Mastitis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Mastitis is the inflammation of the breast. Mastitis commonly affects breastfeeding mothers. This is referred to as puerperal mastitis. Non-puerperal mastitis occurs in non-breastfeeding mothers. Mastitis rarely occurs in men. Inflammatory breast cancer has symptoms very similar to mastitis and so appropriate history and investigation is needed to rule it out.

The use of the term mastitis varies by geographic region. In the United States the term mastitis usually refers to puerperal (referrring to breastfeeding mothers) mastitis with symptoms of systemic infection whereas outside the U.S. it is commonly used for puerperal and non-puerperal cases. The term chronic cystic mastitis, also called fibrocystic disease, is characterized by noncancerous lumps in the breast.

Mastitis was first described by Dr. G. Ranney of Michigan in a paper read before the Section of Obstetrics Medicine at the Brighton meeting of the British Medical Association and in 1887 Dr. Charles J. Wright documented its treatment in the British Medical Journal.^[1] From the 1930s to the 1960s an epidemic form of puerperal mastitis occurred frequently in hospital nurseries in industrialized countries.^[2] During this period, hospital deliveries became more frequent, breastfeeding was not promoted, and the antibiotic era was only just beginning. The dominant role of Staphylococcal infections and transmission between nursery personnel, infants and mothers was repeatedly demonstrated. Epidemic mastitis has been regarded as a hospital acquired disease caused by highly virulent strains of penicillin-resistant Staphylococcus aureus.^[2]

Mastitis can be classified according to several subtypes based on the etiology, the duration of the disease, anatomical location, immunological association and age of the patient. Examples of this classification include puerperal or non-puerperal mastitis, chronic or acute mastitis, periductal or ductal, autoimmune or non-autoimmune (e.g. granulomatous and lupus mastitis)^[3][4][5] and pre-pubertal mastitis.

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue. Development of non-puerperal mastitis is the result of secretory stasis whereas puerperal mastitis occurs when bacteria, often from the patient’s skin or the baby’s mouth/nostrils,^[6] enters a milk duct through a crack in the nipple.

Mastitis is caused by bacteria, mostly Staphylococcus aureus^[7] normally found on the skin, as well as Staphylococcus epidermidis, Streptococcus, E. coli, and Mycoplasma. Mastitis can also be caused by fungi, most commonly Candida, that may be found in the oral cavity of the baby.

Mastitis must be differentiated from other diseases that cause breast pain and/or swelling, such as galactocele^[8][9], breast engorgement^[10][11][12], mastodynia^[13][14][15], fibrocystic breast disease, breast cancer, fibroadenoma, mondor’s disease^[16][17] and breast trauma.

Worldwide, the prevalence of mastitis ranges from a low of 1,000 per 100,000 persons, to a high of 10,000 per 100,000 persons, with an average prevalence of 4,700 per 100,000 persons.^[18] Worldwide, the incidence of puerperal mastitis ranges from a low of 2,900 per 100,000 persons, to a high of 9,500 per 100,000 persons, with an average incidence of 6,200 per 100,000 deliveries within the first seven weeks after delivery.^[19][20][21] Out of this, the incidence of those with mastitis needing hospitalization is 93 per 100,000 persons.^[22]. The percentage of those with mastitis who develop a breast abscess varies from 3% to 11%.^[23] Mastitis commonly affects breastfeeding mothers between the ages of 21 to 35 years, with the highest occurrence in those between the ages of 30 to 34 years, even when parity and full-time employment are controlled.^[2] However, there is no difference between mastitis and breast abscess groups regarding age.^[24] Women are more commonly affected with mastitis than men. There is no racial predilection to mastitis. Geographically the incidence of mastitis is higher in developing countries.^[2]

Mastitis usually occurs in women who are breastfeeding. Women who are breastfeeding are at risk for developing mastitis, especially if they have sore or cracked nipples or have had mastitis previously. Also, the chances of getting mastitis increases if women use only one position to breastfeed or wear a tight-fitting bra, which may restrict milk flow. Mastitis that is not related to breastfeeding might be a rare form of breast cancer. Women with diabetes, chronic illness, AIDS, or an impaired immune system may be more susceptible to the development of mastitis.

According to the World Health Organization, there is no screening modality available for mastitis.^[2]

If left untreated, up to 11% of patients with puerperal mastitis may progress to develop a breast abscess.^[25] Complications that may arise from mastitis include: recurrence, milk stasis and abscess formation. The prognosis is usually good and mastitis clears quickly with antibiotic therapy. 73% of smokers diagnosed with mastitis^[26] have the worst prognosis, especially those with non-puerperal mastitis, and have a higher rate of recurrence of breast abscesses.

The diagnosis of mastitis is mostly clinical. In most cases, patients may present a few days after delivery with localized breast complaints. The affected area is often close to the nipple and areola and commonly occurs on the upper inner side of the breast. The affected area usually occurs only on one breast and very rarely is the whole breast affected.

In most cases, patients may present a few days after delivery with localized breast complaints. The affected area is often close to the nipple and areola and commonly occurs on the upper inner side of the breast. The affected area usually occurs only on one breast and very rarely is the whole breast affected.

The most common symptoms of mastitis include: redness of the affected area, pain local to the affected area and local differential warmth.^[27][28] Some patients may also experience flu-like symptoms, such as aches, shivering, and chills, although this is less common.

Common physical examination findings of mastitis include low to high grade fever, breast tenderness, and swelling.^[29]

Some patients with mastitis have a positive bacterial culture of breast milk.^[29] Culture is rarely used to confirm bacterial infection of the milk because positive cultures can result from normal bacterial colonization, and negative cultures do not rule out mastitis. Culture has been recommended when the infection is severe, unusual, or hospital acquired, or if it fails to respond to two days’ treatment with appropriate antibiotics.^[2] Complete blood count may show an elevated neutrophil count, though this is not specific to mastitis.

There are no characteristic ECG findings of mastitis, however, mastitis has been reported to unmask Type 1 Brugada Syndrome in which the ECG finding resolved when mastitis resolved.^[30]

There is no significant finding diagnostic of mastitis on x-ray, although x-ray irradiation therapy in treating mastitis has been tried with success.^[31][32][33]

There are no CT scan findings diagnostic of mastitis. CT scan is helpful only when there is suspicious metastatic inflammatory breast disease.^[34]

On contrast-enhanced MRI, most non-puerperal mastitis are characterized by non-mass-like lesions with heterogeneous signal intensity. The observation of rim or rim-like enhancement on contrast-enhanced MRI with central hypointensity areas showing as hyperintensity on T2-weighted imaging is suggestive of the possibility of non-puerperal mastitis.^[35]

On MRI, most patients with granulomatous mastitis are characterized by segmental T2 hyperintensity with contrast-enhancement on T1,^[36] however, enhancing T2 hypointense mass with irregular margin was present in minority of patients with granulomatous mastitis.^[36][37] Among the available radiological modalities, MRI is the most specific in the diagnosis of mastitis.^[38]

On ultrasound mastitis may show edema of the fatty tissue, hypoechoic areas in the breast tissue, dilated ducts, fluid collections^[39] or irregular hypoechoic masses suspicious for malignancy^[40][36] or hypoechoic mass-like lesions.^[38]

On mammography, bacterial (puerperal or non-puerperal) mastitis usually shows ill-defined regions of increased density and skin thickening^[37][38][39] as shown below:

Mammogram of Mastitis

Supportive care is the mainstay of therapy for puerperal mastitis. Supportive therapy includes massage, heat application, cold compresses and frequent breastfeeding. The treatment for non-puerperal mastitis is based on the underlying condition. Pharmacological therapies for non-puerperal mastitis include prolactin inhibiting agents, antimicrobial therapy, and nonsteroidal anti-inflammatory drugs (NSAIDs). Granulomatous mastitis has been treated with some success by a combination of steroids and prolactin inhibiting medications.

Surgical intervention is usually not the first treatment option for patients with mastitis. Surgery is usually reserved for complicated mastitis with abscess formation that needs to be drained and granulomatous mastitis that may need excision.^{[41][42][43][44]}

Effective measures for the primary prevention of mastitis include avoidance of the risk factors as well as adhering to the following:^[2]

• Early contact of infants with their mothers, and early start of breastfeeding usually within the first hour.

• Infants should stay in the same bed as their mother, or close to her in the same room.

• Breastfeeding mothers should receive skilled help and support for proper breastfeeding technique, whether or not she has breastfed before, to ensure good attachment, effective suckling and efficient milk removal;

• Every mother should be encouraged to breastfeed ‘on demand’, whenever the infant shows signs of readiness to feed, such as opening the mouth and searching for the breast.

• Every mother should understand the importance of unrestricted and exclusive breastfeeding and of avoiding the use of supplementary feeds, bottles and pacifiers.

• Women should receive skilled help to maintain lactation if their infants are too small or weak to suckle effectively.

• When a mother is in hospital, she needs skilled help at the first feed and for as many of the subsequent feeds as necessary.

• When a mother is at home, she needs skilled help during the first day after delivery, several times during the first two weeks, and subsequently as needed until she is breastfeeding effectively and confidently.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Mastitis was first described by Dr. G. Ranney in Michigan in a paper read before the Section of Obstetrics Medicine at Brighton meeting of the British Medical Association and in 1887 Dr. Charles J. Wright documented its treatment in the British Medical Journal.^[1] From the 1930s to the 1960s hospital deliveries became more frequent, breastfeeding was not promoted, and the antibiotic era was only just beginning.

Mastitis was first described by Dr. G. Ranney in Michigan in a paper read before the Section of Obstetrics Medicine at Brighton meeting of the British Medical Association and in 1887 Dr. Charles J. Wright documented its treatment in the British Medical Journal.^[1] From the 1930s to the 1960s an epidemic form of puerperal mastitis occurred frequently in hospital nurseries in industrialized countries.^[2] During this period, hospital deliveries became more frequent, breastfeeding was not promoted, and the antibiotic era was only just beginning. The dominant role of Staphylococcal infections and transmission between nursery personnel, infants and mothers was repeatedly demonstrated. Epidemic mastitis has been regarded as a hospital acquired disease caused by highly virulent strains of penicillin-resistant Staphylococcus aureus.^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Mastitis can be classified according to several subtypes based on the etiology, duration of the disease, anatomical location, immunological association and age of the patient.

Mastitis can be classified according to several subtypes based on the etiology, duration of the disease, anatomical location, immunological association and age of the patient as follows:

This classification is important when counseling patients on prevention because improper latch of the baby to the breast may result in nipple injuries.

No specific timeline has been used to define the chronicity of the infection.

This classification is based on the anatomical location of the inflammatory process and may not be clinically important.

Examples of autoimmune mastitis include granulomatous and lupus mastitis. This classification is especially important because granulomatous and lupus mastitis are treated differently from other types of mastitis.^[1][2][3]

This is usullay self-limiting and may not need any antibiotic therapy.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue. Development of non-puerperal mastitis is the result of secretory stasis whereas puerperal mastitis occurs when bacteria, often from the patient’s skin or the baby’s mouth/nostrils,^[1] enters a milk duct through a crack in the nipple.

The images below show a general overview of breast anatomy.

1) Chest wall
2) Pectoralis muscles
3) Lobules
4) Nipple
5) Areola
6) Milk duct
7) Fatty tissue
8) Skin

Surface anatomy of the breast

Most clinically significant cases of non-puerperal mastitis start as inflammation of the ductal and lobular system and possibly the immediate surrounding tissue.

Development of non-puerperal mastitis is the result of secretory stasis in about 80% of cases. The retained secretions can get infected or lead to inflammation by causing mechanical injury leading to leakage of the lactiferous ducts. Autoimmune reaction to the secretions may also be a factor.

Development of puerperal mastitis occurs when bacteria, often from patients skin or the baby’s mouth/nostrils,^[2] enters a milk duct through a crack in the nipple.

Several mechanisms, listed below, are thought to lead to the pathogenesis of mastitis:

• Secretory disease or galactorrhea
• Changes in permeability of lactiferous ducts (retention syndrome)
• Blockage of lactiferous ducts, for example duct plugging caused by squamous metaplasia of lactiferous ducts
• Trauma or injury
• Mechanical irritation caused by retention syndrome or fibrocystic condition
• Infection
• Autoimmune reaction to luminal fluid

Approximately a quarter of patients may be hyperprolactinemic. There has been a strong association with fibrocystic condition and thyroid conditions. Up to 50% of patients may experience transient hyperprolactinemia possibly caused by inflammation or treatment and a significant number of patients may have abnormally high prolactin reserve.^[3][4]

TSH, prolactin, and IGF-1 are important systemic factors in galactopoiesis. The significance of these factors in secretory disease is not well documented but it has been asserted that the mechanisms of secretory disease and galactopoiesis are closely related.

Alveolar and ductal epithelia permeability is mostly controlled by tight junction regulation and is closely linked to galactopoiesis and secretory disease. The tight junctions are regulated by a multitude of systemic (prolactin, progesterone, glucocorticoids) and local (intramammary pressure, TGF-beta, osmotic balance) factors.

Acromegaly may present with symptoms of non-puerperal mastitis.

Histopathology of granulomatous mastitis shows characteristic distribution of granulomatous inflammation which remains the gold standard for diagnosis.^[5]

Histologically, lupus mastitis is seen as lymphocytic lobular panniculitis and hyaline sclerosis of the adipose tissue. This histologic finding is required to make an accurate diagnosis.^[6]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Mastitis is mostly caused by Staphylococcus aureus.^[1] Other causes include Staphylococcus epidermidis, Streptococcus, E. coli, Mycoplasma and Candida.

There is no life-threatening cause of mastitis.

The most common cause of mastitis is Staphylococcus aureus^[1] normally found on the skin.

Common causes include:

• Staphylococcus epidermidis
• Streptococcus
• E. coli
• Mycoplasma.
• Fungi, most commonly Candida, that may be found in the oral cavity of the baby.

• ●Tight-fitting brassiere or car seatbelt
• ●Oveproduction of milk
• ●Infrequent breastfeeding
• ●Maternal stress
• ●Maternal malnutrition
• ●Nipple excoriation or cracking
• ●Rapid weaning

Less common causes include:

• Autoimmune reaction to luminal fluid

Cardiovascular	No underlying causes
Chemical/Poisoning	Chloramines in pool water, smoking illicit drugs
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	Vallecular cyst
Endocrine	Oveproduction of milk, Rapid weaning
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	No underlying causes|-
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	Staphylococcus aureus, Staphylococcus epidermidis, Streptococcus, E. coli, Fungi, most commonly Candida, Mycoplasma
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	Autoimmune reaction to luminal fluid
Sexual	No underlying causes
Trauma	Nipple excoriation or cracking
Urologic	No underlying causes
Miscellaneous	Infrequent breastfeeding, Maternal stress, Tight-fitting brassiere or car seatbelt

• Autoimmune reaction to luminal fluid
• E. coli
• Fungi, most commonly Candida
• ●Infrequent breastfeeding
• ●Maternal stress
• ●Maternal malnutrition
• Mycoplasma
• ●Nipple excoriation or cracking
• ●Oveproduction of milk
• ●Rapid weaning
• Staphylococcus aureus
• Staphylococcus epidermidis
• Streptococcus
• ●Tight-fitting brassiere or car seatbelt

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2] Shadan Mehraban, M.D.[3]

Mastitis must be differentiated from other diseases that cause breast pain and/or swelling, such as galactocele^[1][2], breast engorgement^{[3][4] [5]}, mastodynia^[6][7][8], fibrocystic breast disease, breast cancer, fibroadenoma, mondor’s disease^[9][10] and breast abscess.

Mastitis must be differentiated from other diseases that cause breast pain and swelling as shown below:^{[11][12] [13][14][15][16][17][10][18][19]}

Diseases	Laboratory Findings		Physical Examination			History and Symptoms								Other Findings
	Culture of the discharge	Biopsy	Breast tenderness	Skin induration	Cordlike vein appearance	History of trauma	Nipple retraction	Nipple discharge	Erythema	Fever	Warmth	Lymphadenopathy	Itching
Breast abscess	+	–	+	+	–	+	–	+	+	+	+	–	–
Mastitis	+	–	+		–	+	–	+	+	+	+	+	–
Inflammatory breast cancer	–	+	+	+		–	+	–	+	–	+	+	+	*Peau d’ orange appearance of the skin *Metastasis is common.
Galactocele	–	–	–	–		–	–	+	–	–	–	–	–	It is differentiated from other masses by US.
Mondor’s syndrome			+	+	+	–								Retracted breast skin and elevation of the skin may be observed.
Cellulitis	–		+	+					+	–	+	+	–
Fibroadenoma	–	+	–	–		–		–	+					*Peau d’ orange skin apperance. *Enlarged veins on the skin

Other differential diagnosis of mastitis may include:

• Cystosarcoma phyllodes
• Breast cyst
• Breast carcinoma
• Lymphangioma
• Furuncle
• Impetigo
• Neonatal breast hypertrophy
• Breasst engorgement
• Lipoma

Differentiation of different types of breast lumps:

ABBREVIATIONS
LAP=Lymphadenopathy, HRT=Hormonal replacement therapy, FNA=Fine needle aspiration, DCIS=Ductal carcinoma in-situ

Diseases	Benign or Malignant	Clinical manifestation								Paraclinical findings		Gold standard diagnosis
		Demography	History	Symptoms			Signs			Histopathology	Imaging
				Mass	Mastalgia	Nipple discharge	Breast exam	Skin changes	LAP
Fibroadenoma[20]	Benign Very slight increased risk of breast cancer in complex fibroadenoma	Most common benign tumor, women aged 20-30 years	Increases in size during pregnancy or with estrogen therapy, and regress after menopause	+	±	–	Solitary Well-defined Mobile mass	–	–	Proliferative breast lesion without atypia	Ultrasound: Well-defined Solid mass	Mammography Ultrasound Biopsy
Breast cyst[21]	Benign No increased risk of malignancy for simple cyst <1% for complicated cyst <1% to 23% for complex cyst	Common masses found in premenopausal, perimenopausal, and postmenopausal women Mostly seen among HRT users	May resolve after aspiration Further evaluation for unresolved masses	+	±	–	Solitary Cluster of small masses or an ill-defined mass Smooth, firm, and frequently tender	–	–	Nonproliferative breast lesions	Ultrasound: Simple cyst: Well circumscribed, posterior acoustic enhancement without internal echoes Complicated cyst: Homogenous low-level internal echoes due to without solid components Complex cyst: Thick walls greater than 0.5 mm with solid component	Ultrasound Fine needle aspiration (FNA)
Fibrocystic change[22]	Benign No increased risk of malignancy Slightly increased risk of malignancy in presence of positive familial history of breast cancer	Unknown prevalence among adolescents >50% in women of reproductive age	Present before menses and improve during menstruation	+	+	±	Painful breast tissue Tender, nodular swelling	–	–	Nonproliferative breast lesions	Ultrasound: Small cysts in mammary zone Fibroglandular tissue around the mass	Ultrasound Mammography (it is not recommended for adolescents)
Galactocele[23][24]	Benign No increased risk of malignancy	Milk retention cysts with fluid collection among pregnant women and during breast-feeding	After ending lactation, the cysts resolve	+	±	±	Soft masses Cystic masses	–	–	Inflammation of lactate ducts due to extension, results in wall fibrosis	Mammography: Intermediate mass in absence of classic fat-fluid level Ultrasound: Complex mass	Ultrasound Mammography
Cysts of montgomery[25]	Benign No increased risk of malignancy	Most common in age of 10-20 years old	More than 80% resolve spontaneously Drainage is essential in rare cases	+	±	±	Asymptomatic subareolar mass Drainage of clear to brownish fluid	±	–	Acute inflammation due to obstruction of the Montgomery’s gland	Ultrasound: Single cystic lesion in retroareolar area	Ultrasound
Hamartoma[26]	Benign Coexisting malignancy may be present	Common in women older than 35 years old	Asymptomatic ones found incidentally or painless breast lump Usually excised	±	–	–	Soft breast lump Breast enlargement without palpable mass	±	–	Benign proliferation of fibrous, glandular, and fatty tissue Thin capsule of connective tissue	Mammography: Well-described Discrete, solid, and encapsulated lesion	Ultrasound Mammography
Breast abscess[27][28]	Benign No increased risk of malignancy	Complication of lactational mastitis in 14% of cases Common among African-American women, heavy smokers , and obese patients	Resolve after drainage/antibiotic therapy	+	+	–	Localized inflammation of breast Tenderness	+	–	Mixed inflammatory feature by neutrophils. Granulation tissue and chronic inflammation feature caused by Gram-positive cocci	Ultrasound: Fluid collection	Ultrasound
Mastitis[29][30]	Benign No increased risk of malignancy	Common among lactating women (first three months of breast-feeding) Periductal mastitis among smokers and associated with squamous metaplasia	Resolve after drainage/antibiotic therapy	±	+	±	Breast tenderness Swollen breast tissue	+	–	Breast parenchyma inflammation: Acute mastitis: Staphylococcus infection Granulomatous mastitis: Tuberculosis or sarcoidosis infection	Ultrasound: Ill-defined area with hyperechogenicity with inflamed fat lobules Skin thickening	Ultrasound
Diseases	Benign or Malignant	Demography	History	Mass	Mastalgia	Nipple discharge	Breast exam	Skin changes	LAP	Histopathology	Imaging	Gold standard diagnosis
Breast carcinoma[31][32][33]	Malignant	Most common diagnosed cancer among women Leading cause of cancer death in women 40-49 years old	Positive family history	+	–	±	Hard Immobile Solitary Irregular margin	±	±	Molecular alteration in epithelial cells Ductal Lobular Ductal/lobular Mucinous Tubular Medullary Papillary	Mammography: Spiculated soft tissue, mass microcalcification Ultrasound: Spiculated, hypoechoic lesion, shadowing, internal calcification	Ultrasound Mammography
Ductal carcinoma in situ (DCIS)[34][35]	Malignant	Approximately 25% of all breast cancers Increase risk with ageing	Positive family history Nulliparity Obesity	±	–	±	May have normal physical exam	–	–	Noninvasive breast cancer Heterogenous group of neoplastic lesions	Mammography: Suspicious microcalcification	Mammography
Microinvasive breast cancer[36]	Malignant	Rare Commonly referred to DCIS with microinvasion Average age 50-60 years old	Nulliparity Positive family history	+	–	±	Solitary Firm palpable mass	–	±	Associated with high grade DCIS	Mammography: A mass with or without calcification Stromal reaction	Mammography
Breast sarcoma[37]	Malignant	Rare type, < 1% of all breast malignancies Average age of between 45-50 years	Positive history of breast cancer Rapid increase in size	+	–	–	Well-defined Firm mass	±	–	Heterogeneous nonepithelial malignancies from connective tissue of breast	Mammography: Noncalcified oval mass Indistinct margins	Mammography
Phyllodes tumor[38][39]	Benign or Malignant	Most common in premenopausal women (40-50 years)	Represent 1% of breast tumors Grow aggressively Classify in benign, borderline, and malignant groups	±	–	–	Smooth and multinodular Well-defined Firm mass Mobile	–	–	Nonepithelial breast neoplasm with average size of 5 cm	Ultrasound: Solid mass Hypoechoic Well-circumscribed Mammography: Smooth mass Polylobulated mass	Ultrasound Mammography
Lymphoma[40][41]	Malignant	Extremely rare ( 0.04%-0.5%) Average age 55-60 years	Unilateral mass in older women In childbearing women, bilateral and similar to inflammatory breast cancer, possibly having Burkitt lymphoma	+	–	–	Well-defined, firm mass Multiple	–	±	Diffuse growth pattern with large cells like immunoblast associated with neutrophils	Mammography: Nonspecific circumscribed masses Without calcification	Mammography Core biopsy
Duct ectasia[42]	Benign	Common among perimenopausal women	Usually resolve spontaneously	±	±	±	Usually asymptomatic	–	–	Distention of subareolar ducts	Ultrasound: Dilated milk ducts Fluid-filled ducts	Ultrasound
Intraductal papilloma[43]	Benign	Common in women between 35-55 years old	Possibly benign Harbor areas of atypia or DCIS Surgical excision is recommended	+	±	±	Solitary or multiple lesion Large lump near nipple	–	–	Growth of papillary cell into a lumen	Ultrasound: Well-defined Solid nodule	Core needle biopsy
Lipoma[44]	Benign	Common between age of 40-60 years old	Benign tumors May experience recurrence	+	–	–	Solitary Mobile Soft mass	–	–	Mature adipocytes without lipoblasts or atypia	Ultrasound: Well-Circumscribed Hypoechoic lesion	Core needle biopsy Excisional biopsy
Sclerosing adenosis[45][46]	Small risk of malignancy	Recurrent pain during mensturation	May present as a mass or incidental finding on mammogram No treatment is needed	±	+	–	Multiple lesion Firm Tender nodules	±	–	Proliferative disease	Mammography: Well-defined or irregular mass Microcalcification	Mammography
Pseudoangiomatous stromal hyperplasia[47][48]	Benign	Common in reproductive age women	Benign stromal proliferation Stimulation of vascular lesion	+	–	–	Solitary firm mass Thickening	–	–	Slit-like spaces between glandular units Maybe confused with mammary angiosarcoma	Mammography and ultrasound: Well-defined Solid mass Noncalcified	Ultrasound Mammography
Mondor’s disease[49][50]	Benign	Uncommon benign disease Occur on outer side of breast or under nipple	Benign and self-limiting disease Resolve after 4-6 weeks	+	+	–	Thick and tender cord on breast skin	+	–	N/A	Ultrasound: Tubular anechoic structure Multiple narrowing areas	Clinical examination Ultrasound
Diseases	Benign or Malignant	Demography	History	Mass	Mastalgia	Nipple discharge	Breast exam	Skin changes	LAP	Histopathology	Imaging	Gold standard diagnosis
Diabetic mastopathy[51]	Benign	Lymphocytic mastitis or mastopathy Common among premenopausal women Longstanding diabetes mellitus type 1	Suspicious breast mass After diagnosis, excision is not required	+	–	–	Ill-defined mass Immobile	–	–	Dense keloid-like fibrosis Periductal, lobular, and perivascular lymphocytic infiltration	Ultrasound: Irregular mass Hypoechoic Dense lesion	Ultrasound Core needle biopsy
Gynecomastia[52][53]	Benign	Benign breast tissue swelling among men and boys around puberty	Benign proliferation of the male breast glandular tissue Usually underlying nipple mass At least 0.5 cm	+	±	±	Unilateral or bilateral firm mass Breast swelling Rubbery mass	–	–	Glandular breast changes	Ultrasound: Nodular pattern Dendritic pattern Diffuse glandular pattern	Ultrasound
Sarcoidosis[54]	Benign	Rare in patients with systemic involvement	Benign palpable mass May mimic malignancy feature	+	–	–	Firm mass Hard mass	–	–	Epithelioid granulomas with multinucleated giant cell with rare necrosis	Mammography: Irregular Ill-defined Spiculated solid mass	Biopsy
Fat necrosis[55]	Benign	Common among women May mimic malignancy features	Benign breast lumps develop after trauma/ surgery Suspicious lumps required biopsy No excision in established diagnosis	+	±	–	Hard or smooth mass Solitary mass Mobile	–	–	Collections of liquefied fat	Ultrasound: Collections of liquefied fat Oil cysts	Ultrasound

References

1. ↑ Langer A, Mohallem M, Berment H, Ferreira F, Gog A, Khalifa D; et al. (2015). “Breast lumps in pregnant women”. Diagn Interv Imaging. 96 (10): 1077–87. doi:10.1016/j.diii.2015.07.005. PMID 26341843.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
2. ↑ Canlorbe G, Bendifallah S (2015). “[Rare benign breast tumors including Abrikossoff tumor (granular cell tumor), erosive adenomatosis of the nipple, cytosteatonecrosis, fibromatosis (desmoid tumor), galactocele, hamartoma, hemangioma, lipoma, juvenile papillomatosis, pseudoangiomatous hyperplasia, and syringomatous adenoma: Guidelines for clinical practice]”. J Gynecol Obstet Biol Reprod (Paris). 44 (10): 1030–48. doi:10.1016/j.jgyn.2015.09.034. PMID 26530177.
3. ↑ Pustotina O (2016). “Management of mastitis and breast engorgement in breastfeeding women”. J Matern Fetal Neonatal Med. 29 (19): 3121–5. doi:10.3109/14767058.2015.1114092. PMID 26513602.
4. ↑ Leung SS (2016). “Breast pain in lactating mothers”. Hong Kong Med J. doi:10.12809/hkmj154762. PMID 27313273.
5. ↑ Anderson L, Kynoch K (2016). “Implementation of an education package on breast engorgement aimed at lactation consultants and midwives to prevent conflicting information for postnatal mothers”. Int J Evid Based Healthc. doi:10.1097/XEB.0000000000000090. PMID 27465926.
6. ↑ van Bogaert LJ (1986). “[Mastodynia and fibrocystic disease of the breast. Perspectives and methods of medical treatment]”. J Gynecol Obstet Biol Reprod (Paris). 15 (6): 805–11. PMID 3794218.
7. ↑ Songtish D, Akranurakkul P (2015). “Mastalgia: Characteristics and Associated Factors in Thai Women”. J Med Assoc Thai. 98 Suppl 9: S9–15. PMID 26817204.
8. ↑ Sen M, Kilic MO, Cemeroglu O, Icen D (2015). “Can mastalgia be another somatic symptom in fibromyalgia syndrome?”. Clinics (Sao Paulo). 70 (11): 733–7. doi:10.6061/clinics/2015(11)03. PMC 4642489. PMID 26602519.CS1 maint: Multiple names: authors list (link)
9. ↑ Cox EM, Siegel DM (1997). “Mondor disease: an unusual consideration in a young woman with a breast mass”. J Adolesc Health. 21 (3): 183–5. doi:10.1016/S1054-139X(97)00044-X. PMID 9283940.
10. ↑ ^{10.0 10.1} Belleflamme M, Penaloza A, Thoma M, Hainaut P, Thys F (2012). “Mondor disease: a case report in ED”. Am J Emerg Med. 30 (7): 1325.e1–3. doi:10.1016/j.ajem.2011.06.031. PMID 21855258.CS1 maint: Multiple names: authors list (link)
11. ↑ Greydanus DE, Matytsina L, Gains M (2006). “Breast disorders in children and adolescents”. Prim Care. 33 (2): 455–502. doi:10.1016/j.pop.2006.02.002. PMID 16713771.CS1 maint: Multiple names: authors list (link)
12. ↑ Jahanfar S, Ng CJ, Teng CL (2013). “Antibiotics for mastitis in breastfeeding women”. Cochrane Database Syst Rev (2): CD005458. doi:10.1002/14651858.CD005458.pub3. PMID 23450563.CS1 maint: Multiple names: authors list (link)
13. ↑ Lam E, Chan T, Wiseman SM (2014). “Breast abscess: evidence based management recommendations”. Expert Rev Anti Infect Ther. 12 (7): 753–62. doi:10.1586/14787210.2014.913982. PMID 24791941.CS1 maint: Multiple names: authors list (link)
14. ↑ Kleer CG, van Golen KL, Merajver SD (2000). “Molecular biology of breast cancer metastasis. Inflammatory breast cancer: clinical syndrome and molecular determinants”. Breast Cancer Res. 2 (6): 423–9. doi:10.1186/bcr89. PMC 138665. PMID 11250736.CS1 maint: Multiple names: authors list (link)
15. ↑ Dawood S, Merajver SD, Viens P, Vermeulen PB, Swain SM, Buchholz TA; et al. (2011). “International expert panel on inflammatory breast cancer: consensus statement for standardized diagnosis and treatment”. Ann Oncol. 22 (3): 515–23. doi:10.1093/annonc/mdq345. PMC 3105293. PMID 20603440.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
16. ↑ Jaiyesimi IA, Buzdar AU, Hortobagyi G (1992). “Inflammatory breast cancer: a review”. J Clin Oncol. 10 (6): 1014–24. doi:10.1200/JCO.1992.10.6.1014. PMID 1588366.CS1 maint: Multiple names: authors list (link)
17. ↑ Indelicato DJ, Grobmyer SR, Newlin H, Morris CG, Haigh LS, Copeland EM; et al. (2006). “Delayed breast cellulitis: an evolving complication of breast conservation”. Int J Radiat Oncol Biol Phys. 66 (5): 1339–46. doi:10.1016/j.ijrobp.2006.07.1388. PMID 17126205.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
18. ↑ Shetty MK, Watson AB (2001). “Mondor’s disease of the breast: sonographic and mammographic findings”. AJR Am J Roentgenol. 177 (4): 893–6. doi:10.2214/ajr.177.4.1770893. PMID 11566698.
19. ↑ Kadioglu H, Yildiz S, Ersoy YE, Yücel S, Müslümanoğlu M (2013). “An unusual case caused by a common reason: Mondor’s disease by oral contraceptives”. Int J Surg Case Rep. 4 (10): 855–7. doi:10.1016/j.ijscr.2013.07.026. PMC 3785854. PMID 23959419.CS1 maint: Multiple names: authors list (link)
20. ↑ Pinto, Joana; Aguiar, Ana Teresa; Duarte, Hálio; Vilaverde, Filipa; Rodrigues, Ângelo; Krug, José Luís (2014). “Simple and Complex Fibroadenomas”. Journal of Ultrasound in Medicine. 33 (3): 415–419. doi:10.7863/ultra.33.3.415. ISSN 0278-4297.
21. ↑ Courtillot C, Plu-Bureau G, Binart N, Balleyguier C, Sigal-Zafrani B, Goffin V; et al. (2005). “Benign breast diseases”. J Mammary Gland Biol Neoplasia. 10 (4): 325–35. doi:10.1007/s10911-006-9006-4. PMID 16900392.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
22. ↑ Templeman C, Hertweck SP (2000). “Breast disorders in the pediatric and adolescent patient”. Obstet Gynecol Clin North Am. 27 (1): 19–34. PMID 10693180.
23. ↑ Yu JH, Kim MJ, Cho H, Liu HJ, Han SJ, Ahn TG (2013). “Breast diseases during pregnancy and lactation”. Obstet Gynecol Sci. 56 (3): 143–59. doi:10.5468/ogs.2013.56.3.143. PMC 3784111. PMID 24327995.CS1 maint: Multiple names: authors list (link)
24. ↑ Sabate JM, Clotet M, Torrubia S, Gomez A, Guerrero R, de las Heras P; et al. (2007). “Radiologic evaluation of breast disorders related to pregnancy and lactation”. Radiographics. 27 Suppl 1: S101–24. doi:10.1148/rg.27si075505. PMID 18180221.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
25. ↑ De Silva NK, Brandt ML (2006). “Disorders of the breast in children and adolescents, Part 2: breast masses”. J Pediatr Adolesc Gynecol. 19 (6): 415–8. doi:10.1016/j.jpag.2006.09.002. PMID 17174833.
26. ↑ Tse GM, Law BK, Ma TK, Chan AB, Pang LM, Chu WC; et al. (2002). “Hamartoma of the breast: a clinicopathological review”. J Clin Pathol. 55 (12): 951–4. PMC 1769817. PMID 12461066.CS1 maint: Explicit use of et al. (link) CS1 maint: Multiple names: authors list (link)
27. ↑ D’Alfonso TM, Ginter PS, Shin SJ (2015). “A Review of Inflammatory Processes of the Breast with a Focus on Diagnosis in Core Biopsy Samples”. J Pathol Transl Med. 49 (4): 279–87. doi:10.4132/jptm.2015.06.11. PMC 4508565. PMID 26095437.CS1 maint: Multiple names: authors list (link)
28. ↑ Dixon JM (2007). “Breast abscess”. Br J Hosp Med (Lond). 68 (6): 315–20. doi:10.12968/hmed.2007.68.6.23574. PMID 17639835.
29. ↑ Dixon JM, Ravisekar O, Chetty U, Anderson TJ (1996). “Periductal mastitis and duct ectasia: different conditions with different aetiologies”. Br J Surg. 83 (6): 820–2. PMID 8696751.CS1 maint: Multiple names: authors list (link)
30. ↑ Committee on Health Care for Underserved Women, American College of Obstetricians and Gynecologists (2007). “ACOG Committee Opinion No. 361: Breastfeeding: maternal and infant aspects”. Obstet Gynecol. 109 (2 Pt 1): 479–80. PMID 17267864.
31. ↑ Siegel RL, Miller KD, Jemal A (January 2018). “Cancer statistics, 2018”. CA Cancer J Clin. 68 (1): 7–30. doi:10.3322/caac.21442. PMID 29313949.
32. ↑ Li CI, Uribe DJ, Daling JR (October 2005). “Clinical characteristics of different histologic types of breast cancer”. Br. J. Cancer. 93 (9): 1046–52. doi:10.1038/sj.bjc.6602787. PMC 2361680. PMID 16175185.
33. ↑ Parise CA, Bauer KR, Brown MM, Caggiano V (2009). “Breast cancer subtypes as defined by the estrogen receptor (ER), progesterone receptor (PR), and the human epidermal growth factor receptor 2 (HER2) among women with invasive breast cancer in California, 1999-2004”. Breast J. 15 (6): 593–602. doi:10.1111/j.1524-4741.2009.00822.x. PMID 19764994.
34. ↑ Virnig BA, Tuttle TM, Shamliyan T, Kane RL (February 2010). “Ductal carcinoma in situ of the breast: a systematic review of incidence, treatment, and outcomes”. J. Natl. Cancer Inst. 102 (3): 170–8. doi:10.1093/jnci/djp482. PMID 20071685.
35. ↑ Brinton LA, Sherman ME, Carreon JD, Anderson WF (November 2008). “Recent trends in breast cancer among younger women in the United States”. J. Natl. Cancer Inst. 100 (22): 1643–8. doi:10.1093/jnci/djn344. PMC 2720764. PMID 19001605.
36. ↑ Sue GR, Lannin DR, Killelea B, Chagpar AB (October 2013). “Predictors of microinvasion and its prognostic role in ductal carcinoma in situ”. Am. J. Surg. 206 (4): 478–81. doi:10.1016/j.amjsurg.2013.01.039. PMID 23791403.
37. ↑ Smith TB, Gilcrease MZ, Santiago L, Hunt KK, Yang WT (April 2012). “Imaging features of primary breast sarcoma”. AJR Am J Roentgenol. 198 (4): W386–93. doi:10.2214/AJR.11.7341. PMID 22451578.
38. ↑ Geisler DP, Boyle MJ, Malnar KF, McGee JM, Nolen MC, Fortner SM, Broughan TA (April 2000). “Phyllodes tumors of the breast: a review of 32 cases”. Am Surg. 66 (4): 360–6. PMID 10776873.
39. ↑ Chaney AW, Pollack A, McNeese MD, Zagars GK, Pisters PW, Pollock RE, Hunt KK (October 2000). “Primary treatment of cystosarcoma phyllodes of the breast”. Cancer. 89 (7): 1502–11. PMID 11013364.
40. ↑ Brogi E, Harris NL (June 1999). “Lymphomas of the breast: pathology and clinical behavior”. Semin. Oncol. 26 (3): 357–64. PMID 10375092.
41. ↑ Barişta I, Baltali E, Tekuzman G, Kars A, Ruacan S, Ozişik Y, Güler N, Güllü IH, Atahan IL, Firat D (2000). “Primary breast lymphomas–a retrospective analysis of twelve cases”. Acta Oncol. 39 (2): 135–9. PMID 10859001.
42. ↑ Schwartz GF (June 1982). “Benign neoplasms and “inflammations” of the breast”. Clin Obstet Gynecol. 25 (2): 373–85. PMID 6286199.
43. ↑ Wen X, Cheng W (January 2013). “Nonmalignant breast papillary lesions at core-needle biopsy: a meta-analysis of underestimation and influencing factors”. Ann. Surg. Oncol. 20 (1): 94–101. doi:10.1245/s10434-012-2590-1. PMID 22878621.
44. ↑ Guray M, Sahin AA (May 2006). “Benign breast diseases: classification, diagnosis, and management”. Oncologist. 11 (5): 435–49. doi:10.1634/theoncologist.11-5-435. PMID 16720843.
45. ↑ Jensen RA, Page DL, Dupont WD, Rogers LW (1989). “Invasive breast cancer risk in women with sclerosing adenosis”. Cancer. 64 (10): 1977–83. PMID 2804888.CS1 maint: Multiple names: authors list (link)
46. ↑ Wang J, Costantino JP, Tan-Chiu E, Wickerham DL, Paik S, Wolmark N (2004). “Lower-category benign breast disease and the risk of invasive breast cancer”. J Natl Cancer Inst. 96 (8): 616–20. PMID 15100339.CS1 maint: Multiple names: authors list (link)
47. ↑ Celliers L, Wong DD, Bourke A (2010). “Pseudoangiomatous stromal hyperplasia: a study of the mammographic and sonographic features”. Clin Radiol. 65 (2): 145–9. doi:10.1016/j.crad.2009.10.003. PMID 20103437.CS1 maint: Multiple names: authors list (link)
48. ↑ Salvador R, Lirola JL, Domínguez R, López M, Risueño N (2004). “Pseudo-angiomatous stromal hyperplasia presenting as a breast mass: imaging findings in three patients”. Breast. 13 (5): 431–5. doi:10.1016/j.breast.2003.10.011. PMID 15454202.CS1 maint: Multiple names: authors list (link)
49. ↑ Becker L, McCurdy LI, Taves DH (2001). “Superficial thrombophlebitis of the breast (Mondor’s disease)”. Can Assoc Radiol J. 52 (3): 193–5. PMID 11436415.CS1 maint: Multiple names: authors list (link)
50. ↑ Catania S, Zurrida S, Veronesi P, Galimberti V, Bono A, Pluchinotta A (1992). “Mondor’s disease and breast cancer”. Cancer. 69 (9): 2267–70. PMID 1562972.CS1 maint: Multiple names: authors list (link)
51. ↑ Kudva YC, Reynolds C, O’Brien T, Powell C, Oberg AL, Crotty TB (2002). ““Diabetic mastopathy,” or sclerosing lymphocytic lobulitis, is strongly associated with type 1 diabetes”. Diabetes Care. 25 (1): 121–6. PMID 11772912.CS1 maint: Multiple names: authors list (link)
52. ↑ Draghi F, Tarantino CC, Madonia L, Ferrozzi G (2011). “Ultrasonography of the male breast”. J Ultrasound. 14 (3): 122–9. doi:10.1016/j.jus.2011.06.004. PMC 3558246. PMID 23397020.CS1 maint: Multiple names: authors list (link)
53. ↑ Braunstein GD (2007). “Clinical practice. Gynecomastia”. N Engl J Med. 357 (12): 1229–37. doi:10.1056/NEJMcp070677. PMID 17881754.
54. ↑ Lower EE, Hawkins HH, Baughman RP (2001). “Breast disease in sarcoidosis”. Sarcoidosis Vasc Diffuse Lung Dis. 18 (3): 301–6. PMID 11587103.CS1 maint: Multiple names: authors list (link)
55. ↑ Soo MS, Kornguth PJ, Hertzberg BS (1998). “Fat necrosis in the breast: sonographic features”. Radiology. 206 (1): 261–9. doi:10.1148/radiology.206.1.9423681. PMID 9423681.CS1 maint: Multiple names: authors list (link)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

Worldwide, the prevalence of mastitis ranges from a low of 1,000 per 100,000 persons to a high of 10,000 per 100,000 persons.^[1] The incidence of puerperal mastitis ranges from a low of 2,900 per 100,000 persons to a high of 9,500 per 100,000 persons.^{[2][3] [4]}. Mastitis commonly affects breastfeeding mothers between the ages of 21 to 35 years.^[5] Women are more commonly affected with mastitis than men. There is no racial predilection to mastitis.

Worldwide, the prevalence of mastitis ranges from a low of 1,000 per 100,000 persons to a high of 10,000 per 100,000 persons, with an average prevalence of 4,700 per 100,000 persons.^[1]

Worldwide, the incidence of puerperal mastitis ranges from a low of 2,900 per 100,000 persons to a high of 9,500 per 100,000 persons, with an average incidence of 6,200 per 100,000 deliveries within the first seven weeks after delivery but most common during the second and third weeks.^[2][3][4]. Out of this, the incidence of those with mastitis needing hospitalization is 93 per 100,000 persons.^[6]. The percentage of those with mastitis who develop a breast abscess varies from 3% to 11%.^[7]

Mastitis commonly affects breastfeeding mothers between the ages of 21 to 35 years, with the highest occurrence in those between the ages of 30 to 34 years, even when parity and full-time employment are controlled.^[5] However, there is no difference between mastitis and breast abscess groups regarding age.^[8]

Women are more commonly affected with mastitis than men.

There is no racial predilection to mastitis.

Geographically the incidence of mastitis is higher in developing countries.^[5]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

The most potent risk factor in the development of mastitis occurs in women who are breastfeeding, especially if they have sore or cracked nipples or have had mastitis previously.

The most potent risk factor in the development of mastitis occurs in women who are breastfeeding.

Other common risk factors of mastitis include:

• Previous history of mastitis while breastfeeding^[1]
• Infrequent feedings^[1]
• Nipple excoriation or cracking^[1]
• Rapid weaning
• Illness in mother or baby^[1]
• Maternal stress or excessive fatigue^[1]
• Maternal malnutrition^[1]
• Women who use only one position to breastfeed^[1]
• Wearing a tight-fitting bra which may restrict milk flow
• Women with chronic medical conditions, such as diabetes, chronic illness, AIDS, or an impaired immune system, may be more susceptible to the development of mastitis
• Nipple piercings pose a risk due to bacterial infection following the injury and hormonal stimulation by the piercing^[2]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]

According to the World Health Organization, there is no screening modality available for mastitis.^[1]

According to the World Health Organization, there is no screening modality available for mastitis.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: ; Prince Tano Djan, BSc, MBChB [2]

If left untreated, up to 11% of patients with puerperal mastitis may progress to develop a breast abscess.^[1] Complications that may arise from mastitis include: recurrence, milk stasis and abscess formation. The prognosis is usually good and mastitis clears quickly with antibiotic therapy. 73% of smokers diagnosed with mastitis^[2] have the worst prognosis, especially those with non-puerperal mastitis, and have a higher rate of recurrence of breast abscesses.

If left untreated, up to 11% of patients with puerperal mastitis may progress to develop a breast abscess.^[1]

Complications that may arise from mastitis include:

• Recurrence

• Recurrence appears especially in cases of delayed or inadequate treatment.

• Milk stasis
• Breast Abscess

• Abscess is the most severe complication that women can get from this condition.

The prognosis is usually good and mastitis clears quickly with antibiotic therapy. 73% of smokers diagnosed with mastitis^[2] have the worst prognosis, especially those with non-puerperal mastitis, and have a higher rate of recurrence of breast abscesses.

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