levels produced by the fetal-placental unit stimulate an increase in circulating pueperium, lactation , breast-feeding, breast feeding, breastfeeding, postpartum, postpartum depression, postpartum hemorrhage, uterine infection, mastitis, episiotomy infection prolactin; however, the high estrogen-progesterone levels also suppress the number of available prolactin-binding sites in mammary tissue so that lactogenesis is delayed until placental separation leads to a rapid decline in these steroid levels. After delivery, prolactin concentrations remain elevated and increase further during suckling. Because higher prolactin levels lead to more prolactin-binding sites, prolactin can induce an up-regulation of its own receptors, thereby further increasing its biologic activity.
Although both human placental lactogen and growth hormone are structurally similar to prolactin and have intrinsic lactotrophic properties, their role in lactogenesis in humans is unclear. During pregnancy, growth hormone is suppressed to very low levels, whereas placental production of human placental lactogen is parallel to the increase in placental growth during the second half of pregnancy. In animal models, human placental lactogen can mimic the biologic action of prolactin by binding to the prolactin receptor. Because levels of human placental lactogen decline rapidly and become undetectable 24 hours after delivery, a role for human placental lactogen in the maintenance of lactation is unlikely.
In mammary tissues, cortisol induces the development of the rough endoplasmic reticulum and Golgi membranes that are necessary for increased synthesis of milk proteins. Thus, cortisol appears to be essential for prolactin stimu lation of casein production.
During pregnancy, estrogens promote ductal development while progesterone stimulates lobular-alveolar maturation of the mammary gland. In addition, the high levels of estrogens present during pregnancy augment the release of prolactin from the pituitary gland, and the high levels of progesterone act to suppress lactogenesis by reducing the ability of prolactin to up-regulate its own receptors. Progesterone also exerts other anti-lactogenic effects by reducing estrogen binding to mammary tissue.
Thyroid hormones appear to play a permissive role in lactogenesis because administration of T4 augments mammary development and milk production. In patients with