Etiology and pathogenesis
In the vast majority of cases, the causative agent is Staphylococcus, occasionally accompanied by Escherichia coli or streptococci. Anaerobic flora, Pseudomonas aeruginosa, and fungi are less common. Nosocomial (hospital-acquired) infection is of paramount importance in contamination.
Infection most commonly penetrates the tissues through nipple fissures, and less frequently intracanalicular (via the lactiferous ducts) during pumping or breastfeeding. However, the mere presence of the pathogen is insufficient. The primary predisposing factor is lactation stasis (impaired milk outflow, often due to mammary gland immaturity in primiparas).
The mechanism of development proceeds as follows: microbes enter the dilated ducts $\rightarrow$ milk within them curdles $\rightarrow$ duct walls swell, exacerbating stasis $\rightarrow$ epithelium is damaged, and microorganisms break through into the glandular tissue. Inflammation sequentially encompasses the lactiferous ducts, glandular tissue, areola, and subcutaneous fat.
Classification and stages of development
The process is highly dynamic and, in the absence of treatment, progresses rapidly through several phases:
- Serous phase. Begins acutely with chills, malaise, and fever. The gland is enlarged, infiltrated with serous exudate, and extremely tender upon palpation. Leukocytosis reaches $10.0-12.0 \times 10^9$/L, and the ESR is accelerated.
- Acute infiltrative mastitis. Develops within 3–6 days when therapy is ineffective. Temperature rises to $38-40^\circ$C, and the infiltrate in the gland acquires distinct borders.
- Purulent-destructive phase (abscessing, phlegmonous). Serous infiltration is replaced by purulent melting. Small foci coalesce into abscesses. The skin turns red, and a specific fluctuation sign appears (presence of fluid within a cavity).
- Gangrenous form. An extremely severe condition associated with vascular thrombosis. Temperature reaches $40-41^\circ$C. The gland is markedly edematous, with blisters containing hemorrhagic contents and areas of necrosis appearing on the skin. Blood tests show high leukocytosis with a left shift and toxic granulation.
Differential diagnosis: mastitis or lactation stasis?
The initial stages of mastitis must be strictly differentiated from acute milk stasis. Any engorgement of the gland accompanied by a fever should be regarded as serous mastitis, and treatment must be initiated immediately.
- Timing and localization: Lactation stasis typically occurs on days 3–5 (milk ejection) and is usually bilateral. Mastitis is more often unilateral.
- Symptomatology: In lactation stasis, indurations are mobile, lobulated, correspond to lobule contours, and are painless. General condition is minimally affected.
- Pumping/Expression: During stasis, milk is expressed freely, and noticeable relief follows pumping. In mastitis, expression is extremely painful and brings no relief.
Conservative and surgical treatment
Initial forms (serous and infiltrative) are managed conservatively. The gland is elevated (without compression), and fluid intake is restricted. Breastfeeding is not discontinued; regular evacuation is necessary to prevent stasis. Spasmolytics are prescribed to improve outflow, along with antibiotics (penicillins, cephalosporins, macrolides) and retromammary blockades (procaine + antibiotic + enzymes).
Purulent forms require emergency surgery under general anesthesia.
- Incision is performed via wide radial incisions from the periphery toward the center (to avoid damaging the lactiferous ducts).
- For deep or retromammary abscesses, the Bardenheuer incision is used—a semi-oval approach along the lower transition fold. It allows the gland to be detached from the muscle, provides good drainage, and yields an excellent cosmetic result.
- The cavity is cleared of necrotic tissues, irrigated with hydrogen peroxide, and drained.
Approaches in mastitis (RPB): Radial — does not transect ducts; Periareolar — near the nipple; Bardenheuer — in the lower fold for deep abscesses.
Class and exam questions
Is breastfeeding safe during early-stage mastitis?
Yes, during conservative treatment of the serous and infiltrative stages, lactation is not discontinued. Regular expression and feeding are necessary to prevent milk stasis.
How does milk composition change during purulent inflammation?
Due to increased alkaline phosphatase activity, pH shifts toward the alkaline side. Microscopy reveals a large number of leukocytes in the milk.
How to prevent the development of postpartum mastitis?
Prevention includes sanation of infection foci even before childbirth, education on proper breastfeeding, prompt treatment of nipple fissures, and prevention of lactation stasis.
What else to study on this topic
- Complications of mastitis: lymphangitis, lymphadenitis, and sepsis
- Features of chronic non-purulent and purulent mastitis
- Technique and composition of retromammary blockades
- Prevention of nosocomial infections in maternity hospitals
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Other topics from the section "CHAPTER 11. SURGICAL INFECTION (PURULENT-INFLAMMATORY DISEASES)"
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