pathophysiology of mastitis

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Pathophysiology of Mastitis

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Pathophysiology of Mastitis

Pathophysiology of MastitisIn lactational mastitis, milk stasis or milk overproduction, coupled with infection from bacteria entering the breast via a traumatised nipple (e.g., cracked or fissured) and/or from the infant's mouth, can lead to mastitis. Transient breast enlargement from maternal hormones in neonates makes them vulnerable to mastitis.

In duct ectasia (dilated ducts associated with inflammation), the mammary duct-associated inflammatory disease sequence involves squamous metaplasia of lactiferous ducts. This causes blockage (obstructive mastopathy) with peri-ductal inflammation and possible duct rupture. Inflamed ducts are prone to bacterial infection. Left untreated, mastitis may cause tissue destruction resulting in an abscess.A lactational abscess tends to be located in the peripheral breast. Abscesses unrelated to breastfeeding are more commonly sub-areolar in location. An abscess may also occur without apparent preceding mastitis. Rupture of an abscess can lead to a draining sinus with a resulting fistula. In tubercular mastitis, mycobacterial bacilli can enter the breast from:Direct inoculation (primary infection) via a nipple abrasionDistant portals (secondary infection), such as lymphatic spread, haematogenous (miliary) dissemination, or contiguous spread (e.g., empyema necessitans).TB of the breast may present with a nodular, diffuse, or sclerosing reaction. The most common presentation is a painless lump with or without a sinus tract. Most cases of tuberculous mastitis are secondary, and infection occurs via contiguous spread from lymphatics (most commonly axillary, followed by cervical or mediastinal nodes) or less commonly from the pleura or chest wall or via the haematogenous route. Primary TB of the breast is rare. In some cases tubercular mastitis may be mistaken for breast carcinoma.

Necrotising granulomas are the histopathological hallmark of TB infection. In idiopathic granulomatous mastitis, non-necrotising granulomatous inflammation is centred on lobules that clinically may result in a painless mass.