Engorgement: prevalence, presentation, pathophysiology

Prevalence of engorgement

It’s estimated that between one and two-thirds of new mothers experience engorgement.1

Presenting signs and symptoms on the spectrum of inflammation in lactation known as engorgement

Engorgement is a bilateral, generalised inflammation of lactating breasts. The patient experiences her breasts as painful, hot and distended.

Like all breast inflammation, engorgement occurs along a spectrum of severity and is most accurately described by the various combinations of the presenting signs and symptoms shaded in the table below.

Location of inflammation	Dimensions (millimetres)	Erythema	Pain	Systemtic signs + symptoms
Generalised - bilateral		None	None	Feels well
Generalised - unilateral		Mild	Mild when touched only	Fever
Localised WITHOUT lump		Moderate	Mild constant	Myalgia
Localised WITH lump		Severe	Moderate when touched only	Rigor
			Moderate constant
			Severe

A very tense nipple-areolar complex in engorgement is due to milk and hyperaemia, not 'lymphoedema'

Engorgement is not oedema or lymphoedema of the breasts. Although breast inflammation is referred to as 'lymphoedema' in the Academy of Breastfeeding Medicine's Clinical Protocol #36, this term is used inaccurately. You can read more here.

Ultrasound analysis shows that main lactiferous ducts are immediately behind the nipple. Two-thirds of the glandular tissue is found within a three centimetre radius of the nipple.2-4 Peri-areolar engorgement is predominantly due to

• Severely engorged superficial milk ducts, due to high backpressures of milk in the alveoli and ductal lumens, and

• The resultant inflammatory hyperaemia.

• Interstitial fluid plays a small or negligible role.

A 2015 observational study of 20 postpartum women found that those who received intrapartum intravenous fluids had more breast swelling and tenderness in the first 10 days.5 But intravenous fluids are likely to cause increased interstitial fluid of the breasts only if the woman has received a significant dose which also results in lower limb oedema.

Pathophysiology of engorgement in lactation: acute inflammation (bilateral and generalised)

Engorgement in the first days after birth

A 'physiological engorgement' is sometimes differentiated from 'breast inflammation engorgement', without clarity of definitions. NDC considers both as presentations on the spectrum of breast inflammation, focussing on clinical response to relevant signs and symptoms, rather than poorly defined categorisation.

The rate of postpartum synthesis of transitional milk quickly upregulates or downregulates to meet an infant’s needs in the first days post-birth. Women have variable baseline productions of transitional milk in the first week or ten days postbirth, which results from an interaction between her innate milk production capacity and environmental factors.

Postbirth engorgement is most usefully conceptualised as overshoot or temporary excess in initial milk synthesis relative to the infant's needs, since Homo sapiens have the potential for milk production multiple factors above the milk needs of a singleton infant.4

Symptoms and signs of engorgement occur after (not at the same time as) indicators of the onset of transitional milk secretion can be measured in the milk, relative to concentrations in colostrum. These indicators include

• Increased lactose

• Decreased sodium.4

Scenario 1. A woman's innate production of transitional milk upregulates

• If an infant is offered frequent flexible feeds from birth, with generous skin-to-skin opportunities, and

• If underlying clinical problems like conflicting intra-oral vectors of force or restrictive feeding practices are resolved.7

Scenario 2. Applying the mechanobiological model and a complex systems perspective, engorgement of the lactating breasts is due to excess production of milk relative to the infant's needs, which results in

• High intraluminal pressures of milk, which

• Trigger an inflammatory cascade, which results in

• Hyperaemia (arterial capillary dilation and proliferation), accompanied by

• Leakage of proteins from the widened junctions of the venules, which

• Osmotically increase the amount of fluid in the interstitium of breast stroma, which

• Increases associated stromal tension or pressures, which then

• Compress the lactiferous ducts, resulting in

• Worsening backpressure of milk in the alveoli, in an inflammatory cascade.

• The mechanical load of high intra-alveolar and intra-ductal pressures and microscopic areas of alveoli rupture trigger the wound-healing environment of inflammation, microscopic involution, and downregulation of milk synthesis.7,8

You can find out about the NDC mechanobiolological model of breast inflammation here.

Scenario 3. Applying the mechanobiological model and a complex systems perspective, engorgement of the lactating breasts may emerge when environmental factors (e.g. restrictive feeding practices) or clinical problems (e.g. nipple pain) interfere with the infant removing milk he or she needs from the breast. This downregulation of milk production relative to the infant's needs may result in poor infant weight gain, or poor satiety and unsettled behaviour.

Engorgement after the first week postbirth

After the first week postbirth, engorgement is typically due to compromised milk removal, perhaps due to clinical problems, or to restricted breastfeeding practices.

For example, engorgement may be associated with damaged nipples, which are a marker of conflicting intra-oral vectors of force during breastfeeding. Engorgement is also often associated with weaning an infant from the breast.

The Academy of Breastfeeding Medicine's Clinical Protocol #36 'The mastitis spectrum' erroneously excludes engorgement from the spectrum of breast inflammation

Clinical Protocol #36 classifies postpartum engorgement as “a distinct clinical entity related to interstitial edema and hyperemia”, which does not belong on the spectrum of breast inflammation.

Paradoxically, by claiming that engorgement does not fall on the spectrum of breast inflammation, Clinical Protocol #36 implicitly acknowledges the implausibility of its underlying pathogenic biofilm hypothesis, implicitly acknowledging that engorgement is unlikely to result from a generalised narrowing of all of a breast’s lactiferous ducts due to whole-of-breast pathological biofilm.

But Clinical Protocol #36 fails to offer pathophysiological mechanisms which explain the interstitial fluid and hyperaemia of engorgement.9,10

You can read about the scientific flaws in the pathogenic theory of breast inflammation here.

Recommended resources

Clinical inflammation of the stroma of the lactating breast: NDC mechanobiological model

NDC mechanobiological model: hydrostatic stretching and compression acts as a mechanical Feedback Inhibitor of Lactation, downregulating breastmilk secretion

Knowledge of mechanobiology is essential for management of breastfeeding and lactation-related problems

The pathogenic microbiota theory of breast inflammation lacks biological plausibility

Engorgement: management, possible outcomes, and what doesn't help

References

1. Berens P, Brodribb W. Engorgement, Revised 2016. ABM Clinical Protocol #20. Breastfeeding Medicine. 2016;11(4):159-163.

2. Geddes DT. The use of ultrasound to identify milk ejection in women - tips and pitfalls. International Breastfeeding Journal. 2009;4(5):doi:10.1186/1746-4385-1184-1185.

3. Ramsay DT, Kent JC, Hartmann RA, Hartmann PE. Anatomy of the lactating human breast redefined with ultrasound imaging. Journal of Anatomy. 2005;206:525-534.

4. Geddes DB. The anatomy of the lactating breast: latest research and clinical implications. Infant. 2007;3(2):59-61.

5. Kujawa-Myles S, Noel-Weiss J, Dunn S, Peterson W, Cotterman KJ. Maternal intravenous fluids and postpartum breast changes: a pilot observational study. Inernational Breastfeeding Journal. 2015;10(18):doi:10.1186/s13006-13015-10043-13008.

6. Hartmann PE, Atwood CS, Cox DB, Daly SEJ. Endocrine and autocrine strategies for the control of lactation in women and sows. In: Press P, editor. Intercellular signalling in the mammary gland. New York1995.

7. Douglas PS. Re-thinking benign inflammation of the lactating breast: a mechanobiological model. Women's Health. 2022;18:https://doi.org/10.1177/17455065221075907.

8. Douglas PS. Re-thinking benign inflammation of the lactating breast: classification, prevention, and management. Women's Health. 2022;18:17455057221091349.

9. Mitchell KB, Johnson HM, Rodriguez JM, Eglash A, Scherzinger C, Cash KW, et al. Academy of Breastfeeding Medicine Clinical Protocol #36: The Mastitis Spectrum, Revised 2022. Breastfeeding Medicine. 2022;17(5):360-375.

10. Douglas PS. Does the Academy of Breastfeeding Medicine Clinical Protocol #36 'The Mastitis Spectrum' promote overtreatment and risk worsened outcomes for breastfeeding families? Commentary. International Breastfeeding Journal. 2023;18:Article no. 51 https://doi.org/10.1186/s13006-13023-00588-13008.