Lactation and Breastfeeding

• During pregnancy, high oestrogen and progesterone prepare the breast but inhibit prolactin''s effect on milk production. The abrupt fall in progesterone after delivery of the placenta removes that block and copious milk production begins.
• Colostrum, produced in the first days, is lower in fat and lactose and rich in secretory IgA, protein and antibodies.
• Suckling maintains supply through prolactin release and by relieving the local inhibitory feedback of retained milk; supply follows demand.
• Prolactin suppresses GnRH, producing lactational amenorrhoea — real but unreliable as contraception unless strict criteria are met.
• Benefits include reduced infant infection rates and, for the mother, reduced breast and ovarian cancer risk.
• Contraindications are narrow and worth knowing precisely: maternal HIV in settings where safe replacement feeding is available, active untreated tuberculosis (until treated, though expressed milk may be given), active herpes lesions on the breast, certain maternal medications and substances, and infant galactosaemia.

Endocrine causes of impaired lactation

• Retained placental fragments: sustained progesterone secretion blocks prolactin action on the alveolar epithelium, so lactogenesis II never occurs — classic stem is delayed "milk coming in" plus ongoing lochia rubra.
• Sheehan syndrome: postpartum haemorrhage → pituitary infarction → low prolactin; failure to lactate is often the earliest sign, followed by amenorrhoea and secondary hypoadrenalism.
• Hypothyroidism, poorly controlled diabetes, PCOS/obesity: blunt prolactin signalling and delay secretory activation.

Anatomic/mechanical causes

• Prior breast surgery: periareolar or reduction incisions transect lactiferous ducts and the fourth intercostal nerve, abolishing the afferent limb of the suckling reflex.
• Insufficient glandular tissue (tubular/hypoplastic breasts, wide intermammary space), flat or inverted nipples.
• Infant factors: prematurity, ankyloglossia, cleft palate, neurologic hypotonia — all produce ineffective milk removal.

Pharmacologic (modifiable)

• Dopamine agonists (bromocriptine, cabergoline), combined oestrogen-containing contraceptives started early postpartum, ergot alkaloids, and pseudoephedrine all reduce supply.

• Delayed first feed, mother–infant separation, scheduled rather than on-demand feeding, early formula supplementation, unrelieved nipple pain, maternal smoking, and lack of professional support. The USPSTF gives a B recommendation for interventions to support breastfeeding during pregnancy and postpartum, and the AAP endorses Baby-Friendly practices (skin-to-skin within the first hour, rooming-in).

• Mammogenesis: oestrogen drives ductal branching, progesterone drives alveolar (lobuloalveolar) growth, and human placental lactogen plus prolactin complete differentiation. Prolactin rises steadily through gestation, but high circulating progesterone occupies the prolactin receptor pathway and blocks casein/lactose synthesis — the breast is loaded but locked.
• Lactogenesis I (mid-pregnancy): limited secretion of colostrum, protein- and IgA-rich because tight junctions between alveolar cells remain leaky, allowing paracellular passage of immunoglobulin and sodium.
• Lactogenesis II (roughly 2–3 days postpartum): delivery of the placenta causes abrupt progesterone withdrawal while prolactin stays high. Tight junctions close, lactose synthase is activated, and lactose — the osmotic driver — pulls water into the alveolar lumen, producing the sudden increase in volume mothers perceive as milk "coming in."
• Galactopoiesis is under autocrine control: retained milk accumulates feedback inhibitor of lactation (FIL) and mechanically flattens alveolar cells, downregulating synthesis. Removing milk removes the brake — hence supply follows demand, and stasis begets further decline.
• Neuroendocrine reflexes: suckling stimulates nipple mechanoreceptors → fourth intercostal nerve → spinal cord → hypothalamus. Dopamine (prolactin-inhibiting factor) release falls, so anterior pituitary prolactin surges (synthesis); simultaneously paraventricular/supraoptic neurons release oxytocin from the posterior pituitary, contracting myoepithelial cells for ejection. Oxytocin release is conditionable (the infant's cry), and the acute let-down reflex is the component blocked by pain and psychological stress or circulating catecholamines, whereas prolactin-driven milk synthesis is comparatively unaffected in the short term.
• Oxytocin also contracts the uterus, explaining afterpains and faster involution during feeds.
• Prolactin suppresses hypothalamic GnRH pulsatility → low LH/FSH → anovulation, hypo-oestrogenism, vaginal dryness, and lactational amenorrhoea.
• When drainage fails: alveolar distension plus interstitial and lymphatic oedema produce engorgement; persistent stasis raises intraductal pressure so hyperosmolar milk leaks paracellularly into stroma, triggering a sterile inflammatory response (inflammatory mastitis), which bacterial colonisation via a cracked nipple can convert to infectious mastitis and then a walled-off abscess.

Normal lactation

• Drops of thick yellow colostrum in the first 48 hours; breast fullness, warmth and heaviness at days 2–4 as lactogenesis II occurs.
• Let-down: tingling or pins-and-needles sensation, contralateral leaking, and uterine cramping during feeds (oxytocin acting on myometrium).
• Infant with 8–12 feeds per 24 hours, audible swallowing, and stool transitioning from meconium to yellow seedy by days 4–5.

Nipple pain patterns

• Shallow latch: pain throughout the feed with a compressed, creased nipple and fissuring.
• Candidal infection: burning, shooting pain radiating into the breast after feeds, shiny pink nipples, often with infant oral thrush.
• Raynaud phenomenon of the nipple: triphasic white–blue–red blanching with cold exposure, severe biphasic pain.

Step 2 — quantify infant intake objectively

• Serial nude weights: loss of more than roughly 7% of birth weight warrants evaluation and more than 10% is clearly abnormal; birth weight should be regained by about 10–14 days of life. The AAP endorses plotting weight loss on newborn weight nomograms rather than using a single fixed percentage.
• Output: at least six voids per day and yellow seedy stools by day 4–5.
• Test weighing (pre- and post-feed on a digital scale) quantifies milk transfer when supply is in question.

Step 4 — targeted testing for specific syndromes

• Mastitis: clinical diagnosis; ABM advises against routine milk culture, reserving it for severe, recurrent, hospital-acquired or non-responding cases and for MRSA risk.
• Suspected abscess: breast ultrasound is the confirmatory study and guides aspiration; aspirated fluid goes for Gram stain and culture.
• Erythema not resolving after appropriate therapy: image and obtain a skin punch biopsy to exclude inflammatory breast cancer.
• Primary lactation failure: check TSH, prolactin, and consider pelvic ultrasound for retained products; a low prolactin with other anterior pituitary deficits supports Sheehan syndrome.
• Galactosaemia is detected on state newborn screening (GALT enzyme/erythrocyte galactose-1-phosphate).
• For maternal drug safety questions, the reference standard is the NIH LactMed database.

Maternal

• Nipple fissure: shallow latch → epithelial breakdown → portal for S. aureus; signals impending mastitis.
• Engorgement → plugged duct → mastitis → abscess is a continuum driven by stasis. A fluctuant mass with fever persisting past 48–72 hours of antibiotics signals abscess and requires drainage rather than a change of antibiotic.
• Galactocele: retained-milk cyst; painless, smooth, mobile, fluid-filled on ultrasound.
• Inflammatory breast cancer masquerading as refractory mastitis — peau d'orange, non-resolving erythema. This is the must-not-miss diagnosis; biopsy rather than a third antibiotic course.
• Hypo-oestrogenism from prolactin-mediated GnRH suppression → vaginal atrophy, dyspareunia, and transient reversible bone mineral density loss.
• Unintended pregnancy when lactational amenorrhoea is relied on outside its strict criteria.

Infant

• Hypernatraemic dehydration from inadequate intake — lethargy, fever, weight loss beyond 10%, markedly elevated serum sodium. This is an emergency; correct sodium slowly to avoid cerebral oedema.
• Breastfeeding (suboptimal intake) jaundice in the first week from volume depletion and exaggerated enterohepatic circulation; breast milk jaundice peaks later and resolves without stopping feeds. Unchecked severe unconjugated hyperbilirubinaemia risks acute bilirubin encephalopathy and kernicterus — an emergency requiring intensive phototherapy or exchange transfusion per the AAP guideline.
• Nutrient deficiencies: vitamin D deficiency rickets without supplementation; iron deficiency after ~4–6 months; vitamin B12 deficiency with megaloblastic anaemia and neurologic regression in infants of vegan or B12-deficient mothers. Late vitamin K deficiency bleeding, presenting as intracranial haemorrhage, occurs in exclusively breastfed infants whose parents declined intramuscular vitamin K — an emergency.
• Galactosaemia: continued lactose exposure produces vomiting, hepatomegaly, cataracts and E. coli sepsis.

• Progesterone withdrawal is the trigger. Milk "comes in" because the placenta leaves, not because prolactin rises. A woman who never establishes supply and has ongoing bleeding has retained placental fragments; one who cannot lactate after a haemorrhagic delivery and later develops amenorrhoea and fatigue has Sheehan syndrome.
• Two hormones, two jobs. Prolactin = production (blocked by dopamine agonists); oxytocin = ejection (conditioned by the infant's cry, inhibited by pain and stress). Uterine cramping during a feed is oxytocin, not pathology.
• Mastitis: keep breastfeeding. The single best next step is continued/increased milk removal plus NSAIDs; add dicloxacillin or cephalexin if systemically unwell or not improving. Weaning is the classic wrong answer.
• Fever persisting past 48–72 hours on antibiotics → ultrasound for abscess → needle aspiration. Erythema that never resolves → biopsy for inflammatory breast cancer.
• Bilateral, days 3–5, no focal erythema = engorgement (physiologic). Unilateral, wedge-shaped, week 2–6, cracked nipple = mastitis (S. aureus).
• The jaundice pair: breastfeeding jaundice is early, from not enough milk (dehydration, enterohepatic recycling) — treat by feeding more; breast milk jaundice is later-peaking in a thriving infant — continue breastfeeding. Do not swap them.
• Galactosaemia is the infant contraindication — switch to a soy/lactose-free formula. Untreated PKU is managed with monitored partial breastfeeding, not automatic cessation.
• Supplements every board exam wants: vitamin D 400 IU daily for all breastfed infants and iron from about 4 months (AAP); intramuscular vitamin K at birth prevents late vitamin K deficiency bleeding.
• Common distractors: the lactational amenorrhoea method works only if all three criteria hold (exclusive breastfeeding, amenorrhoeic, under 6 months); combined oestrogen-containing contraception is the wrong early postpartum choice — pick a progestin-only method.