Immediately after vaginal delivery, the cervix has a loose, pliable tone and may have several small excoriations. Over the first week postpartum, the cervix assumes a more typical gross appearance, although it may remain slightly dilated for the first few days. Persistent heavy bleeding and a continued open cervical os should alert the physician to the possibility of retained placental fragments. Cervical dysplasia may regress in the postpartum period. Kaplan et al¹⁰ studied 157 women with antepartum cervical squamous intraepithelial neoplasia and their subsequent postpartum course. Sixty-two percent of patients with low-grade antepartum dysplasia had regression, while only 6% experienced disease progression, although 60% developed recurrent disease within 5 years. All 28 cases of antepartum high-grade dysplasia in this study persisted postpartum.

The typical rugated appearance of the vagina is temporarily lost, with it appearing more edematous, vascular, and smooth after delivery. Rugae typically reappear about 3 weeks postpartum as these changes resolve. The vagina may initially appear
relatively estrogen deficient in postpartum lactating women or women using progesterone-only contraception. A vaginal lubricant may be beneficial if dyspareunia occurs.

Resumption of ovulation and subsequent menses differs greatly in breastfeeding compared with nonbreastfeeding mothers. Nonlactating mothers experience ovulation on average 45 days after delivery with return of menses in many by 7 to 9 weeks postpartum. Lactating mothers experience a delayed and much more variable return to both ovulation and menstruation, which may relate to specific breastfeeding practices.^11,12 Lactational amenorrhea is useful in predicting the return of fertility in nursing women. During the first 6 months after delivery, women who are amenorrheic and breastfeeding frequently (≥8 times/24 hours) without giving supplements to the neonate have a less than 2% risk of pregnancy.^{13,14,15,16,17,18,19}

The control of fertility generated by lactation is incompletely understood. However, the current theory suggests a prolactin-mediated dysfunction of the gonadotropin-releasing hormone pulse generator in the hypothalamus as the underlying cause of lactation-related reduction in fertility.²⁰

The urinary system and pelvic floor are altered by pregnancy and the birthing process. Intravenous fluids and oxytocin (which is antidiuretic during infusion) may increase postpartum diuresis. Conduction anesthetics may also disrupt neural bladder control and cause postpartum urinary retention.^21,22 Urinary retention with overdistention, urinary tract infection, and stress urinary incontinence are common transient problems. Dilation of the ureters may persist for 3 months or more postpartum.^23,24

Recently, ultrasound imaging of the lactating breast has raised questions regarding the permanent existence of lactiferous sinuses.⁵⁰ During pregnancy, lobuloalveolar growth increases dramatically. Terminal end buds differentiate into alveoli composed of a single layer of milk-secreting epithelial cells surrounding a central lumen. Alveoli are surrounded by myoepithelial cells and capillaries. The lumen of the alveoli empty into intralobular ducts, which coalesce to form a central duct in each lobe exiting through one of 5 to 9 ductal orifices.

By 16 weeks’ gestation, the breast is fully competent to produce milk. Prior to this time, milk production is prevented by the high level of circulating progesterone, which blocks prolactin activation of alpha-lactalbumin formation. Onset of copious milk production (lactogenesis stage II or LS-II) begins after delivery of the placenta and subsequent fall in progesterone.⁵¹ The mean time for LS-II is 50 to 73 hours postpartum.⁵² LS-II occurs later following stressful deliveries⁵³ and in primiparious,⁵⁴ obese^55,56,57 women with excessive gestational weight gain⁵⁸ and in women with preexisting diabetes.⁵² Delayed onset of LS-II is a risk factor for premature weaning, and dyads with risk factors should be monitored closely. Tissue swelling and edema are common during LS-II, but the experience of painful engorgement varies. Analgesics are appropriate treatment for pain.

Early lactation failure or partial inhibition of milk production can result from primary glandular insufficiency, retained placenta,⁵¹ and severe postpartum hemorrhage resulting in ischemic pituitary necrosis and Sheehan syndrome.⁵⁹

Following LS-II, milk production increases to a mean of 750 mL/d by 4 weeks after delivery and remains at that level throughout exclusive breastfeeding.⁶⁰ For individual women, milk volume increases or decreases in response to alterations in mammary stimulation and the degree of breast emptying.

Prolactin is the primary endocrine regulator of milk production. Baseline levels vary with physiological state. Prolactin increases from 8 to 14 ng/mL prepregnancy to 200 to 500 ng/mL at term and declines to 30 to 40 ng/mL between 180 and 360 days of lactation. Suckling causes a sharp rise in prolactin levels at all stages of lactation through at least the second year postpartum.^61,62,63,64 Suckling triggers prolactin increase, which peaks at 30 minutes and returns to baseline after 2.5 to 3 hours. Relationships between milk production and prolactin levels are not straightforward. This may reflect numerical or functional differences in prolactin receptors.

Milk ejection results from oxytocin-induced contraction of myoepithelial cells surrounding the alveoli. Lactiferous ducts then increase in diameter facilitating milk flow.^50,65 Pituitary release of oxytocin is triggered by suckling, auditory, olfactory, or emotional cues.⁶⁶ Unlike prolactin, oxytocin can be released through a conditioned reflex.

Involution of the mammary gland is triggered by prolonged milk stasis and termination of suckling. Peaker and Wilde⁶⁷ detected a feedback inhibitor of lactation (termed FIL), which accumulates during milk stasis and blocks the secretion of milk constituents. Locally produced serotonin has been identified as a possible candidate for FIL,⁶⁸ although additional milk proteins may be involved.

Human milk is a complex, highly structured fluid containing a wide variety of nutrients and other bioactive factors which impact infant growth, development, and immune function. Its composition is dynamic and varies with duration of lactation, degree of breast emptying, during a nursing, with the mother’s diet, with maternal antigen response, based on maternal genotype, and other particulars. Changes over the course of lactation appear to match the changing needs of the growing infant.⁶⁹

Human milk components are multifunctional, serving not only as nutrients but also in a variety of ways that promote infant health and development. Proteins, for example, are a source of peptides, amino acids, and nitrogen and are also involved in the development of the immune response (immunoglobulins), nonimmunologic defense (lactoferrin, lysozyme), growth stimulation (neural growth factor), and other functions. Carbohydrates provide nutritional support (lactose) and prevent bacterial adhesion to mucosal surfaces (oligosaccharides).^{70,71,72,73,74} Human milk oligosaccharides (HMOs) are dietary fibers that pass through the digestive tract largely intact,⁷⁵ acting as prebiotics, and presumably promote gastric motility. Concentrations of HMOs vary over time^{76,77,78,79,80} and this, along with variations in the type of oligosaccharides present, may be genetically determined.^{72,76,77,81,82,83}

Human milk is commonly differentiated into colostrum, transitional, and mature milk. Colostrum, the initial milk produced in the first 3 to 7 days postpartum, is uniquely suited for the neonate. It contains a threefold higher protein concentration than mature milk, higher concentrations of immunoglobulins, leukocytes, and other immunologically active proteins, and lower concentrations of lactose and fat than more mature milk.^48,84 Colostrum appears to act also as an infant growth promoter.⁴⁸ Throughout lactation, the specificity of secretory immunoglobulin A (sIgA), the primary antibody which defends the mucous membranes, in milk depends on the mother’s antigen exposure and response. In this sense, human milk is location-specific.

Infants themselves can also control the nutrient content of received milk by varying the degree of breast emptying. Fat content (and calorie density) increases with the degree of breast emptying, progressing from low-fat “foremilk” to high-fat “hindmilk” during the course of a feed. The influence of maternal diet is more pronounced among malnourished women and relatively minor among those with normal body nutrient stores.

In well-nourished women, normal dietary fluctuations influence the flavor and odor of milk, which influences infant dietary preferences.⁸⁵ In general, the nutrient content of milk is more responsive to maternal diet during lactation in malnourished than in well-nourished women,⁸⁶ and current data suggest that it is not diet, but rather the maternal body composition and body mass index that may be associated with the nutritional value of human milk.⁸⁷ Women can and do produce adequate and abundant milk on inadequate diets.⁶¹ Complicated “rules” about diet during lactation that fail to consider the mother’s nutrient stores and dietary preferences can undermine maternal resolve to breastfeed.⁸⁸

Two nutrients may not be supplied in adequate amounts in milk from normal, well-nourished women: vitamin K⁸⁹ and vitamin D.⁹⁰ Routine intramuscular injection of vitamin K1 at birth provides all the vitamin K the infant needs. The American Academy of Pediatrics recommends daily supplementation with 200 IU of vitamin D to all infants unless they consume at least 500 mL/d vitamin D-fortified formula.⁹¹

Other nutritional deficiencies may be observed in breastfed infants of severely malnourished or diet-restricted mothers, including deficiencies in vitamin A, D, B1, B2, B3, B6, and B12, folic acid, ascorbic acid (AA), iodine, zinc, and carnitine.^92,93 A healthy and varied diet during lactation ensures adequate maternal nutrition and optimal concentration of some nutrients in human milk.⁹³ Without supplements, strict vegans will eventually develop B12 deficiencies and produce milk deficient in B12.^94,95 Infants may become symptomatic before
the mother.⁹⁵ Although infant symptoms can be partially reversed with B12 shots, neurologic deficits can be irreversible. Therefore, women following a vegetarian or vegan diet should consume B12 supplements, particularly during pregnancy and lactation. Other circumstances that may lead to B12-deficient breast milk are severe maternal malnutrition, particularly if accompanied by intestinal parasites and resulting nutrient malabsorption,^96,97 and gastric bypass surgery or partial gastrectomy.^98,99 In these cases, maternal oral supplementation may not be sufficient, and intravenous vitamin B12 may be required.⁹⁸