09/08

BENIGN DISORDERS AND DISEASES OF THE BREAST

NL ALLORTO
COMMENTATORS: DRS P MOGABE / M MANGRAY
MODERATOR: DR C. CACALA

EMBRYOLOGY
Breast tissue is a highly modified sweat gland derived from ectoderm that occurs as
two ventral bands (mammary ridges) extending from axilla to groin at around 6 weeks
of gestation.
Anomalies occur along this mammary ridge as accessory nipples or glands, or
unilateral or bilateral absence.
ANATOMY
Macroscopic Anatomy
The breasts extend from the second to the sixth ribs, extending into the axilla via the
axillary tail. The nipple protrudes from the areola which is rugose and pigmented,
containing smooth muscle responsible for nipple erection and montgomerys glands,
which are modified sebaceous glands, responsible for lubrication during suckling.
The breast is composed of 15 20 lobes of tubular alveolar type glandular tissue.
Suspensory ligaments of Cooper are fibrous bands extending from the deep layers of
the superficial fascia to the dermis of the skin. They permit mobility while providing
structural support.

Microscopic Anatomy
The distal terminus of the ductal network is the terminal ductal lobular unit (TDLU).
Each of the lobes in the breast contains thousands of TDLUs, which form the
functional secretory unit. The secretory units produce milk, which drains via the
branching ducts to their terminus as the ampullae at the surface of the nipple. The
TDLU is complex and consists of the extralobular and intralobular terminal ducts, and
the blindly ending lobules (or ductules). An inner layer of secretory cells and an outer
layer of myoepithelial cells which contain contractile fibers that eject the milk into the
ducts during lactation surround this inner layer. Hence the lobules are referred to as
acini during pregnancy and lactation.
Lymphatic Drainage and Blood Supply
Most of the lymphatic drainage of the breast is into the axilla, although the lower
inner quadrants may drain to the infraclavicular and sometimes to the internal
mammary nodes. The lymphatic channels travel through the axilla, along the sternum,
and above and below the clavicle. Arterial blood supply is abundant, while the venous
drainage is variable. Most major venous pathways lead to the pulmonary capillary
network, or the vertebral veins.

2
DEVELOPMENT
Prepuberty
Puberty

Breasts are in resting state with ducts present but nonfunctional.

Ducts elongate due to estrogen; breast bud appears and is sometimes
mistaken for a mass and removed! Breast buds do not always develop
simultaneously.
Young adult Effects of progesterone are influenced by initiation of ovulation; ducts
elongate; side branches of ducts and lobular elements form.
Maturity
Breasts become pendulous after many ovulatory cycles; lobular
elements are well formed. Distinct morphologic changes occur with
the menstrual cycle. During the first 5 menstrual days, there is minimal
oedema in the intralobular stroma and no mitoses or apoptosis is seen
in the lobular epithelium. Intraluminal secretions are common. During
the following 2 weeks, (the follicular phase), the lobular acini develop
a distinct double-cell layer appearance with basal layer vacuolation.
The stroma becomes oedematous until the third
week, (the midluteal phase). In the last few days prior to menstruation,
(the late luteal phase), there is extensive vacuolation and oedema. In
premenopausal women, the breast is most sensitive just prior to
menstruation. Thus, mammography may be more comfortable in early
menstruation.
Pregnancy Distal ducts grow and branch; breasts enlarge to twice their normal
weight; increase in mammary blood flow leads to vascular
engorgement and areolar pigmentation; sometimes bloody nipple
discharge occurs due to hypervascularity.
Lactation
Acini are dilated and engorged with colostrum and then milk.
Menopause Lobules begin to recede, leaving mostly ducts, adipose tissue, and
fibrous tissue; histologically, postmenopausal and prepubertal breasts
are very similar. Hormone therapy may delay postmenopausal changes
in the breast and mimic a more active physiologic or premenopausal
state (ie, cyclic tenderness due to increased nodularity, etc).

ANDI Classification of benign breast disease

Normal

Benign disorder

Benign disease

Development
Duct development
Lobular development
Stromal development

Nipple inversion
Fibroadenoma
Hypertrophy

Mammary fistula
Giant fibroadenoma
Tubular breast

Cyclical change
Hormonal activity

Mastalgia

Epithelial activity

Duct papilloma

Pregnancy
Epithelial hyperplasia

Blood-stained
discharge

Lactation

Galactocoele

Involution
Duct involution
Cysts
Epithelial hyperplasia
Sclerosing adenosis

Duct ectasia
Nipple retraction
Micropapillomatosis

Other conditions outside ANDI Classification:

Galactorrhooea
Hamartomas
Granular cell tumours
Phyllodes tumour
Traumatic Fat Necrosis
Infection
Mondors disease
Gynaecomastia

Periductal mastitis
Ductal hyperplasia
Lobular hyperplasia

FIBROCYSTIC CHANGE:
A benign condition of the breast, it is actually a spectrum of morphologic changes in
the TDLU. Some of these changes result from cellular proliferation (hyperplasia) and
can cause palpable masses and/or mammographic lesions.
Types of Fibrocystic Change
Adenosis
A benign proliferation of glandular acini within a lobule, which may
also be referred to as sclerosing adenosis when acini are deformed by sclerotic
reaction. A subtype of adenosis is called blunt duct adenosis, in which there is
dilatation of acini within the TDLU. Blunt duct adenosis can show calcifications
within the acinar secretions.
Apocrine metaplasia A change in which the cells of the TDLU resemble those of
apocrine sweat glands; it is often associated with cysts of various sizes.
Cysts and duct ectasia
A dilation of medium to large ducts lined by flattened
cells and filled with secretions and amorphous debris, which can include some
calcifications ("milk of calcium"). These dilated spaces, when large, are referred to as
cysts. Smaller dilated ducts are often referred to as duct ectasia, particularly when
associated with periductal inflammation. Duct ecasia is a common cause of nipple
discharge. With extravasation of ductal contents into periductal tissue, the condition is
called retro areolar mastitis. Another complication of duct ectasia is mammary duct
fistula. Treat with excision of the fistula and the duct up to the nipple.
Fibrosis
Replacement of the normal fatty stroma by increased fibrous tissue.
Epithelial hyperplasia
A spectrum of complexity in the proliferation of benign
cells lining the TDLU, both quantitatively and qualitatively:
- Mild hyperplasia contains only a few more cells beyond the normal cell layer,
and the cells do not have any significant nuclear changes.
- Moderate or florid hyperplasia contains many more cells than the usual 2-cell layer
and is found in 20% of breast biopsies.
- Atypical ductal hyperplasia (ADH) and atypical lobular hyperplasia (ALH) are 2
forms of epithelial hyperplasia that have some of the histologic features of carcinoma
in situ. As a "borderline" category, pathologists often have difficulty making this
diagnosis. ADH has a relative risk of four, for the development of breast carcinoma,
the risk associated with ALH is less.
CYSTS
Excessive secretion of the apocrine epithelium in the terminal duct lobular unit leads
to progressive dilatation and the formation of microcysts which then enlarge.
Type I : contain actively secreting apocrine epithelium
=intracellular fluid
prone to multiplictity and recurrence
Type II : flattened epithelium
=extracellular fluid
There is no inflammatory component unless there is cyst leak or rupture.
Calcification is common.

5
Management
See attached protocol

FIBROADENOMA
This is a benign breast lesion, not part of fibrocystic change. Fibroadenoma represents
a focal hyperplasia of the stroma and the epithelial component of the TDLU and
creates a distinctive round and well-circumscribed mass on physical exam or imaging.
The stromal hyperplasia often compresses and stretches the hyperplastic glands. With
age, the stroma will become more sclerotic and may undergo dystrophic calcification,
and the epithelial hyperplasia may decrease. The natural history of fibroadenoma is to
grow to 1-3cm in size, get smaller or resolve ( one third to one half), most stay the
same size and only a small percentage enlarge. Although rare, the surrounding tissue
of a fibroadenoma may undergo changes like sclerosing adenosis, epithelial
calcifications, or papillary apocrine changes. In this tissue there is a risk of malignant
change and hence the excision of a fibroadenoma with a rim of adjacent tissue rather
than being shelled out.
Management
Solitary lump/ likely fibroadenoma

Imaging

<35 years
>35 years
ultrasound
mammogram+ultrasound

FNA / Core Biopsy

Confirmation of fibroadenoma

<25 years

>25 years

excision of all fibroadenomas

excision
if desired

one year follow up

ascertain if excision desired

NOTE:

Screen detected fibroadenomas- manage with triple assessment and excison

with localisation if positive family history.

Multiple fibroadenomas- core the larger lesions and excise the symptomatic
ones with annual follow up.
Giant multiple fibradenomas (rare) are treated with mastectomy and
reconstruction.

NIPPLE DISCHARGE
See attached protocol
GALACTORRHOEA

Milk production is stimulated by prolactin. Most cases of galactorrhoea are associated

with hyperprolactinaemia and those that are not, are poorly understood.
CAUSES
Physiological
Pregnancy and Suckling
Stress
Coitus
Pathological
Prolactinomas
Hypothalamic/ Pituitary tumors
Polycystic ovarian syndrome
Primary Hypothyroidism
Renal/Liver Failure
Drug Induced
Dopamine Antagonists
Oestrogen
Opiates
Cimetidine
Methyldopa

MANAGEMENT
1. Investigation for tumours with the appropriate treatment according to findings.
2. Cessation of offending drugs.
3. Medical therapy: Cabergoline (dostinex) or Bromocriptine dopamine agonist

7
PAPILLOMA
These are finger-like hyperplastic epithelial growths with a fibrovascular core. The
epithelial hyperplasia may be of varying degrees. Papillomas can occur in large or
small ducts and may be solitary or multiple. When multiple and small, the term
"papillomatosis" is used and is considered to be part of the spectrum of fibrocystic
change.
Solitary intraductal papillomas are tumours of major lactiferous ducts, most
frequently observed in women 30 to 50 years of age. They commonly cause a serous
or sero-sanguinous discharge, from a solitary duct. The discharge is bloodstained in
approximately one half of women with solitary papillomas .
Papilloma is the commonest pathological finding in women with Pathological Nipple
Discharge.
There is no potential for malignancy.
Management
Microdochectomy in younger patients.
Major duct excision (Hatfields procedure) in older patients
Multiple intraductal papillomas occur in approximately 10% of cases of intraductal
papillomas. Compared to solitary intraductal papillomas, these tend to occur in the
younger patients, are less often associated with nipple discharge, more frequently
peripheral, and more often bilateral. Essentially, these lesions appear to be susceptible
to the development of carcinoma: Studies have shown malignancy to develop in 10%
(7 33%) of patients with multiple peripheral lesions.
ManagementConsider close surveillance or bilateral prophylactic mastectomy with immediate
reconstuction.
Juvenile papillomatosis (JP ) is a rare condition that affects women between the
ages of 10 and 44. Patients typically present with a painless mass that, on physical
examination, is circumscribed, easily mobile, and most often thought to be a
fibroadenoma . Follow up studies have suggested that JP is associated with an
increased risk of breast cancer in the patient's female relatives, and the patient herself
may be at increased risk for developing carcinoma, particularly if the lesion is
bilateral and the patient has a family history of breast cancer.
ManagementExcision.
NOTE: There is no role for ductogram!

8
Hamartoma:
An encapsulated area of normal breast tissue. It may present as a lump, be found
incidentally at screening or surgery. Management is by way of triple assessment and
excision if the patient desires.
Granular Cell Tumours:
These present as a lump. They clinically and mammographically simulate carcinoma.
Histologically the granules are secondary lysosomes. They occur more commonly in
pre menopausal women, and particularly African- American. Typically occurs in the
upper inner quadrant (vs carcinoma, upper outer)
Treatment is wide local excision as these can recur locally.
PHYLLODES TUMOR

Phyllodes (formerly labelled as cystosarcoma phyllodes) is a rare tumour that occurs

almost exclusively in the female breast. Its name is derived from the Greek words
sarcoma, meaning fleshy tumour, and phyllo, meaning leaf. Grossly, the tumour
displays characteristics of a large malignant sarcoma, takes on a leaflike appearance
when sectioned, and displays epithelial cystlike spaces when viewed histologically
(hence the name). Because tumours are mostly benign, the name may be misleading.
Thus, the favoured terminology is now phyllodes tumour.
Phyllodes tumour is the most commonly occurring nonepithelial neoplasm of the
breast but represents only about 1% of tumours in the breast. It has a sharply
demarcated smooth texture and is typically freely movable. It is a relatively large
tumour, and the average size is 5 cm. However, lesions more than 30 cm in size have
been reported.
About 90% of phyllodes tumours are benign and about 10% are malignant or
uncertain malignant potential . The benign tumours, although they will not
metastasize, do have a tendency to grow aggressively and recur locally.
Unfortunately, the pathologic appearance does not always predict the clinical
behavior, so there may be uncertainty about the classification of some cases, hence
the term uncertain malignant potential.
Phyllodes tumours can occur in people of any age; however, the median age is the
fifth decade of life. Some juvenile fibroadenomas in teenagers can look histologically
like phyllodes tumors, but they behave in a benign fashion similar to other
fibroadenomas.
Clinical Presentation
May occur in any age, however commonly in the fifth decade. Clinically and
histologically they may be mistaken for fibroadenoma.
Management
Triple assessment of a lump is mandatory.

9
Due to tendency of aggressive local recurrence , the surgical treatment is wide local
excision if histology is known and wide re-excision of the cavity if confirmed after
excision biopsy of a lump.
TRAUMATIC FAT NECROSIS
Type I
Occurs in elderly patients, presenting as a lump. There may be overlying ecchymosis,
or simulation of cancer or mastitis. Mammaography may features suggesting
carcinoma, and biopsy is mandatory, with excision if diagnosis is doubtful.
Type II
In younger women, this presents as a tender cystic mass. Diagnosis is readily made on
mammography as striking translucent cystic areas. Triple assessessment is still
mandatory with aspiration of the cystic areas. Excise if there is non concordance
between imaging and pathology or the patient desires.

INFECTION
Lactational mastitis/abscess
Seen commonly in our setting , it is usually a staph aureus infection gaining access
via a cracked nipple. Mothers are most vulnerable during the first month of lactation
and during weaning when the breasts are engorged. There may be progression to an
abscess, which can be parenchymal , subcutaneous, subareolar, retromammary.
Management :
1. nipple and infant hygiene
2. early antibiotic therapy flucloxacillin
3. surgical drainage for abscess
4. manual expression of the breast milk.
5. feeding can continue in both breasts.
6. Resistant mastitis may be due to secondary candidial infection add
antifungal.
Non lactational mastitis/abscess
Normally a manifestation of periductal mastitis, it occurs in older woman, with
variable bacteriology. Incision and drainage with antibiotics as for lactational disease,
but biopsy of the abscess wall is mandatory.
Chronic Granulomatous Mastitis
Granulomatous lobular mastitis is an inflammatory breast disease of unknown
etiology that generally affects women of child-bearing age within a few years of
giving birth. Clinically, it may present as a hard mass resembling a malignancy or as a
firm, red, tender lesion suggestive of an abscess. Histologically, the granulomas are
centered on lobules, are often suppurative, and may be associated with microabscess
formation. The granulomas may also surround empty spaces, consistent with
dissolved lipid. Other causes of mammary granulomas, such as tuberculosis and
sarcoidosis, must be excluded. The pathogenesis of granulomatous mastitis is

10
unknown, though there is a suggestion of a continuum from subclinical mastitis to
mastitis and finally to a breast abscess. Various theories have been postulated
regarding the etiology of granulomatous mastitis, including autoimmune and
hypersensitivity processes, an association with the oral contraceptive pill, a reaction
of extravasated luminal secretions, trauma, and infection, but they have not been
substantiated. Taylor et al. recently published a review suggesting a link with
Corynebacterium infection, particularly with C. kroppenstedtii. Their study also
suggested that breast-feeding for lactating women is a significant risk factor in the
pathogenesis of inflammatory breast disease in view of their predisposition to develop
static secretions.
As corynebacteria constitute part of the normal skin flora, it can be difficult to
distinguish between infection, colonization, and contamination with these organisms.
Despite the uncertainty, it is important to consider Corynebacterium species causative
organisms in abscesses, especially when isolated as a pure or predominant growth of
>104 CFU/ml. Funke et al. proposed that the presence of gram-positive bacilli
associated with polymorphonuclear cells in the clinical specimen is strong evidence
for a causal role. Pure cultures support a possible disease association, and the
predominance of coryneform bacteria in material from normally sterile sites should
also be considered an indicator for a possible disease association.
Management
Diagnosis is made by fresh tissue sent for MC&S.
Three months of doxycycline 100mg daily with aspiration or I&D of abscesses.
(due to the chronic nature of the disease, recurrent abscess with sinus formation and
breast destruction led to mastectomy being performed in the past for disease control)

TB

Tuberculosis of the breast is a rare entity due to the infertile environment of the breast
for the bacilli. Although it may be increasing with the HIV epidemic. The low
incidence may also be due to misdiagnosis as pyogenic abscesses or carcinoma.
TB breast may be primary, where the breast lesion is the only manifestation of
disease, and secondary where there is a demonstrable focus elsewhere in the body.
Spread is most commonly retrograde lymphatic from lung, occasionally contiguous
spread from bone or joint, and rarely haematogenous. Direct inoculation from the
infected tonsils of suckling infants may be the onlyexample of primary breast TB, and
infects the ducts and spares the lobules.
It has three distinct presentations: an abscess, a painful lump or mimicking
inflammatory carcinoma, with fixity and skin changes. Rarely it presents as a nipple
discharge.
A high index of suspicion is vital to make the diagnosis, with pathological and
microbiological confirmation.
It is difficult to diagnose. Ultrasonography is the tool of choice that also fascilitates
fine needle aspiration if there is a discrete area of change. If not, random cores are
taken with/out lymph node biopsy.
The prognosis is good with adequate anti tuberculous therapy and minimal surgical
intervention. Mastectomy is rarely required and then only for extensive disease where
breast preservation is impossible.

11
MONDORS DISEASE
This is phlebitis of the thoracoepigastric vein. The course of this vein is from the
axilla laterally across the breast to the subareolar area where it crosses medially and
then extends to the epigastrium. It may be idiopathic or may occur after trauma,
surgery, or radiation to the breast. Clinical manifestation is a visible cord like vein,
skin retaction or pain. The condition is self limiting and symptomatic management
includes non steroidal analgesia.
MASTALGIA
Breast pain (mastalgia) alone or in association with lumpiness is reported in up to a
half of all women attending breast clinics. Two thirds of a group of working women
and 77% of a screening population admitted to having had recent breast pain when
directly questioned. Most mastalgia is of minor or moderate severity and is accepted
as part of the normal changes that occur in relation to the menstrual cycle.
Classification
Breast pain can be separated into two main groups, cyclical (2/3) and non- cyclical
(1/3).
Cyclical mastalgia
Patients with cyclical pain are by definition premenopausal, and their average age is
34. Normal changes in relation to menstrual cycle are heightened awareness,
discomfort, fullness, and heaviness of the breast during the three to seven days before
each period. Women often report areas of tender lumpiness in their breasts and
increased breast size at this time. Patients with cyclical mastalgia typically suffer
increasing severity of pain from mid-cycle onwards, with the pain improving at
menstruation. The pain is usually described as heavy with the breast being tender to
touch, and it classically affects the outer half of the breast. The pain varies in severity
from cycle to cycle but can persist for many years.
Cyclical mastalgia is relieved by the menopause, but pregnancy, oral contraceptives,
and parity do not affect its course. Physical activity can increase the pain: this is
particularly relevant for women whose occupations include lifting and prolonged use
of the arms. The impact of mastalgia on quality of life is often underestimated.
Non-cyclical mastalgia
This affects older women (mean age 43).
Ensure that the pain is from the breast itself.
Treatment as for cyclical mastalgia.
Other conditions that can mimic mastalgia must be treated on their own merit.
Non-breast causes
* Cervical and thoracic spondylosis
* Bornholm disease
* Lung disease
* Gall stones
* Exogenous oestrogens such as hormone replacement therapy
* Thoracic outlet syndrome

12
Assessment of patients
A careful history is necessary to exclude non-breast conditions. Clinical examination
must be performed to exclude a clinically important mass lesion in the breast. If no
mass is identified further investigation is not indicated and the patient should be
reassured that there is no sinister cause for her symptoms. The impact of the pain on
the patient's quality of life should then be determined. A pain chart for at least two
months to allow identification of the pattern of pain and to assess the number of days
of pain in each menstrual cycle.
Aetiology
Despite the close temporal relation with the menstrual cycle, hormonal studies have
failed to reveal any clear differences in patients with mastalgia, although a few reports
indicate that there may be a slight elevation of prolactin stores. Women with
mastalgia have also been found to have abnormal plasma fatty acid profiles, but the
role of dietary factors such as caffeine and fats in the aetiology of breast pain is
unclear. An abnormal profile of certain essential fatty acids might explain the
response of breast pain to agents such as evening primrose oil. Many women with
cyclical mastalgia report breast swelling and abdominal bloating in the luteal phase of
their menstrual cycles, but studies measuring total body water show no difference
between patients with mastalgia and controls: this is consistent with the observation
that diuretic treatment is of no value in mastalgia.
Treatment
Cyclical breast pain
1.
2.
3.
4.
5.
6.
7.

reassurance
supportive bra day & night
decrease caffeine intake
stop smoking
start or stop oral contraceptive pill
voltaren emugel
evening primrose oil:
3 grams daily (1gram tds) for 8 weeks then decrease to 2grams daily
indefinitely
mechanism of action: contains linoleic acid which functions as an anti
inflammatory agent stabilising adenyl cyclase in the breast.
8. modalities reserved for severe mastalgia
-danazol (s/e weight gain, acne, hirsutism)
-bromocriptine ( s/e nausea, dizziness)
-tamoxifen (s/e hot flushes, weight gain, DVT, post menopausal
uterine carcinoma)

13
GYNAECOMASTIA
* Commonest condition affecting male breast
* Due to enlargement of both ductal and stromal tissue
* It is benign and often reversible
* Usually presents as unilateral non-tender breast enlargement
Aetiology
* Most cases are idiopathic
* Physiological causes are due to relative oestrogen excess
* Physiological causes
o Neonatal
o Puberty
o Senile
* Pathological causes
o Primary Testicular Failure
+ Anorchia
+ Klinefelter's Syndrome
+ Bilateral Cryptorchidism
+ Acquired Testicular Failure
+ Mumps
+ Irradiation
o Secondary Testicular Failure
+ Generalised hypopituitarism
+ Isolated gonadotrophin deficiency
o Endocrine Tumours
+ Testicular
+ Adrenal
+ Pituitary
o Non-Endocrine Tumours
+ Bronchial carcinoma
+ Lymphoma
+ Hypernephroma
o Hepatic Disease
+ Cirrhosis
+ Haemochromatosis
o Drugs
+ Oestrogens and oestrogen agonists - digoxin, spironolactone
+ Hyperprolactinaemia - methyldopa, phenothiazines
+ Gonadotrophins
+ Testosterone target cell inhibitors - cimetidine, cyproterone Acetate
+ antiretrovirals
Prevalence peaks in pubescent years, and then a slow incline with age.
Management

See attached protocol

14
CONCLUSION
The spectrum of the benign breast ranges from aberrations of development to
disease. The approach to management must include triple assessment and while the
exclusion of malignancy is important, the impact of benign disorders on a womans
life must not be underestimated.

DIAGNOSTIC APPROACH TO NIPPLE DISCHARGE

15

NIPPLE DISCHARGE

NO ASSOCIATED
LUMP

ASSOCIATED LUMP

<35 YEARS
CLINICAL
ASSESSMENT

TRIPLE ASSESSMENT

>35 YEARS
CLINICAL
ASSESSMENT
MAMMOGRAM

CYTOLOGY

BENIGN /
INCONCLUSIVE

MAMMOGRAM
& USS

MALIGNANT

LOCALIZED TO ONE
DUCT

MULTIDUCTAL & / OR
BILATERAL
GALACTORRHOEA

MICRODOCOTOMY

TFT S (&
PROLACTIN if milky)

NO ABNORMALITY

DEFINITIVE
TREATMENT

TREAT /
INVESTIGATE IF
ABNORMAL

CYTOLOGYHB OR EPITHELIAL
CELLS

CYTOLOGY NORMAL

HADFIELDS
PROCEDURE

REVIEW 3/12 REPEAT

CYTOLOGY
NADDISCHARGE

DIAGNOSTIC APPROACH TO BREAST CYSTS

ABNORMAL

STEREOTACTIC /
USS BIOPSY

TX PATHOLOGY AS
INDICATED

16
PALPABLE
BREAST LUMP

<35 YEARS USS

>35 YEARS USS
& MAMMOGRAM

BREAST CYST

SIMPLE CYST

COMPLEX CYST

ASPIRATE

TRIPLE
ASSESSMENT

NON- BLOODY /
BENIGN
CYTOLOGY
NO RESIDUAL
MASS

RESIDUAL MASS

ATYPICAL
CYTOLOGY

BLOODY /
MALIGNANT
CYTOLOGY

FOLLOW-UP 3/12

TRIPLE
ASSESSMENT

SURGICAL CYST
EXCISION

DEFINITIVE
SURGICAL TX

RECURRENT
CYST
ASPIRATE AND
FOLLOW-UP 3/12

BENIGN
DISCHARGE
FROM FOLLOW-UP

MALIGNANT

FURTHER
RECURRENCE /
SYMPTOMATIC
CYST EXCISION

BREAST INFECTION MANAGEMENT

BENIGN
FOLLOW-UP
USS & SOPD 3/12

17

BREAST
INFECTION

LACTATING

NOT-LACTATING

MASTITIS
(USS OR NEEDLE
CHECK FOR
ABSCESS)

ABSCESS

FLUCLOXACILLIN
10/7

SURGICAL
INCISION &
DRAINAGE

? AUGMENTININDIVIDUALIZE
PATIENTS

BX =
TUBERCULOSIS

RETROAREOLAR
MASTITIS

BX =CHRONIC
GRANULOMATOUS
MASTITIS
Corynebacterium

NON-SETTLING
CONSIDER
ANTIFUNGAL TX /
USS

? FLUCLOX
INDIVIDUALIZE
PATIENTS

? MAMMOGRAM
WHEN
HEALED
(INDIVIDUALIZE
PATIENTS)

CHECK HIV AND

CD4
CXR

INCISION AND
DRAINAGE +
BIOPSY
RECURRENCES

DOXYCYCLINE
100mg/ daily 3/12
ASPIRATE
RECURRENT
ABSCESSES

TB TREATMENT
REFER FOR HIV
COUNSELLING &
ARVD IF +

RECURRENT
PROBLEM
CONSIDER MAJOR
DUCT EXCISION

FOLLOW-UP
3-6/12
LONG TERM

GYNAECOMASTIA

SURGICAL
INCISION &
DRAINAGE & Bx
ABSCESS WALL

CHRONIC NONLACTATING

MAMMOGRAM

INCISION
AND DRAINAGE
AND
BIOPSY

18

GYNAECOMASTIA
HISTORY &
EXAMINATION

DRUGS
THAT:
Oestrogen
Testosterone
Oestrogen
like
Marujuana
AntiRetrovirals
ELIMINATE
DRUG WHERE
POSSIBLE

SIGNS OF
LIVER
DISEASE
THYROID
DISEASE

TESTICULAR
LUMP

NO OBVIVOUS
CAUSE
GYNAECOMASTIA

CHECK LFTs
TFTs

TESTICULAR
ULTRASOUND
SCAN
= MASS

CHECK HCG
TESTOSTERON
E
E2
LH

TREAT
UNDERLYING
DISEASE IF
POSSIBLE

CHECK HCG &

OESTROGEN

LFTs
TFTs

pain/ cosmesis
DANAZOL
100mgb.d.1/52
100mg tds 5/52
or
Tamoxifen 20
od SOPD 1/12

SURGICAL TX
SUBCUT
MASTECT-OMY
+/LIPOSUCTION

HCG
(>5iu/L)
NO
TESTICULAR
MASS

TESTOSTERONE
LH

HCG =
TESTICULAR
GERM CELL
TUMOUR

CT ABDOMEN
+/CHEST

ANDROGEN
RESISTANCE

E2 =
TESTICULAR
TUMOURLEYDIG OR
SERTOLI CELL

ADRENAL
GERM CELL
TUMOUR
HCG
SECRETING
NONTROPHOBLAS
TIC NEOPLASM

References

PRIMARY
HYPO
GONADISM

TESTOSTERONE

LH

N
TESTOSTERONE
E2

/N
LH

NO
TESTICULAR
MASS

PROLACTIN

ADRENAL CT
+/- DHEAS

PROLACTIN
=
HYPER
PROLACTIN
AEMIA

MASS =
ADRENAL
NEOPLASM

N/
SLIGHTLY
LH
=
2NDARY
HYPO
GONADISM

NO MASS =
EXTRA
GLANDULAR
AROMATASE
ACTIVITY

19

1. Al Sarakbi W, Worku1 D, Escobar PF, et al. Breast papillomas: current

management with a focus on a new diagnostic and therapeutic modality.
Int Semin Surg Oncol . 2006;3;1.
2. Ang LM, Brown H,. Corynebacterium accolens isolated from breast
abscess: possible association with granulomatous mastitis. J Clin
Microbiol. 2007;45(5):1666-8.
3. Mansel RE. ABC of Breast Diseases: Breast Pain. BMJ 1994;309:866868.
4. Mallika T, Shukla HS. Breast tuberculosis: diagnosis, clinical features &
management. Indian J Med Res. 2005;122:103-110.
5. Dixon JM, Mansel RE. ABC of Breast Diseases: Congenital Problems
and Aberrations of Normal Breast Development and Involution. BMJ
1994;309:797-800.
6. Hamed H, Fentiman IS. Benign breast disease. Int J Clin Pract
2001;55;464-464.
7. Marchant DJ. Benign breast disease. Obstet Clin North Am. 2002;29;120.
8. Spear S. Surgery of the Breast: Principles and Art. Philadelphia:
Lippincott Williams & Wilkins, 1998.
9. Silva OE, Zuraida S. Breast Cancer: A Practical Guide. Orlando:
Elsevier Saunders, 2001.