||It has been suggested that this article be merged into Mastitis. (Discuss) Proposed since August 2010.|
|Postpartum nonpurulent mastitis|
|Classification and external resources|
Puerperal mastitis is the inflammation of breast in connection with pregnancy, breastfeeding or weaning. It is caused by blocked milk ducts or milk excess and is relatively common; estimates range depending on methodology between 5–33%. However only about 0.4–0.5% of breastfeeding mothers develop an abscess.
Some predisposing factors are known but their predictive value is minimal. It appears that proper breastfeeding technique, frequent breastfeeding and avoidance of stress are the most important factors that can be influenced.
Light cases of mastitis are often called breast engorgement, the distinction is overlapping and possibly arbitrary or subject to regional variations.
Mastitis can be classified as milk stasis, non-infectious or infectious inflammation and abscess. It is impossible to correlate this classification with clinical symptoms, in particular milk stasis, non-infectious and infectious inflammation can be distinguished only by leukocyte count and bacteria culturing. Symptoms like fever, intensity of pain, erythema or rapid onset of symptoms can not be used to distinguish these.
Signs and symptoms 
Early stages of mastitis can present with local pain, redness, swelling, and warmth, later stages also present with systemic symptoms like fever and flu-like symptoms and in rare cases an abscess can develop. However it is pretty common that symptoms develop very quickly without any warning.
Except in severe cases it is not necessary to wean a nursling because of mastitis; in fact, nursing is the most effective way to remove the blockage and alleviate the symptoms. Sudden weaning can cause or exacerbate mastitis symptoms and cause hyponatremic shock in the infant.
Breast abscess 
Breast abscess develops only rarely, most sources cite about 0.4-0.5% of breastfeeding women. Known risk factors are age over 30, primiparous and late delivery. No correlation was found with smoking status however this may be in part because much fewer smoking women choose to breastfeed. Antibiotics were not shown effective in prevention of this kind of abscess but are useful to treat a secondary infection.
Keratinizing squamous metaplasia of lactiferous ducts may play a similar role in the pathogenesis of nonpuerperal subareolar abscess.
Aspiration or incision and drainage may be used to relieve the abscess. Breastfeeding from the affected breast should be continued where possible.
Infectious pathogens commonly associated with mastitis are Staphylococcus aureus, streptococcus spp., gram negative bacilli such as Escherichia coli. Salmonella spp., mycobacteria, candida, and Cryptococcus have been identified in rare instances.
Recent research suggests that infectious pathogens play a much smaller role in the pathogenesis than was commonly assumed only a few years ago. Most detected pathogens are very common species that are natural part of the breast fauna and simple detection of their presence is not sufficient to prove a causative role. Furthermore treatment with antibiotics appears to have minimal impact.
The presence of cracks or sores on the nipples increases the likelihood of infection. Tight clothing or ill-fitting bras may also cause problems as they compress the breasts. There is a possibility that infants carrying infectious pathogens in their noses can infect their mothers; the clinical significance of this finding is still unknown.
Frequent emptying of both breasts by breastfeeding is essential. Also essential is adequate fluid supply for the mother and baby. Use of pumps to empty the breast is now considered somewhat controversial.
In cases of light mastitis massage and application of heat prior to feeding can help as this may aid unblocking the ducts. However in more severe cases of mastitis heat or massage could make the symptoms worse and cold compresses are better suited to contain the inflammation.
Antibiotics are not needed in the overwhelming majority of cases and should be used only for bacterial infections. Dicloxacillin or cephalexin are sometimes recommended, because of the high rates of penicillin resistant staphylococci.
Breast engorgement or mastitis occur frequently after weaning. The pregnancy/lactation related hormones usually return to normal levels shortly after weaning but for some women it can take several months and there is an increased risk of rebound lactation and mastitis before hormone levels settle. Avoiding stress is important because the same hormones are also stress hormones. Even after hormone levels settle it takes some time for the breast gland to rebuild to its nonlactating state and it may be particularly prone to mastitis during this time.
Most cases of post weaning mastitis or breast engorgement resolve with relatively little treatment. Recurrent post weaning mastitis on the other hand can be an indication of a developing hyperprolactinemia or thyroid disorders and endocrinological examination must be considered.
Cold compresses, lactation inhibiting herbs or medication can be used.
Salvia officinalis is commonly used for weaning (Veldhuizen-Staas C. 2007), but no peer reviewed literature is known on this subject. Chasteberry extract can improve prolactin levels which may reduce risk of recurrence but no data is available for use in mastitis.
Prolactin lowering medication has been frequently used for weaning in the past but is much less used since Parlodel (bromocriptine) approval for weaning has been withdrawn in the US over safety concerns. While the question of bromocriptin safety for weaning purposes was never completely resolved it became apparent that it was not very effective in the prescribed dose and did rarely justify the unpleasant side effects.
Granulomatous (non-puerperal) mastitis is known to occur on average 2 years and almost exclusively up to 6 years after pregnancy. It is an extremely rare condition and believed to be in many cases related to an autoimmune reaction to milk proteins following incomplete inhibition of milk secretion and hyperprolactinemia.
Distinction between puerperal (but post-weaning) and nonpuerperal mastitis is somewhat arbitrary.
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