Breast Surgery A Companion to Specialist Surgical Practice

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93. Fruhstorfer BH, Malata CM. A systematic approach
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94. Eltahir A, Jibril JA, Squair J, et al. The accuracy of
‘one stop’ diagnosis for 1110 patients presenting to
a symptomatic breast clinic. J R Coll Surg Edinb
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95. Dey P, Bundred N, Gibbs A, et al. Costs and ben-
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96. Harcourt D, Ambler N, Rumsey N, et al. Evaluation
of a one-stop breast clinic: a randomised controlled
trial. Breast 1998;7:314–9.
97. Dixon JM, Lamb J, Anderson TJ. Fine needle as-
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98. Robinson IA, McKee G, Nicholson A, et  al.
Prognostic value of cytological grading of fine-
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18
Tim Davidson
Tom Bates
Litigation in breast surgery
Introduction
Litigation for clinical negligence has accelerated
at an alarming rate. In 2009/10 the NHS paid out
£787 m (including £164 m for defence and claimant
legal costs).1 In the USA, the value of malpractice
claims for delay in the diagnosis of breast cancer
15 years ago was second only to that for neurologi-
cal damage to neonates2,3 and today this situation
remains unchanged.4 Poor cosmetic outcome is also
a frequent cause for litigation and heightened pub-
lic awareness has increased patients' expectations of
recompense for real or perceived injury following
both cosmetic and reconstructive breast surgery.
Basic principles
The legal process differs between countries and
although this chapter is based on civil law in
England and Wales, the general principles in use
elsewhere are similar.5 For a claimant to succeed
in law, she must satisfy the court (in the UK a
judge, or in some countries a jury) that there was
a failure or breach of duty of care (liability) and
that as a foreseeable result she suffered an injury
(causation). For the case to succeed, the court must
find in favour of the claimant with regard both
to liability and to causation. Clinical negligence
cases are heard in civil court and the judge deter-
mines on the balance of probabilities whether the
­defendant is liable. This is entirely different from
a criminal court determining guilt or innocence
where the level of proof is beyond all reasonable
doubt (which many equate to a degree of confi-
dence >95%). If the court finds in favour of the
claimant, the court awards financial recompense
to redress, as far as money is able, the injury that
she has suffered.
Breach of duty
Duty of care
Any doctor – GP, radiologist, surgeon or pathologist –
owes each individual patient a duty of care. This is
rarely an issue. In the NHS the doctor acts as an em-
ployee of the hospital or health board, which is covered
by the NHS Litigation Authority, which administers a
scheme that acts as a mutual insurer for participating
trusts (Clinical Negligence Scheme for Trusts).6 When
acting in a private capacity, the doctor is covered by a
professional defence organisation of his or her choice.
The Bolam test
A doctor is not negligent if he or she acts in ac-
cordance with a practice accepted at the time as
proper by a responsible body of medical opinion.
The Bolam test arises from the case of a patient
who received electroconvulsive therapy and sus-
tained fractures.7 Negligence was alleged because
the patient was not given muscle relaxants and

Litigation in breast surgery
295
was ­inadequately restrained. Some doctors would
have used muscle relaxants and restraints, others
not. The doctor was not found negligent because
he acted in accordance with a practice accepted at
the time, even though other doctors may have advo-
cated a different practice.
The Bolitho modification of Bolam adds the re-
quirement that for the practice or opinion formed
to be acceptable, it must be based on logical argu-
ment; an irrational practice cannot be argued as rea-
sonable in court simply because a body of medical
opinion agrees with its use.8
The Bolam test requires a higher degree of skill
from a specialist in his or her own field than from
a GP. If a patient is referred to a breast surgeon and
the standard of care falls below that which the pa-
tient could reasonably have expected from a breast
specialist, there has been a breach of the duty of
care. The standard of care needs to be determined
by an appropriate peer group, so a GP expert would
be asked by the court to advise on breach of duty on
the part of a GP whereas a specialist expert would
be asked to give an opinion on the standard of care
delivered by a breast surgeon.
Guidelines
National and local guidelines of good clinical prac-
tice are now in use throughout the NHS with guide-
lines covering patient referral, diagnosis, treatment
and organisational arrangements within breast
units.9,10 Breaches of guidelines are not indicative
of, or equivalent to, negligent practice and guide-
lines are constantly being amended in the light of
scientific knowledge, healthcare resources, govern-
ment targets, etc. Consideration must always be
given to the time at which the alleged breach of duty
took place and for a guideline to be relevant it must
have been in the public domain at the time.
Clinical practice that complies with guidelines
is inevitably much easier to defend against allega-
tions of negligence. A diagnostic excision biopsy
exceeding 20 g, as set out in NHS Breast Screening
Programme guidelines, does not equate to negligent
practice; however, a patient claiming excessive de-
formity after such a procedure is unlikely to succeed
in litigation if her biopsy specimen weighed under
20 g. There is ongoing debate regarding the medico-
legal implications of surgical guidelines.11 Carrick
et al.12 reported that whereas 41% of surgeons sur-
veyed believed that guidelines would protect them
against litigation, 37% believed that they would
increase their exposure to claims.
Consent
Doctors have been made increasingly aware of the
need to warn patients of the risks involved with
any diagnostic or therapeutic procedure, to in-
volve patients in decision-making and to seek fully
informed consent. Patient information leaflets, in-
volvement of breast-care nurses and more detailed
consent forms signed by the operating surgeon are
now standard practice but have done little to stem
the tide of litigation as expectations continue to
rise. Consent obtained by a junior doctor without
the knowledge and skill to undertake the intended
procedure or to discuss the possible complications
is no longer considered acceptable. The degree of
disclosure is primarily a matter of clinical judgment,
but major complications (such as loss of a flap in
breast reconstruction) must be included even if their
occurrence is rare.5,13 Where a procedure (such as
breast reduction) is being undertaken primarily for
cosmetic reasons, the surgeon is advised to include
even minor potential consequences in the documen-
tation of informed consent.
Causation
The second hurdle to be overcome by the claimant
is to prove that the negligent act caused an injury
that was forseeable. Causation may be obvious
(from clinical examination or photographic records)
where there is a poor cosmetic outcome from breast
reduction, but may be difficult to prove where there
has been a delay in the diagnosis of breast cancer.
The award of damages
The sole remedy available to the successful claimant
is an award of damages – a sum of money intended
to restore the claimant to the position she would
have been in but for the negligent act. Explanation
and apology to the claimant or her family, desirable
though they may be, are not within the power of
civil law, nor are recommendations for retraining,
suspension or deregistration of doctors who find
themselves as defendants. Patients seeking to hold
their doctor to account are, however, increasingly
turning to the fitness to practice procedures of the

Chapter 18
296
General Medical Council (GMC), with such enqui-
ries rising 30% between 2004 and 2009.14 An un-
happy patient may both embark on litigation and
report the doctor to the GMC, with the practitioner
facing so-called double jeopardy.
The award comprises two components, general
and special damages. General damages compensate
for pain, suffering and loss of amenity, and are based
upon judicial guidelines that are upgraded regularly
to allow for inflation. Special damages are specific
to the individual claimant and include past losses,
which can be identified with some accuracy, and es-
timated future losses. It is the future loss of earnings
and the costs of providing care for the claimant or
dependants that generate very high claims. A young
woman with children and a high income will attract
a high value award if she (or her surviving family)
can demonstrate that her premature death resulted
from substandard care.
In English law the perceived culpability or magni-
tude of the negligent act has no bearing on the sum
awarded. This contrasts with the position in the
USA, where cases that proceed to trial (the minor-
ity) rely on jury decisions that often incorporate an
element of punitive or exemplary damages, a sum
the jury considers warranted by the wrongfulness
of the defendant's act. The extent to which this af-
fects the size of the award can be seen by comparing
the average value of claims concluded by settle-
ment ($282 000) with that secured by jury verdict
($870 000).3
The Woolf report
In a review of the UK civil justice system, Lord
Woolf singled out clinical negligence cases15 be-
cause the difficulty in proving both liability and
causation accounts for much of the excessive cost
and the high proportion of cases that fail. The root
of the problem, however, lies less in the complex-
ity of the law than in the climate of defensiveness.
The patient's disappointment when treatment goes
wrong is heightened by what she perceives to be
a refusal to acknowledge fault and an attempt to
cover up.
The general rule is that ‘costs follow the event’ –
so the unsuccessful party is responsible for the costs
of both sides. Privately financed claimants or law-
yers acting on a no-win, no-fee basis are therefore
­reluctant to pursue actions where the chances of
success are small. However, if the claimant is sup-
ported by legal aid and loses the case, costs are not
recoverable by the defendant. Most claims in the UK
are legally aided because of the high costs of litiga-
tion; often the defendant is an NHS Trust, hence ex-
penses incurred by both the claimant and defendant
are funded from the public purse. In cases valued at
less than £12 500, the median figure for the costs of
litigation was 137% of the value of the claim. This
explains the pressure to settle low-value claims even
if defensible and a reluctance to appeal a doubtful
judgment.
The recommendations of the Woolf report are
intended to improve the resolution of disputes be-
tween patients and doctors, and reduce delay and
costs while treating both parties fairly:
• Pre-litigation protocol where claimants should
notify defendants with a written intention
to sue 3 months before action. If liability is
disputed, defendants should provide a reasoned
answer.
• Lists on the Queen's Bench to include a list of
judges familiar with clinical negligence cases
and training of trial judges in medical issues.
• Fast-track options for claims under £10 000 so
that these can be litigated on a modest budget
with a single expert acceptable to both parties
appointed by the court.
• The medical expert is now required to address
his report to the court and not to the instructing
party,16 with an overriding duty ‘to provide
objective unbiased opinion to the court on
matters within his expertise, never assuming the
role of an advocate’.
The burden (level) of proof
In civil litigation the court determines the facts,
which means that the judge makes a decision on the
balance of probabilities. This means that the suc-
cessful claimant will normally recover damages in
full, although in one case where the claimant was
held to have lost an 80% chance of cure, a deputy
high court judge directed that damages should be
calculated accordingly.17
The all-or-none nature in awarding damages is
arguably the most troubling aspect for experts in-
volved in clinical negligence.18 For example, if the

Litigation in breast surgery
297
court finds that as a result of negligence a woman
has suffered a reduction in her chance of survival
from 60% to 40%, she will be awarded the full
amount to compensate her (or her family) as though
the loss had already occurred, on the basis that on
balance she is now more likely to die. If the court
finds, however, that her chance of survival has re-
duced from 90% to 60%, it may award her nothing
on the basis that on balance her chance of survival
remains unchanged.
In the case of Hotson v. East Berkshire Area Health
Authority (1987), the House of Lords formulated
the current UK position on causation. The defen-
dant was in breach of duty in failing to diagnose a
fracture of a femoral epiphysis following a fall. The
child developed avascular necrosis with significant
disability. The evidence was that the child had a
75% risk of developing this complication due to the
accident and the trial judge and the Court of Appeal
held that he was entitled to 25% of his damages
for the 25% loss of a chance that prompt treatment
might have prevented the complication. However,
the House of Lords overturned the decision and
held that on balance he was going to develop it even
in the absence of negligence or, put another way, he
had failed to establish that he was within the 25%
who would not develop it.
The position on causation was again recognised
in the appeal case of Gregg v. Scott (2002), a claim
for failure to diagnose an axillary lump as non-­
Hodgkin's lymphoma. The Court of Appeal held
that the delay had reduced his chance of survival,
although this had always been less than 50%, from
42% to 25% survival at 10 years. The case was ap-
pealed to the House of Lords who dismissed the
claimant's appeal for loss of a chance and upheld
the traditional approach. So the burden of proof in
deciding causation, for the time being at least, re-
mains unchanged.
Delay in the diagnosis of
breast cancer
Delay in diagnosis may occur as a result of failure
to refer the patient from primary care or, once refer-
ral has taken place, for example with false-negative
mammography, failure to perform triple assess-
ment, misinterpretation of equivocal results or the
misfiling of a positive test result.19
Litigation arising from delay in diagnosis concerns
two main areas:
• Did the delay necessitate more extensive
treatment?
Where the patient has had a mastectomy on
the basis of tumour size, it is often claimed that
­earlier diagnosis would have made breast conser-
vative surgery an option. For multifocal tumours,
it can be argued that mastectomy would have
been needed from the outset. With the advent of
sentinel node biopsy, a claimant who has under-
gone axillary clearance for involved nodes may
contest that earlier diagnosis at a time when her
nodes were clear would have allowed less radical
axillary surgery. When the patient has received
chemotherapy it might be argued that this would
not have been necessary if the diagnosis had been
made sooner when, for example, the axillary
nodes would on balance have been negative.
• Did the delay in diagnosis reduce the chance
of cure?
This is a controversial area since there is public
expectation, promoted over the years by health
campaigners, that earlier diagnosis offers bet-
ter chance of a cure. Where expert opinion is
divided, the court often prefers the evidence in
favour of the delay having caused a reduced
survival time. A review of claims for diagnostic
delay in breast cancer in Sweden over a 10-year
period concluded that delays had an impact
on treatment in 23% of cases and adversely
affected prognosis in 11% of those patients for
whom the delay was longer than 12 months.20
Delay in primary care
The GP who sees many cases with benign breast symp-
toms each year but only one or two breast cancers is
in a difficult position and GPs are increasingly fac-
ing litigation for delays in referral. The main area of
contention is where long-standing or recurrent breast
nodularity coexists with an (initially) undetected
lump. Relying on a negative mammogram without an
expert clinical examination, ultrasound or needle bi-
opsy may increase the risk of false reassurance.19
GPs today are therefore faced with referring most
women with breast symptoms for a specialist opinion
and referral guidelines have been in use in the UK
since 1995.21–23

Chapter 18
298
Delay after specialist referral
Breast units throughout the UK submit audit data
on compliance with 2-week target referrals for sus-
pected cancers.24 The prioritisation of referral let-
ters can be counter-productive if non-urgent cases
have to wait longer, but current NHS guidelines
stipulate all symptomatic breast referrals are now
seen within 2  weeks. NHS ‘31/62’ cancer targets
(allowing 31 days from urgent referral to diagnosis
and 62 days to commencing treatment) will identify
units in breach of national guidelines.
The role of triple assessment, and the circum-
stances in which it fails, are critical. The specialist
centre is also faced with the problem that women
under 35 form the majority of the diagnostic
­workload (66%) but the fewest number of breast
cancers (3%).21
The North American experience
Two studies commissioned by the Physician Insurers
Association of America (PIAA)2,3 showed delay in
the diagnosis of breast cancer to be the common-
est cause of clinical litigation, and a striking feature
of both studies was young age: women under 50
accounted for 69% of claimants and received 84%
of the damages paid, whereas only 25% of cancers
occur in women under 50.
The most common reasons cited for the delay were
(in descending order):
• physical findings failed to impress;
• failure to follow up the patient;
• negative mammogram report or misreading of
the mammogram;
• failure to perform a biopsy.
In 487 cases where liability was admitted, the
mean delay was 14 months. The mean payout was
$301 000, with higher damages for longer delays
and to younger patients.3
Diagnosis of breast cancer
Triple assessment is the foundation upon which cli-
nicians diagnose breast lumps. However, the extent
to which the accuracy of these tests is reduced in
younger women is not well appreciated (Fig. 18.1).
It has been suggested that perfection of diagnosis will
require removal of every solid mass,25 but this would
represent a retrograde step. The practice of defensive
medicine, in place of conventional wisdom, may well
be encouraged by a litigious public and diagnostic
tests where the sensitivity falls below 95%.
Physical examination
About 70% of all breast cancers are palpable, but
with tumours of 0.6–1 cm diameter this figure falls
100
80
60
40
20
0
30–39
40–49
Clinical examination
50–59
60–69
≥70
Age (years)
% detection of malignant or
probably malignant lessions
100
80
60
40
20
0
30–39
40–49
Mammography
50–59
60–69
≥70
Age (years)
% detection of malignant or
probably malignant lessions
Figure 18.1  •  Sensitivity of clinical and mammographic examination by age. Reproduced from Dixon JM, Mansel RE.
Symptoms, assessment and guidelines for referral. In: Dixon JM (ed.) ABC of breast diseases, 2nd edn. London: BMJ
Books, 2000; p. 6. With permission from Wiley Publishing Ltd.

Litigation in breast surgery
299
to 50%.26 The larger the breast and the greater the
density of breast tissue, the more difficult physical
examination becomes. Cyclical changes in breast
parenchyma may require repeat examination at
different phases of the menstrual cycle. Coexisting
benign lumps, scars and distortion from previous
surgery, the ridge of tissue above the inframam-
mary fold, changes during pregnancy and lactation,
and the underlying ribs all add to the uncertainty
of clinical examination. Other difficulties include:
inflammatory cancers masquerading as infection;
the presence of implants with an associated fibrous
capsule; and the effect of hormone replacement
therapy, which increases the density of breast pa-
renchyma both clinically and radiologically.
The sensitivity of clinical examination in women
aged 30–39 can be as low as 25%.26 A sensitivity over
90% can only be expected in older women, when the
atrophic nature of the breast parenchyma and the low
incidence of benign disease combine to make clinical
diagnosis a relatively simple task. The low sensitivity
of clinical examination, coupled with the low inci-
dence of breast cancer and the considerable numbers
of young women attending breast clinics, must largely
explain why failure of physical findings to impress the
clinician was one of the most common reasons for
delay in diagnosis in the PIAA study.3
Mammography
False-negative mammography is one of the principal
reasons for delay in diagnosis,3,27 since it gives the
clinician and patient false reassurance. Age is an im-
portant factor in false-negative reporting (Fig. 18.1),
with the number of cancers missed inversely pro-
portional to age: 36% of cancers in women aged 40
compared with just 9% in those aged 75. The net
result of medicolegal pressure on breast radiologists
has been an increase in recall and biopsy rates.28,29
Ultrasound
The use of ultrasound is now an integral part of
breast imaging in a patient of any age with a lump
(see Chapter 1), especially when an abnormality is
not detectable on clinical or mammographic exami-
nation. Ultrasound-guided core biopsy has replaced
fine-needle aspiration cytology (FNAC) in screen-
detected tumours, although both techniques are
currently acceptable in the symptomatic clinic. The
expertise required for ultrasound examination and
guided core biopsy has placed breast imaging out-
side the competency of the general radiologist. The
breast surgeon using ultrasound in the clinic may be
similarly compromised unless training in the tech-
nique can be verified.
Cytology
For many years FNAC has allowed rapid and cost-
effective tissue diagnosis of a palpable lump. How
reliable is FNAC? Dixon et al.26 reported that the
sensitivity of FNAC could be increased from 66%
to 99% by restricting the biopsy to one aspirator. In
comparison, the sensitivity of FNAC in women un-
der 36 was as low as 78%,25 though Dixon et al.26
found that accuracy was not related to age if inade-
quate samples were excluded from the calculations.
In a review of 112 reports of FNAC of breast
masses by Layfield et al.30 the overall accuracy was
over 95% but delays in diagnosis of greater than
50 days still occurred, and 85% of such delays were
in women under 5531 and with smaller tumours.32
In small tumours, a sampling error is probably more
common than misinterpretation of the cytology and
ultrasound-guided core biopsy is advisable.
Efficacy of triple assessment
If it is assumed that breast cancer detection by clini-
cal examination, imaging and FNAC are indepen-
dent of each other, it is possible to calculate the
theoretical rate at which all three tests will give a
false-negative result. The false-negative rates of the
three investigations have been multiplied and ex-
pressed as a percentage in Table 18.1. It is probable
that the sensitivities of these tests are not totally in-
dependent of each other, and therefore the predicted
rate that all three tests will be false negative for an
individual is a conservative estimate. For a woman
under 35 with breast cancer, there may be a 12%
chance that all three tests will give a false-negative
result. Using optimal sensitivities, the chance that
all three tests will produce a false-negative result
falls to approximately 1 in 1000 patients with these
data skewed towards the older age groups; the likely
overall rate of false-negative triple assessment in the
clinic is between 1.4% and 4%.32,33

Chapter 18
300
Tumour doubling time
The usual threshold diameter for detection of a
breast cancer by physical examination is 1 cm; such
a tumour consists of 109 cells and is the result of
30 doublings. It is possible for mammography to
detect tumours as small as 2 mm, which equates to a
tumour of 107 cells and about 23 doublings.
Assuming a constant doubling time, early detec-
tion of breast cancer is a misnomer, since at least
two-thirds of the biological life of the tumour will
have been completed by the time of detection.34
In medicolegal terms, if the alleged delay in diag-
nosis was 14 months for a cancer with a doubling
time of 90 days, such a delay would equate to the
number of cells increasing by one order of magni-
tude (i.e. from 109 to 1010 cells). This represents a
major increase in tumour load but is a very short
period in the lifespan of the tumour and it is diffi-
cult to be sure that this period of delay would have
a significant effect. In civil law, however, the court
wants to know whether such an effect is more
likely than not to alter the patient's prognosis or
treatment.
Lymph node status remains the most important
prognostic indicator at the time of primary treat-
ment. Tubiana and Koscielny35 suggested that breast
cancer represents a continuum from slow-growing
tumours with late axillary involvement and distant
dissemination to the most aggressive, rapidly grow-
ing and early metastasising subtype. Assuming the
growth rate of the nodal metastasis approximates to
that of the primary tumour, it is possible to estimate
the theoretical time at which the tumour must have
metastasised, and not infrequently this would have
occurred before the threshold size for detection of
the primary tumour.34
It is generally accepted that breast cancer begins
as a single cell or a small group of cells that exhibit
an exponential growth pattern. The time taken for
a tumour to double in volume is known as the dou-
bling time. Doubling times for breast cancers have
been estimated by measuring the size of mastectomy
scar recurrences36 and by serial mammographic
evaluation.37
Pearlman36 categorised patients as having fast-
(<25  days), intermediate- (26–75  days) and slow-
growing (>76 days) tumours based on measurement
of tumour doubling time; 5-year survival rates were
5%, 62% and 100% respectively. Peer et al.38 esti-
mated mean doubling time in women under 50 to
be 80 days (confidence limits 44–147 days) and in
women over 50 to be 157 days (confidence limits
121–204  days). Although lymph node metastases
are more commonly found in fast-growing tumours,
it would be wrong to assume that the survival of
patients was entirely a consequence of tumour
doubling time. Galante et al.37 emphasised the im-
portance of the metastatic potential of the tumour,
suggesting that within fast-, intermediate- and slow-
growing tumours there may be subsets with high
and low metastasising potential.
The premise that early detection of a tumour will
lead to cure depends on the concept that at the time
of earlier treatment the tumour has not metasta-
sised. The period of time between the earliest pos-
sible detection of the cancer and the time at which
the tumour metastasises has been described as the
cancer control window.39 If the tumour has already
metastasised by the time it reaches the threshold size
for detection, there is no window and only effective
systemic therapy might cure the patient. It is often
argued by the claimant and her legal team that delay
in treatment is the cause of metastasis rather than
the inherent biology of the tumour itself.
Vignettes on breach of duty
The following vignettes illustrate areas of breach
of duty that have arisen in medicolegal breast cases
and the comments following each vignette raise is-
sues that might be discussed in conference with
counsel.

False-negative rate

Women <35 years
Optimal
Clinical
examination
0.75
0.12
Mammography
0.75
0.12
Fine-needle
cytology
0.22
0.05
All three false
negative
12.3%
0.072%
Table 18.1  •  False-negative rates of triple assessment
for women under 35 compared with the
generally quoted results19,31

Litigation in breast surgery
301
Vignette 1: False-positive cytology,
lymphoedema and alteration of
records
A 60-year-old patient was referred to a breast
clinic with a clinically suspicious breast lump.
Mammography was suspicious (M4) and FNAC
was malignant (C5). The patient underwent wide
local excision and axillary clearance for what subse-
quently proved to be a histologically benign condi-
tion. She complained of a poor cosmetic outcome
and a painful swollen arm, which she had not been
warned about. The nursing records stated ‘patient
was warned of the risk of lymphoedema’.
Comments
• A false-positive cytology result is a rare but
potentially devastating event. From a medico-
legal standpoint, an expert review of the
cytology should be the first step. If experts are
agreed that the cytologist acted reasonably in
reporting the slides as malignant, attention will
then focus on the surgeon.
• The surgeon has to be aware that a false-positive
cytology can occur and for this reason most
surgeons will not carry out mastectomy without
histological confirmation from a core biopsy.
Histology is mandatory in the absence of a fully
concordant malignant triple assessment and
should have been obtained in this case. Axillary
clearance for a benign condition is a potentially
significant injury and it is unfortunate that this
patient developed lymphoedema.
• The tense of the warning suggested to the judge
that this was a retrospective note. Judges place
most reliance on contemporaneous records and
alterations to the notes are often quite obvious.
Any addition to the notes must be clearly
identified as such by signing and dating the
record and any temptation to alter the record
after the event must be firmly resisted.
Vignette 2: Failure of preoperative
assessment and postoperative
management
A 69-year-old woman presented with a small but
obvious carcinoma in the tail of the breast. The sur-
geon performed FNAC, which showed malignant
cells (C5), and he carried out wide local excision of
the tumour without preliminary breast imaging and
without performing axillary staging. The tumour
was grade 2 but the resection margins were not re-
ported. The patient was started on tamoxifen but
was not referred for consideration of radiotherapy.
Comments
• The management of this patient falls short of
an acceptable standard in a number of respects
(breach of duty), but until such time as she
develops evidence of recurrence, which may
never occur, any resultant harm (causation)
remains potential.
• A preoperative mammogram might have shown
widespread microcalcification or multifocal
tumour and in this situation conservative
surgery would not have been appropriate.
There might also have been an undetected
cancer in the contralateral breast.
• To fail to report the margin status and
managing a patient with conservative surgery
without consideration of radiotherapy is
unacceptable.
• It is clear that this case was not discussed at a
multidisciplinary meeting.
• Axillary node status should have been assessed
and has been recommended in UK guidelines
since 1995.9
Vignette 3: False-negative
cytology, trainees in the clinic and
lobular carcinoma
A 38-year-old patient was referred to a breast clinic
with a breast lump. Mammography was negative
and a specialist registrar found an indefinite lump
of which he was not suspicious. He carried out
FNAC but failed to achieve an adequate specimen
(C1). At follow-up 6 weeks later a repeat FNAC
showed an adequate benign sample (C2). She
was discharged from the clinic but re-presented
6 months later with an invasive lobular carcinoma
at the same site.
Comments
• Trainees must be adequately supervised and
only permitted to see patients by themselves
when their trainer is satisfied that they are
competent and understand local protocols.10

Chapter 18
302
• There is a learning curve in achieving adequate
samples with FNAC. The rate of inadequate
FNAC samples should be monitored for each
clinician.
• Clinicians should be aware that lobular cancers
are prone to false-negative mammography.
There is also an increased difficulty with false-
negative cytology interpretation.
• The diagnosis of breast cancer in young women
is difficult and in the situation where a patient
complains of a lump but on clinical examination
or mammography nothing is obvious,
ultrasound is advisable, with guided biopsy if a
lesion is seen.
Vignette 4: Pneumothorax
following FNAC
A dental nurse aged 32 presented with a lump in the
tail of the breast. An experienced clinical assistant in
the breast clinic carried out FNAC. Unfortunately,
he pierced the pleura and caused a pneumothorax
that required hospitalisation and pleural drainage.
The patient was not warned of the risk and com-
plained of persistent chest pain over a period of
many months.
Comments
• Did the clinician fail in his duty of care by
advancing the needle too far or by failing to
warn the patient? The literature suggests a risk
of around 1 in 10 000.40–42 It is not rare to strike
a rib with the needle at FNAC. Piercing the
pleura may be more common because a trivial
pneumothorax may go undetected.
• In several cases the court has found
pneumothorax to be a rare but recognised
complication that can occur without breach
of duty, although one case ruled this injury
to be negligent, which was an unexpected
judgment.42 There is often a reluctance on the
part of trusts to defend or appeal low-value
cases under £10 000 (as would be the case for
damages here).
• In defending a claim of negligence, it is
important to be able to show that the clinician
was experienced in the technique. Were this to
be a trainee, it would be necessary to establish
that he or she had been properly supervised.
• Pneumothorax has been reported following
needle localisation by a radiologist and
following aspiration of axillary seroma,
performing FNAC and core biopsy. Using image
guidance should theoretically reduce the risk.
Delay in diagnosis: causation
issues
In a case of delay in diagnosis, it is often relatively
straightforward to establish whether there has been
a breach of duty of care. The next hurdle to be over-
come by the claimant is to satisfy the court, on the
balance of probabilities, that this delay caused her
harm. Expert opinion is often divided and if the ex-
perts cannot agree then the court makes a judgment.
The public and the judiciary have the expectation
that early diagnosis carries a better outlook. It is
not surprising therefore that counter-arguments of
lead-time bias and innate tumour biology tend to
fall on deaf ears.
Having established breach of duty, the issue of cau-
sation may include the allegation that less treatment
would have been required. It may also be argued
that psychological damage has ensued. However,
the main issue centres around whether the claim-
ant has suffered a reduced expectation of life or, if
she has died by the time the matter comes to court,
whether she would have lived longer. Richards
et  al.,43 after a systematic review, concluded that
there is an average reduction in 5-year survival of
7% with a delay of 3–6 months and 12% with a
delay of more than 6 months. Dische et al.44 extrap-
olated a 1.8% decrease in survival from Richards
et al.'s data for each 1-month delay up to 6 months.
In the same issue of the Lancet, Sainsbury et al.45
reported no such effect but produced the apparently
contradictory finding that patients with the shortest
delay had the worst prognosis, a finding previously
reported by Afzelius et al.46
The survival in patients with the best-prognosis
tumours (small, special type, grade 1, node nega-
tive) approaches that of the normal population, and
clearly a formula attributing a reduction in survival
for each month of delay would be inappropriate in
such tumours. However, if one accepts this, then for
some tumours with a worse prognosis there must
be a greater loss of survival.44 It would nevertheless
seem intuitive that the most aggressive tumours with
rapid metastatic potential are likely to be ­incurable

Litigation in breast surgery
303
from early in their natural history, suggesting diag-
nostic delays in such cancers are less likely to have
an impact on survival.
Vignettes on causation
The following vignettes illustrate some of the causa-
tion issues that have arisen once liability has been
established. Delay in diagnosis remains an area of
considerable uncertainty and the comments reflect
our experience of differing arguments presented to
the court.
Vignette 5: 12-month delay
in diagnosis of node-positive
carcinoma
A 32-year-old woman was referred to a breast clinic
with a lump in the breast. Ultrasound showed an
indeterminate opacity 1 cm in diameter consistent
with a fibroadenoma but no sample was taken by
FNAC or core biopsy. She was discharged from the
clinic but returned a year later with a clinical car-
cinoma at the same site. This measured 2.1 cm on
both ultrasound and histology and was grade 3; one
of four nodes was positive. Liability for delay in di-
agnosis was admitted in failing to carry out a biopsy
at the first visit.
Comments
• The Nottingham Prognostic Index (NPI)47–49
and Adjuvant!Online50 are often used to
determine the difference in outcome over the
period of delay.
• Both NPI and Adjuvant!Online rely on the
following assumptions about the individual
case:
Assumption 1: the tumour grade remains
constant – this is usually agreed by both sides.
Assumption 2: earlier tumour size. In this
particular case a record of tumour size at
the first visit was available, but if no clinical
measurement was recorded and there was
no imaging, an approximate tumour size
has to be derived by working back from the
tumour volume at diagnosis using tumour
doubling times. This calculation assumes (i)
that tumour growth is exponential, (ii) that
in calculating tumour diameter the tumour
­approximates a sphere or an ellipsoid, and
(iii) that the doubling time chosen is appro-
priate. Tumour size itself is a weak deter-
minant of prognosis but the derived earlier
tumour size is further used to calculate the
likely nodal status.
Assumption 3: the nodal status at the time of
the breach of duty is usually unknown and
often disputed by the experts. Axillary node
status is invariably presumed to have been
negative by the claimant, and this claim is
supported by tables for tumour grade and
tumour size that show the probability of posi-
tive nodes.51 Only in grade 2 and 3 tumours
greater than 2.5 cm does the probability of
positive nodes rise above 50%. Therefore, on
balance it may often be argued that the nodes
would have been negative at the earlier time
when the tumour was smaller.
Vignette 6: 2-year delay in
diagnosis of node-negative grade
1 carcinoma
A 40-year-old woman presented with a lump in the
breast and a triple assessment was carried out. The
tumour measured 1.5 cm on ultrasound and mam-
mography, and FNAC was reported as benign (C2).
She was discharged but 2 years later returned with
a carcinoma 3 cm in diameter on histology. The pa-
tient was treated by breast conservation and post-
operative radiotherapy.
The tumour was grade 1 and four nodes sampled
were clear. Review of the original cytology indicated
that this had been under-reported and an expert
opinion graded the slides unequivocally malignant
(C5). Breach of duty was admitted.
Comments
• The standard of care must be judged against
the standard reasonably to be expected of a
cytologist working at the same level and not
that of a world expert in the field.
• Although the tumour doubled in diameter over
the 2-year period of delay, it remained within
the good prognosis group. The treatment would
have been the same with an earlier diagnosis
and therefore the case did not succeed on
causation.

Chapter 18
304
Vignette 7: 3-year delay in
diagnosis of a carcinoma missed
on screening
A woman of 50 responded to an invitation for
screening and was recalled for a localised area of
microcalcification. There was a soft-tissue opac-
ity and the appearance was judged benign on fur-
ther magnification views and ultrasound. She was
returned to routine screening but 3 years later the
screening films showed an obvious carcinoma at
the same site. This was a 2-cm grade 2 infiltrating
carcinoma with an extensive in situ component;
four of 10 nodes were positive. An expert opinion
from a breast-screening radiologist rated the origi-
nal films as suspicious for ductal carcinoma in situ
(DCIS; M4) and stated that the microcalcification
should have been biopsied by any competent breast
radiologist.
Comments
• Delay due to radiological misinterpretation
tends to be a matter of years rather
than months. Screening by 3-yearly
mammography probably reduces breast cancer
deaths by up to 25%, and it is likely that a
delay in diagnosis of 3 years will affect survival
in a proportion of cases.
• The potential loss of survival in this case would
be considerable since the original lesion would,
on the balance of probabilities, have been an
area of high-grade DCIS with a near-normal
expectation of life if adequately treated at age
50. At age 53 the patient now has a relatively
poor prognosis but on balance is still more
likely to survive 10 years (Table 18.2).
Vignette 8: 14-month delay in
the breast clinic and failure to
recommend chemotherapy
A 30-year-old woman was referred with a lump in the
breast and was seen by a succession of specialist reg-
istrars. An initial ultrasound showed a 1-cm opacity
consistent with a fibroadenoma but the FNAC was
reported as mildly atypical (C3) and the pathologist
advised ‘consider biopsy to confirm’ but no action was
taken. A series of 6-month follow-up appointments
were given. Finally the GP referred the patient again to
the consultant, who immediately diagnosed breast can-
cer. The tumour was 4 cm, grade 3 and heavily node
positive. The patient was treated by wide local exci-
sion, axillary clearance and radiotherapy. She was not
given chemotherapy or hormone treatment until she
developed bone secondaries 16 months later. Breach of
duty was admitted for the delay in diagnosis and the
failure to give chemotherapy at the time of diagnosis.
Comments
• Discussion of the discordant triple assessment at
the breast multidisciplinary meeting (MDM) did
not take place.
• Arranging a 6-month follow-up for a breast
lump that is presumed benign is illogical.
• The judge took evidence from five expert
witnesses. It was agreed that when first seen the
tumour would have been grade 3, 1 cm in diameter
and node negative. The tumour had increased in
size to 4 cm in the 14 months of delay and opinion
was divided as to whether this was ever potentially
curable. The experts for the claimant were far
more optimistic than those for the defence but in
the event the judge preferred the latter.52
• The judge considered that, on balance, the
breach of duty ‘caused her to die 18 months
before, sadly, she would have died anyway’.
• Unfortunately, the damages amounted to less than
the defence had already paid into court. Civil
litigation rules resulted in the family winning the
case but receiving none of the settlement.
Vignette 9: 8-month delay in
diagnosis in primary care
A 46-year-old woman attended her GP with a new
lump that the GP assessed as a 1.5-cm smooth
Group
NPI value
10-year
­survival (%)
Excellent (EPG)
2.0–2.4
96
Good (GPG)
2.41–3.4
93
Moderate I (MPGI)
3.41–4.4
82
Moderate II (MPGII)
4.41–5.4
75
Poor (PPG)
5.41–6.4
53
Very poor (VPG)
≥6.41
39
Table 18.2  •  Nottingham Prognostic Index groups
From the Nottingham Primary Breast Cancer Series. Data relate
to patients with primary operable breast cancer, treated from
1990 to 1996.47

Litigation in breast surgery
305
­benign lump; in view of the past history of benign
breast nodularity, the GP recommended a conserva-
tive approach and it was only when she saw a dif-
ferent GP 8 months later that referral to the clinic
and a diagnosis of breast cancer was made. She
underwent mastectomy and axillary clearance for a
42-mm grade 2 carcinoma with seven of 20 nodes
involved, followed by chemotherapy, radiotherapy,
trastuzumab and endocrine therapy. She had suf-
fered persistent shoulder discomfort since the time
of axillary surgery.
Comments
• Following an opinion from a GP expert, breach of
duty on the part of the GP was admitted and the
claim for causation was both for more extensive
treatment and loss of chance of survival.
• The claimant's breast expert maintained that
she would had undergone wide excision and
sentinel node biopsy at the earlier time and that
her expected survival had been reduced from
93% to 53%.
• At a pre-trial meeting of experts, they agreed
jointly that the nodes would still have been
involved at the earlier time and that the
axillary surgery would have been unchanged,
and agreed that she was, on balance, still
more likely to survive than die from the breast
cancer.
• The experts agreed that she had lost the chance
of breast conservation as a result of the delay
and following their joint report the case was
settled for £50 000 on the basis that she had
undergone mastectomy and would require
future breast reconstruction.
• Less than 5% of clinical negligence cases are
contested in court with over 95% of cases either
dropped or settled before the trial date.
• Since the discussion of discordant triple
assessments in breast MDMs has become
widespread good practice, claims for delay in
diagnosis against breast specialists have reduced
and are now mainly against GPs who fail to
refer cases to the breast clinic.
Poor cosmetic outcome
The mastectomy rate in the UK remains close to
40%, and where mastectomy is required the in-
creasing demand for reconstruction has been
­addressed in national guidelines53 and detailed au-
dit.54 Litigation has risen in line with patients' ex-
pectations,55 although the typical size of claim for
an unsatisfactory cosmetic outcome is considerably
less than for delay in diagnosis.
Clinical notes should record evidence of discus-
sions with the patient regarding either immedi-
ate or later breast reconstruction and should
document that alternative treatment options and
potential complications of surgery have been
discussed. The presence of the breast-care nurse
to augment and further document the surgeon's
counselling is advisable and her written record,
usually kept separately from the clinical notes,
can make all the difference when allegations of
inadequate preoperative information are part of a
claim for breach of duty on the part of the recon-
structive surgeon.
Preoperative markings should be made on the
ward by the operating surgeon, explained to and
agreed with the patient without pressure of time,
and a record kept of this operative planning. Hasty
skin marking in the anaesthetic room or on a pa-
tient already anaesthetised are not compatible with
a reasonable standard of care.
A request for immediate reconstruction can pres-
ent difficulties in offering the most appropriate
reconstruction and yet not breach guidelines for
commencing treatment. This tension has presented
medicolegally with a patient offered a more basic
form of reconstruction with a subpectoral implant in
order to expedite mastectomy who, once the cancer
had been dealt with, felt that the advice fell below a
reasonable standard. The breast surgeon must make
available to the patient the appropriate range of re-
constructive options, including those that might re-
quire the involvement of a plastic surgical colleague.
Should a patient pursue litigation for her cosmetic
outcome, the Bolam principle7 would apply in de-
termining breach of duty, i.e. the practice would
be compared with that held to be reasonable by a
similar body of professionals, in this case breast sur-
geons trained to undertake breast reconstruction.
An audit of the surgeon's operative results is not
currently expected by the court, nor are there pre-
scribed minimum numbers of procedures to comply
with good practice. At present there is no certificate
of competency in training in breast reconstruction
within the UK, but current reconstructive guide-
lines53 outline the requirements for good practice.

Chapter 18
306
When a poor cosmetic outcome is due to a recog-
nised complication rather than poor judgment and
provided the patient has been warned of the risk,
she does not have a case against the surgeon.
Reduction mammoplasty, breast augmentation and
surgery for gynaecomastia remain high-risk areas for
patient dissatisfaction and should never be under-
taken on an occasional basis. Breast operations rep-
resent the biggest group of plastic surgical procedures
giving rise to claims.56 It is vital that evidence of ap-
propriate discussions about potential problems is
adequately recorded in the notes and the correspon-
dence, together with the use of appropriate informa-
tion leaflets and clinical photographs to explain the
proposed procedure. Consent forms should record
the signed informed consent as well as documenting
that the literature has been received and understood.
Operation notes, where relevant, should include
details of implant type, serial and lot number, and
manufacturer, for possible future reference.57
Vignette 10: Poor cosmetic
outcome after immediate breast
reconstruction
A 52-year old patient with multifocal cancer was
advised to have a mastectomy by a breast surgeon
and after discussion with the breast-care nurse she
requested immediate reconstruction. He offered her
a tissue expander, which was inserted at the time
of mastectomy, but it was not possible to achieve
symmetry with the large contralateral breast.
Contralateral breast reduction was carried out, with
a poor cosmetic outcome. She was subsequently
referred to a plastic surgeon for revision surgery and
then sued her first surgeon.
Comments
• With cosmetic and reconstructive surgery, the
damage is self-evident, i.e. causation is less of
an issue than breach of duty. With delay in
diagnosis the converse is often the case.
• Patient expectation of a good cosmetic outcome
is arguably less demanding for postmastectomy
reconstruction than for purely cosmetic
surgery of the breast. Nevertheless, there is
growing demand for a wider choice and more
sophisticated reconstruction techniques.
• The first question that must be addressed is the
adequacy of training in reconstructive surgery. If
the level of training was appropriate, the second
question is whether the standard of advice and
operative skill met that which the patient could
reasonably have expected. Unless the answer to
both questions is in the affirmative, the surgeon
is liable.
• Most breast surgeons undertaking
reconstruction in the UK have attended training
courses on the use of subpectoral and latissimus
dorsi techniques. Some breast surgeons
undertake pedicled transverse rectus abdominis
muscle reconstruction, but free tissue transfer is
beyond the training and theatre time constraints
of most breast surgeons.
Risk management
Failure of communication and poor rapport often
prompt patients into taking legal action. A woman
who feels that her complaints have been taken seri-
ously and investigated thoroughly is less likely to
sue. In cases where the doctor–patient relationship
breaks down, referral to another specialist may be
the best course of action.
A rapid and timely diagnosis will best be achieved
by establishing and adhering to a multidisciplinary
approach in the care of breast patients, and for the
breast clinician this is arguably the most robust
safeguard of good practice in both diagnostic and
treatment aspects of breast surgery.
Key points
• Missed diagnosis of breast cancer is the commonest cause of litigation, and the settlements
highest, in premenopausal women.
• False reassurance from a negative mammogram is a common factor: always obtain a tissue
diagnosis in a palpable mass with a negative mammogram.

Litigation in breast surgery
307
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of the procedure.
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informed.

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52. Taylor v. West Kent Health Authority [1997] 8 Med
LR 251–7.
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Oncoplastic breast surgery – A guide to good prac-
tice. Eur J Surg Oncol 2007;33:S1–23.
54. National Mastectomy and Breast Reconstruction
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ic.nhs.uk/mbrreports; 2011[accessed 30.06.12].
55. Richards E, Vijh R. Analysis of malpractice claims
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309
Index
NB: Page numbers followed by f indicate figures,
t indicate tables and b indicate boxes.
A
Abdominal flap reconstruction 151
see also Lower abdominal tissue, reconstruction
Abdominal scars, multiple 154
Abscess see Breast abscess
Accessory breast tissue 268, 269f
Acellular dermal matrix (ADM) 136–138, 149–150
Acupuncture 261–262
Acute myeloid leukaemia (AML) 205, 206
Adenoma 275, 275f
Adjuvant therapy 199–218
angiosarcoma 174
bisphosphonates 209–210
chemotherapy see Chemotherapy
ductal carcinoma in situ (DCIS) 188–192
endocrine see Endocrine therapy
locally advanced breast cancer 226
male breast cancer (MBC) 170
melanoma 173
radiotherapy see Radiotherapy (RT)
systemic 36
triple-negative breast cancer 212
see also Trastuzumab
Adjuvant!Online (AO) 35, 36, 303
Oncotype DX 209
Adriamycin 203, 206, 209, 210
dosage 205, 206
see also CAF therapy
Advanced breast cancer (ABC) index 36
Afimoxifene 277
Age
cardiotoxicity 206
chemotherapy 204
ductal carcinoma in situ (DCIS) 182t, 187
endocrine therapy 203, 203t
fertility 166, 167
genetic predisposition 127–128
male breast cancer (MBC) 168–169
malignancy 273
primary breast lymphoma (PBL) 173
radiotherapy (RT) 250–251
tamoxifen 199–200, 203, 203t, 225–226, 233, 233b
Agnus castus 276
Alkylating agents 233t
AlloDerm® 149–150
ALMANAC (Axillary Lymphatic Mapping Against
Nodal Axillary Clearance) trial 21–22, 118, 260
‘aTTom:adjuvant Tamoxifen - To offer more?’
trial (UK) 200
AMAROS (‘After Mapping of the Axilla, Radiotherapy
or Surgery?’) 118
Ameliorative interventions 261, 261t
American College of Surgeons Oncology Group
(ACOSOG) 113
Z1071 114
Z-0011 trial 116, 117–118, 117f, 119–120,
251–252
American Joint Committee on Cancer (AJCC) 114, 173
American Society of Clinical Oncology (ASCO) 28
American Society for Radiation Oncology (ASTRO),
Consensus statement 248, 249, 249b
Amitriptyline 236
Amoxicillin-clavulanate 276
Analgesia 235, 236
Anastrozole 202, 203–204, 225–226, 233
psychosocial issues 262–263
recommendations 204t
vs tamoxifen 192, 200–201
ANDI (aberrations of normal breast development and
involution) 268, 270–278, 270t
Angiosarcoma 174, 174f
staging 174
‘Angel wings’ management 75, 75f
Ann Arbor Classification, lymphomas 173
Anthracyclines 206–207, 209, 210, 212, 234
dose 205–206
side-effects 233t
Antibiotics 279–281, 286b
Anticonvulsants 236
Antidepressants 236
Antimetabolites 233t
Anti-oestrogens 232t
Antiulcer drugs 286b
Apocrine carcinoma 181
Arazoxifene 140
Areola reconstruction 158
Areola-sparing mastectomy (ASM) 133b, 135
ARM (axillary reverse mapping) technique 119
Aromatase inhibitors (AI) 200–203
extended therapy 202
first line 200–201, 200f, 201t
bad prognosis/subgroups 201
comparative toxicities 201
gynaecological problems 262
issues 202–203
male breast cancer (MBC) 170
metastatic disease 233
musculoskeletal problems 262–263
postmenopausal women 225–226, 233
psychosocial issues 261
recurrence 226
risk-reducing 140
sequential after tamoxifen 201–202
side-effects 232, 232t
vs tamoxifen 226b
types 233
Arthralgia 262–263
Ascites 237
Ashkenazi Jewish population 129b

310
Index
Assessment failure, preoperative 301
ATAC (Arimidex®, Tamoxifen, Alone or in
Combination) trial 200, 200f, 201, 201t, 202,
203–204
Oncotype DX 209
ATLAS (Adjuvant Tamoxifen Longer Against Shorter)
trial 200
Atlas and principles of oncoplastic surgery (OPS) 98–99
ATM gene 128t
Atypical ductal hyperplasia (ADH) 179–180, 193–194
Atypical hyperplasia 140
Atypical lobular hyperplasia (ALH) 181–182,
193–194
Augmentation breast complications 287–288
Austrian Breast and Colorectal Cancer Study Group
(ABCSG)
ABCSG-6 trial 203–204
ABCSG-12 trial 203, 209–210
Autologous breast reconstruction 147, 148, 151–158
background 151
see also Latissimus dorsi (LD) flap reconstruction
Autologous latissimus dorsi (LD) flap 84
Autologous myocutaneous flaps 136b
with implant 136b
Axilla 109–126
anatomy 110f
imaging techniques 119–120, 119f
radiotherapy (RT) 118, 251–252, 252t
reverse mapping (ARM) technique 119
seromas 116–117
Axillary lymph node
chemotherapy 204–205
see also Sentinel lymph node (SLN) biopsy
Axillary staging 166, 170, 172
ductal carcinoma in situ (DCIS) 185–186
Axillary surgery 109–126
biopsy see Sentinel lymph node (SLN) biopsy
complications 118–119, 119t
cosmetic outcome 63
locally advanced breast cancer 220–221
lymph node dissection (ALND) 251–252
non-sentinel node metastases 115–118, 115t
node positive, dissection 116–118, 117f
prediction models 115–116
see also Lymphoedema
AZURE trial 209–210
B
Balance of probabilities (litigation) 294, 296
Bandaging, lymphoedema 121
Basal markers 30
Batwing incision 134f
Becker expander/prostheses 136–138
Bed biopsies 54–55
Benign breast cancer 268–293
ANDI conditions 270–278, 270t
non-ANDI conditions 279–283
congenital abnormalities 268–270
cosmetic surgery, complications 287–288
future management 289
patient assessment 288–289
Benzopyrones 121
Bevacizumab 212
Beyond all reasonable doubt, defined 294
BIG 1-98 trial 200f, 201, 201t, 202
BIG 2-04 SUPREMO trial 250
Bilateral risk-reducing salpingo-oophorectomy
139–140
Biological agents 226–227
Bird's beak deformity 93–94, 94f
Bisphosphonates 236–237
Blood-brain barrier 234
BOADICEA (Breast and Ovarian Analysis of Disease
Incidence and Carrier Estimation Algorithm)
program, risk estimation 128, 130b
Bolam test 294–295
BOLERO-2 trial 234f
Bolitho modification of Bolam 295
Bone pain 237
Bone scintigraphy 234–235
Bony metastases 236
Bowel obstruction 238t
Brain stem disease 238t
BRCA1 gene 1, 10, 10b
histopathology 10, 30, 32, 33
male breast cancer (MBC) 169
models 130
risk factors 127–129, 128t, 139
risk reduction 130–131, 131b, 138, 139–140, 140b
scoring system 129t
testing 129
BRCA2 gene 1, 10
histopathology 30, 32, 33
male breast cancer (MBC) 169
models 130
risk factors 127–129, 128t, 139
risk reduction 130–131, 131b, 138, 139–140, 140b
scoring system 129t
testing 129
BRCAPRO program, risk estimation 130, 130b
Breach of duty 294–295
vignettes 300–302
Breast abscess 279, 280–281, 281f
aspiration 280b, 280f
lactating 281f
Breast cancer
benign see Benign breast cancer
diagnosis 298–300, 298f
genetics see Genetic predisposition
invasive see Invasive breast cancer (IBC)
key issues 2b
locally advanced see Locally advanced breast cancer
male see Male breast cancer (MBC)
pathology 20–43
high-throughput molecular techniques 31–34
histopathology 30
minimum dataset 37f, 38
molecular factors 25–30
predictive factors 20, 25–30, 31–33
prognostic factors 20, 31–33, 34–36, 34t,
35f, 35t
traditional factors 20–25
pregnancy see Pregnancy-associated breast cancer
(PABC)
risk estimation 130
subtypes 208t
Breast Cancer Care 271
Breast Cancer International Research Group
(BCIRG)-006 trial 206–207, 206b, 211, 211t
Breast Cancer Linkage Consortium (BCLC) 127–128, 130

311
Index
Breast displacement see Oncoplastic surgery (OPS);
Volume displacement
Breast hypoplasia 268–270, 269f
Breast Imaging and Reporting Data System (BI-RADS)
183–184
Breast International Group (BIG)
BIG 1-98 trial 200f, 201, 201t, 202
BIG 2-04 SUPREMO trial 250
Breast oedema 246
Breast Screening Programme (NHS) 5, 6t, 9, 9t, 38, 183–184
Breast-conserving surgery (BCS) 51–70, 83, 244b
complications 63, 279–280
cosmetic outcome 60–64, 60f, 82–83, 83t
deformities 89–90, 89f
drug treatment effects 64
neoadjuvant therapy 63–64
patient factors 60
poor results 64, 64f, 65f
radiotherapy (RT) 64, 243–244, 245f, 246f, 247,
247b, 251–252
surgical factors 61–63, 63f
tumour factors 60–61
ductal carcinoma in situ (DCIS) 184–185
endocrine therapy 191–192, 192b
local recurrence (LR) 66–67, 66t, 82–83, 83t
male breast cancer (MBC) 169–170
mammary ductoscopy (MD), adjunct 49
patient selection 51–53, 52b
pregnancy-associated breast cancer (PABC) 165–166
procedures 53–56
recurrence rates 56–60, 56f
adjuvant systemic therapy 59–60
patient-related factors 56–57
treatment-related factors 56f, 58–59, 59t
tumour-related factors 57–58, 57t
trials 51
see also Oncoplastic surgery (OPS); Volume
replacement
BRIP1 gene 128t
British Association of Surgical Oncology 38, 57
British Breast Group 38
Bromocriptine 277
Burden (level) of proof 296–297
C
CAF (cyclophosphamide/adriamycin/fluorouracil)
therapy 203, 206
dosage 205, 206
CALGB (Cancer and Leukaemia Group B)
8541 trial 29–30, 206
9344 trial 205, 206, 207b, 212
9741 trial 208
40101 trial 208
49907 trial 204
postoperative radiotherapy (RT) 246, 246b, 247
Cambridge predictive model 115–116, 251–252
Cancer see Benign breast cancer; Breast cancer; Locally
advanced breast cancer; Male breast cancer
(MBC); Pregnancy-associated breast cancer
(PABC)
Capecitabine 204, 234
Capsular contracture 150–151, 287–288, 288b
Capsulectomy 150
Capsulotomy 150
Carboplatin 206
Carcinoma 8f
delay in diagnosis 304, 304t
lobular 301–302
node-positive 303
node-negative 303
see also Ductal carcinoma in situ (DCIS)
Cardiac morbidity, radiation-induced 252–253
Cardiotoxicity
anthracyclines 206, 248
trastuzumab 212
Cardiovascular drugs 286b
Care pathways 239
Causation
defined 294
issues 295, 302–305
Cavity shavings 54–55
CB11 test 28
CEF (cyclophosphamide/epirubicin/fluorouracil)
see FEC therapy
Cerebral metastases 237
nausea/vomiting 238t
CHEK2 gene 128t
Chemopreventive agents 140
Chemotherapy 204–209
age 204
anthracycline-based see Anthracyclines
dose density 208
duration 208
fertility 166, 167
male breast cancer (MBC) 170
metastatic disease 231, 233–234, 233t
molecular markers 208–209, 208t
nausea/vomiting 238t
neoadjuvant 112–114, 220–221, 220f, 221b,
223–225, 224f
nodal status 204–205
oestrogen receptor (ER) status 205
Oncotype DX 209
pregnancy-associated breast cancer (PABC) 166, 167
premenopausal breast cancer 203
primary breast lymphomas (PBLs) 174
recurrence 226–227
tamoxifen 199–200
taxanes see Taxanes
trastuzumab 211
Chest-wall reconstruction 159
Chloramphenicol 279
Chromogenic in situ hybridisation (CISH) 27, 28, 29
Ciprofloxacin 279
Circumareolar mastectomy 79, 80f
with immediate nipple reconstruction 77, 77f
Claus dataset, risk estimation 130, 130b
Clinging (flat) carcinoma 181
Clinical Negligence Scheme 294
Clinics
delay in diagnosis 304
one-stop 288–289
Clomifene 286b
Clonidine 264
CMF (cyclophosphamide/methotrexate/fluorouracil)
therapy 205, 208, 209, 250
dosage 205, 206
Co-amoxiclav 279
Cochrane reviews 188, 191, 237, 243, 263–264
College of American Pathologists (CAP) 28

312
Index
COMICE trial 3–4
Communication of information 239
Complex cysts 277
Complex sclerosing lesions (CSLs) 278
Compression garments, lymphoedema 120b, 121
Computed tomography (CT) 4, 219, 234–235, 237
three-dimensional 242
Congestive heart failure (CHF) 206, 212
Consent 295
Constipation 237
Contraceptives, oral 270
Contralateral prophylactic mastectomy (CPM) 139
Corynebacterium amycolatum 282
Corynebacterium kroppenstedtii 282
Corynebacterium tuberculostearicum 282
Cosmetic issues
implant-based reconstruction 148, 150–151, 151b, 151f
litigation 295, 305–306
local recurrence (LR) 82–83, 83t
surgical complications 287–288
see also Breast-conserving surgery (BCS); Oncoplastic
surgery (OPS); Volume replacement
Cowden's disease 128t
Cribriform carcinoma 181
Cyclical mastalgia 270t, 276
Cyclical nodularity 270t
Cyclizine 238t
Cyclo-oxygenase-2 (COX-2) 182–183
Cyclophosphamide 166, 203, 205, 206, 207, 250
dosage 205, 206
HER-2-positive disease 206
node-negative disease 209
SWOG 8814 trial 209
trastuzumab 210, 210b
see also CAF therapy; CMF therapy; FEC therapy
Cyrillic program, risk estimation 130b
Cysts, breast 8f, 277
imaging 277
inclusion 288
management 277
para areola 284
simple/complex 277
Cytokeratin-19 183
Cytology
false-positive 301
false-negative 301–302
see also Fine needle aspiration (FNA); Needle core
biopsy
D
Damages, award of 295–296
Danazol 277b, 286, 286b
Danish Breast Cancer Cooperative Group (DBCG) 167
DBCG 82b trial 250
DBCG 82c trial 250
Decongestive exercises 121
Deformities, breast-conserving surgery (BCS) 89–90, 89f
types 89, 89b
Denosomab 236–237
Department of Health (UK) 2b, 263
Advisory Committee on screening 5
Desmoid tumour 278
Dexamethasone 236, 238t
Diabetic mastopathy 284
Diagnosis, delay in 297–298
Diclofenac 237
DIEP (deep inferior epigastric perforator) flap 84–85, 136b
complications 157t
free 154, 155f, 157b
reconstruction 151, 156–157, 156f
Diffuse large B-cell lymphoma 173
Digital mammography 273
Diuretics 121
Docetaxel 206, 207–208, 234f
‘Dog ear’ 72, 75, 75f
Dome scar design 78, 79
Domperidone 238t
Donor sites, free flap 157–158
Down's syndrome 166
Doxorubicin 29–30, 166, 206, 207
Dual tracer technique 111b
Duct ectasia 270t, 274
Ductal carcinoma in situ (DCIS) 3, 10, 46, 179–198
adjuvant therapy 188–192
endocrine therapy 191–192
radiotherapy (RT) 188–191, 189t, 191f, 192b, 242–244
clinicopathological features 182t
excision 14
follow-up/prognosis 192–193
future 193–195
ongoing trials 193
optimising treatment 194–195
Sloane Project 193–194
stem cell therapy 194
histopathology 37f
investigation/diagnosis 183–184
diagnostic procedures 184
localisation-guided biopsy 184
stereotactic core/vacuum-assisted biopsy (VAB)
183–184
male 168, 193
mammary ductoscopy (MD) 48
natural history 179–180
nipple discharge 275
non-comedo types 181
oncoplastic surgery (OPS) 16
pathology 180–182
classification/features 180–181
lobular intraepithelial neoplasia (LIN) 181–182
presentation 183
psychosocial issues 259, 260–261
receptors/markers 182–183, 183f
recurrence 186–188
age at diagnosis 187
excision margin, assessment 186
high-grade/comedo tumours 186
histological type/tumour architecture 187
invasive 193
markers 188, 188t
scoring systems 187–188
in situ 193
tumour size/palpability 187
risk factors 179
screening 5, 5b, 9f
sentinel lymph node (SLN) biopsy 112
stem cells 180
treatment 184–186, 185f
axillary staging 185–186
breast-conserving surgery (BCS) 184–185
mastectomy 184

313
Index
Ductal lavage 273
Ductal papillomas 274–275
Ductography 46
nipple discharge 273
Ductoscopy see Mammary ductoscopy (MD)
Duloxetine 263
Duty of care 294
see also Breach of duty
Dying patient 237–238, 238t, 239
E
Early Breast Cancer Trialists' Collaborative Group
(EBCTCG) 151, 199–200, 201, 202, 207, 208
overview analyses 203b, 205, 208
EBC-1/MA.5 study 205
ECOG (Eastern Cooperative Oncology Group)
1199 trial 207–208
E5194 study 188, 191, 243
Eczematous changes 172
Edinburgh randomised trial 251–252
Ekland technique 287
ELIOT (electron intraoperative therapy) 248–249
Encysted papillary carcinoma 181
Endocrine receptor-positive tumours 207
Endocrine therapy 199–204
aromatase see Aromatase inhibitors
ductal carcinoma in situ (DCIS) 191–192
ER-negative breast cancer 231
male breast cancer (MBC) 170
metastatic disease 231–233, 232t
neoadjuvant therapy 223, 225–226
pregnancy 167
premenopausal women 203, 203t
recommendations 204t
tamoxifen see Tamoxifen
Epidermal growth factor (EGF) 180
Epidermal growth factor receptor (EGFR) 25–26, 27, 182
prognostic/predictive value 27
testing methods 27
Epirubicin 205, 206, 210b
see also FEC therapy
Epstein–Barr virus 270
ERB1 gene 26
ERISAC trial 192
Erythromycin 276, 279
Escitalopram 262
Estring® 203b, 262
Ethnic groups 129
European Commission, Working Group for Breast
Screening Pathology 22, 38
European Organisation of Research and Treatment of
Cancer (EORTC) 247–248
10853 trial 180b, 186, 187, 188–191, 189t, 191f, 243
22881-10882 trial 247
AMAROS trial 118, 251–252
BIG 2-04 SUPREMO trial 250
European Society for Therapeutic Radiology and
Oncology (ESTRO) 249
Evening primrose oil (EPO) 276
Examination, physical 298–299
Excision, tissue 96f, 97
impalpable cancers 55–56
margin, assessment 186
wire guided 13–15, 14f
Exemestane 202, 203, 204t, 262–263
Exercise 120b, 263–264
Expanders 136–138, 136b
implants 148, 269
Extensive in situ component (EIC) 58, 59
F
FAC (fluorouracil/adriamycin/cyclophosphamide)
see CAF therapy
False-positive cytology 301
False-negative cytology 301–302
FASG (French Adjuvant Study Group)
FASG-01 trial 208
FASG-05 trial 205
Fast-track options 296
Fat necrosis 283, 288
Fat transfer (lipofilling) 150–151, 269
FEC (fluorouracil/epirubicin/cyclophosphamide) therapy
206, 208, 210b
dosage 205, 208
Fertility 166, 167
FHO1 study 10
FHO2 study 10
Fibroadenomas 270–272, 270f, 270t
simple 270–271, 271f
management 271
tubular/lactating 271
Fibromatosis 278
Fibrotic lesions 278
Field-in-field technique 242
Film mammography 273
Fine-needle aspiration (FNA) 3, 3b, 165
axilla 119–120
lipomas 283–284
litigation 299
vs needle core biopsy 12, 289
pneumothorax 302
FinHer trial 210b, 211, 211t
Fishtail technique 75, 75f
Flap donor site 158
Flavonoid derivatives 121
Flucloxacillin 279
Fluorescence in situ hybridisation (FISH) 219
HER-2 27, 28, 234
5-fluorouracil 166, 203, 205, 206, 209
dosage 205, 206
HER-2-positive disease 206
metastatic disease 234
node-negative disease 209
postmastectomy radiotherapy (PMRT) 250
trastuzumab 210b
see also CAF therapy; CMF therapy; FEC
therapy
Fluoxetine 262
Food and Drug Administration (FDA) 28
‘4:1 ratio’ 244–246, 244b
Fractionation regimens 248
Fractures 237
Free lower abdominal tissue flap 148
Free myocutaneous flap 269
Free transverse rectus abdominis myocutaneous
(TRAM) flap 72
Fulvestrant 226, 233
Fusiform mammaplasty 102

314
Index
G
Gabapentin 236, 264
Gadolinium-enhanced MRI 120
Gail model, risk estimation 130, 130b
GAIN (German Adjuvant Intergroup Node-Positive)
study 209–210
Galactorrhoea 44, 45t, 273
Gasperon mammaplasty 102–103
G-CSF (granulocyte colony-stimulating factor) 208
Gel implant 269
Gemcitabine 234
Gene expression, assessment 32
General Medical Council (GMC) 295–296
Genetic predisposition 127–129, 128t, 129t
bilateral risk-reducing salpingo-oophorectomy
139–140
chemopreventive agents 140
counselling 131
high-risk women with breast cancer 139
management options 130–131
testing 129
see also BRCA1 gene; BRCA2 gene; Risk-reducing
mastectomy (RRM)
Genome-wide association studies 128t
Genomic Health 33–34, 188
Genomics 31–32
gene expression, assessment 32
genetic aberrations, mechanisms 31
status, assessment 31–32
Glandular defect, re-approximation 16–17
Glandular density 94
Glue 80
Gluteal artery perforator flaps 136b
Goldilocks mastectomy 75–76, 76f, 77–78
Goserelin 203, 231–232
Goserelin acetate 170
Gracilis-base thigh flaps 136b
Granular cell tumours 284
Granulomatous mastitis 282, 283f
Gravid breast 165
Greater omental flaps 121
Gregg v. Scott (2002) 297
Groupe Européen de Curiétherapie (GEC) 249
Growth factor receptors, type 1 26–30
Growth pathway, oestrogen receptor-negative breast
tumour cells 183f
Guidelines 295
Gynaecological problems 262
Gynaecological surgery 201
Gynaecomastia 169, 284–287, 285f
aetiology 285, 285b
associated drugs 286b
classification 285, 286b, 286t
treatment 285–287, 287f
H
HABITS trial 261
Haematomas 284
Haemocult testing 273
Haloperidol 238t
Hamartomas 271–272
Hemicircumareolar scar pattern 79
HER-1 (human epidermal growth factor receptor 1) 194
HER2 gene 27, 28, 29, 206–207
HER-2 (human epidermal growth factor receptor 2)
25–26, 27–30, 219, 250, 289
ductal carcinoma in situ (DCIS) 182–183, 183f, 187,
188, 188b, 192, 193, 194
predictive factors 29–30
prognostic factors 29
recurrence 199, 226
testing methods 28–29
trastuzumab 210, 234
HER-2 (human epidermal growth factor receptor 2)-
positive disease
adjuvant therapy 201, 206–207, 207b, 210b, 211–212
locally advanced breast cancer 220–221, 223–224
trastuzumab 234
HER-2 (human epidermal growth factor receptor
2)-negative disease 201, 207b, 209, 223–224
HER-4 (human epidermal growth factor receptor 4) 188
HERA (Herceptin in Adjuvant Breast Cancer) trial,
trastuzumab 210, 211–212, 211t
HercepTest (DAKO) 28
Herceptin® see Trastuzumab
Hidradenitis suppurativa 282–283
HIF-1α 183
High-throughput molecular techniques 31–34
Histopathology 30
Hormonal therapy
HER-2 29–30
male breast cancer (MBC) 170
psychosocial issues 261–264
Hormone receptor-negative tumours 204
Hormone replacement therapy (HRT) 140, 261–262
ductal carcinoma in situ (DCIS) 179, 180
Hormones, gynaecomastia 286b
Hospice 239
Hot flushes 261
‘Hot spots’ 242
Hotson v. East Berkshire Area Health Authority
(1987) 297
Hydrocortisone 232
Hyoscine butyl bromide 238t
Hypercalcaemia 238t
Hyperoestrogenism 285
Hypnosis 262
Hypofractionated whole breast irradiation (HF-WBI) 248
Hypofractionation 244b
Canadian trials 248
I
Ibandronate 236–237
IBIS II DCIS trial 192, 193
ICICLE trial 193
IGAP (inferior gluteal artery perforator) flap 157
Image-guided breast biopsy 11–13
results 13
samples 13
techniques 12–13
Imaging 1–19
breast cancer screening see Screening
surgery 13–17
symptomatic breast cancer 1–2
techniques 2–4
Immunohistochemistry (IHC) 22, 27
HER-2 27, 28
oestrogen/progesterone receptors (ERs/PRs) 26

315
Index
IMPACT (Immediate Preoperative Arimidex®
Compared with Tamoxifen) trial 201
Impalpable cancers 55–56
Implants 136–138, 136b
antibiotics 279–280
complications 280
implant-based reconstruction 78, 147, 148, 149f, 150,
151b, 151f
palpable edge 288
rippling 150–151, 288
rupture 287, 288
silicone 85, 154
In situ hybridisation (ISH) 27, 28–29
Inclusion cyst 288
Independent Review Group (UK) 89, 154b
Infections 279–283
granulomatous mastitis 282, 283f
hidradenitis suppurativa 282–283
lactational 279
non-lactational 279
postsurgical 279–280
treatment 280–282, 280f, 281f, 282f
Inferior pedicle mammaplasty 101
Infiltrating lobular carcinoma 230
Inflammatory breast cancer 219, 220f
treatment 167
INFORM test 28
Information, communication of 239
Inframammary fold (IMF) 73
implants 78, 79f
mastectomy 74, 79
scar 75
Inguinal lymph nodes 121
INT-101 trial 203
Intensity-modulated radiotherapy (IMRT) 242
dose distribution 242b
trial 242b
Intercostal perforators 74
Intergroup Exemestane Study (IES) 201–202
Intermittent pneumatic compression 121
International Agency for Research on Cancer (WHO) 4b
International Breast Cancer Study Group (IBCSG), 23-01
trial 117–118
International Prognostic Index 174
International Union Against Cancer (UICC) 173
Intrabeam device 248–249
Intraduct lesions 48, 48f
Intraductal breast biopsy (IDBB) 48–49
Intranasal fentanyl 236
Intraoperative radiotherapy (IORT) 248–249
Invasive breast cancer (IBC)
early (EBC) 260
radiotherapy (RT) 242–243, 243b, 244–247
boost 247
Oxford overview 244–246, 245f, 246f
subgroups for omission 246–247
Invasive carcinoma
ductal (IDC) 23, 24b
of no special type (ductal NST) 23
lobular (ILC) 23, 25b, 52
Inverted-T scar design 77–78, 99–100, 99f, 100f
modified 104
Inverted-V scar design 77–78, 78f
Ipsilateral breast tumour recurrence (IBTR) 243, 246, 247
Irradiation see Radiotherapy (RT)
Isotope imaging 4
J
J mammaplasty (Gasperon) 102–103
Juvenile hypertrophy 270t
Juvenile papillomatosis 274–275
K
Kaplan–Meier estimate 248–249
Karnofsky Performance Scale 238
Ketamine 236
Klinefelter's (Kleinfelter's) syndrome 169, 284
L
Lactating abscess 281f
Lactating fibroadenomas 271
Lactational infections 279
Lapatinib (laptinib) 223–224, 226–227, 234
Lasofoxifene 140
Lassus mammaplasty 100
Lateral intercostal artery perforators (LICAP) flap 85
Latissimus dorsi (LD) flap 136b
autologous 84
musculocutaneous 148
myocutaneous 84, 84f, 85b
myosubcutaneous 84b, 85f
Latissimus dorsi (LD) flap reconstruction 151–154, 152f
complications 153–154
contraindications 152
flap options 152–153
indications 152
planning 153
silicone issues 154
technique 153
Latissimus dorsi (LD) miniflaps
volume replacement 87
perioperative outcome 87–88, 88f
Laxatives 237
Left ventricular ejection fraction (LVEF) 212, 212b
Lejour mammaplasty 100
LENT-SOMA (late effects normal tissue - subjective,
objective management–analytic) 248
Letrozole 225–226, 262–263
extended therapy 202
recommendations 204t
vs tamoxifen 200–201
Leukaemia 206
Levomepromazine 238t
LFSPD gene 128t
Liability, defined 294
Lipofilling (fat transfer) 150–151, 269
Lipomas 283–284
Lipomodelling techniques 85
Liposuction 121, 286–287
Litigation 294–308
basic principles 294–297
breach of duty 294–295, 300–302
burden (level) of proof 296–297
causation 295
damages 295–296
Woolf report 296
breast cancer, diagnosis 298–300, 298f
cytology 299
mammography 299

316
Index
Litigation (Continued)
physical examination 298–299
triple assessment 297, 299, 300t
tumour doubling time 300
ultrasound 299
cosmetic issues 295, 305–306
delay in diagnosis 297–298
causation issues 302–305
North America 298
primary care 297
specialist referral 298
vignettes 300–302, 303–305
Liver metastases 231
Llubjana predictive model 251–252
Lobular carcinoma 301–302
Lobular carcinoma in situ (LCIS) 168, 181–182, 193–194
clinicopathological features 182t
tamoxifen 140
Lobular intraepithelial neoplasia (LIN) 181–182, 182t
Local recurrence (LR)
breast-conserving surgery (BCS) 66–67, 66t, 82–83, 83t
cosmetic issues 82–83, 83t
reconstruction 159
Localisation-guided biopsy 184
Locally advanced breast cancer 219–229, 220f, 220t
radiotherapy (RT) 221–223, 221b
recurrence 226–227
surgical management 219–221
treatment 167
systemic 223–227
Locoregional recurrence rate (LRR) 247, 248
Long transverse/oblique scar 79
Louisville predictive model 115–116, 251–252
Lower abdominal tissue, reconstruction 149f,
154–158, 155f
contraindications 154
flap options 154–155, 156, 157–158
complications 157, 157t
techniques 156–157
indications 154
techniques 154–156
Luteinising hormone-releasing hormone (LHRH) 203
agonist 231–232, 233
Lymph node, staging 20–22, 21f
see also Axillary lymph node; Sentinel lymph node
(SLN) biopsy
Lymphangitis carcinomatosa 231
Lymphatic exercises 121
Lymphatic/vascular invasion (LVI) 57–58
Lymphaticolymphatic bypass 121
Lymphaticovenular bypass 121
Lymphazurin blue 166
Lymphoedema 21b, 116–117, 118, 119t, 120–121, 120f
complete decongestive therapy 121
pharmaceutical interventions 121
surgery 121
treatment, cornerstones 120b
vignette 301
Lymphoma (PBL), primary breast 173–174, 173f
Lymphoscintigraphy 111, 111f
Lymphovascular invasion (LVI) 25, 25b
M
MA17 trial 202
Macrocysts 270t
Macromastia 269–270
Macrometastases 114, 115f
Magnetic resonance imaging (MRI) 10–11,
120, 184
-guided biopsy 12–13
Magnetic resonance mammography (MRM) 3–4
Magnetic resonance spectroscopy 120
Major duct excision 46–47
Male breast cancer (MBC) 168–170, 168f
adjuvant therapy 170
clinical presentation 169
diagnosis 169
ductal carcinoma in situ (DCIS) 168, 193
family history 169
metastatic disease 170
pathology 168–169
prognosis 170
risk factors 169
treatment 169–170
local therapy 169–170
Mammaplasty
Gasperon (J) 102–103
inferior pedicle 101
round block 101
superior pedicle see Superior pedicle mammaplasty
V 100
Mammary duct fistula 280–281, 282f
Mammary ductoscopy (MD) 47, 184
breast conservation surgery (BCS), adjunct 49
history/technology 47, 47f
intraduct lesions 48, 48f
limitations 49
nipple discharge 273
pathology 48–49
technical considerations 47–48
Mammography 2, 46
digital 273
film 273
‘increased risk’ women 10, 11f
litigation 299
magnetic resonance (MRM) 3–4
neoadjuvant chemotherapy 224–225
Paget's disease 172
risk reduction 130–131
surgery complications 287
volume replacement 88
Mammotome device 183–184
Manchester manual method 128
Manual lymphatic drainage 120b, 121
Manual model, risk estimation 130
MAP.3 trial 180, 192
MARIBS study 10–11
Mastalgia 276–277
assessment 276
cyclical 270t, 276
treatment 276–277
Mastectomy 71–81, 83
angiosarcoma 174
areola-sparing (ASM) 133b, 135
bilateral simple 76
vs breast conserving surgery (BCS) 51, 51b
ductal carcinoma in situ (DCIS) 184
flap necrosis 80
Goldilocks 75–76, 76f, 77–78
with immediate reconstruction 76–80
planning 77–78
recurrence rates 77t

317
Index
Mastectomy (Continued)
nipple-areola complex-sparing 132, 133b
pregnancy-associated breast cancer (PABC) 165–166
prophylactic 112, 139
psychosocial issues 259
radical 80–81
radiotherapy (PMRT) 249–250
risk-reducing see Risk-reducing mastectomy (RRM)
scar patterns 76, 77
simple 72–76, 72f, 73f
closure 75
‘dog ear’ management 75, 75f
inframammary fold (IMF) 74, 80f
intercostal perforators 74
lighting 74
‘plane’ identification 74
planning 72–75
posterior margin 74
retraction 74
shoulder fat 75
surgical tools 74
suturing 75
technique 73–75, 73f, 74f
simple total (STM) 133b
skin flap necrosis 159
skin-sparing (SSM) 76–77, 77t, 133–134, 133b, 146
smoking 71–72, 76, 80f
Wise pattern risk-reducing 135f, 137f, 138f
wound healing, risk factors 71–72
see also Sentinel lymph node (SLN) biopsy
Mastitis, granulomatous 282, 283f
Mayo predictive model 115–116, 251–252
MD Anderson predictive model 115–116, 251–252
Medical experts 296
Medical Research Council (MRC), BIG 2-04 SUPREMO
trial 250
Medroxyprogesterone 232
Megesterol acetate 232
Melanoma 173
Memorial Sloan–Kettering predictive model 115–116,
251–252
Meningeal disease 238t
Metastatic disease 230–241
dying patient 237–238, 238t, 239
macrometastases 114, 115f
male breast cancer (MBC) 170
micrometastases 114–115, 114f, 115t
non-sentinel node 115–118, 115t
palliative care 230, 231–238, 238t, 239
chemotherapy 231, 233–234, 233t
endocrine therapy 231–233, 232t
radiotherapy (RT) 237
response, assessment 234–235
symptom control 235–237
systemic treatment 231, 232f
presentation/prognosis 230, 231t
staging 230–231
to breast 175
Methadone 236
Methotrexate 167, 209, 250
see also CMF therapy
Methylene blue 166
Methylnaltrexone 237
Metochlopramide 238t
Metronidazole 276
Microdochectomy 46–47, 275–276
Micrometastases 114–115, 114f, 115t
Micropapillary carcinoma 181
Microvascular lymph node transfer 121
Milan III trial 247
MINDACT trial 209
Mindfulness 262
Minimally invasive carcinoma (MIC) 22–23
Minimum dataset 37f, 38
MIRROR study 112–113
mTOR (mammalian target of rapamycin) inhibitors 233
Molecular factors 25–30
Mondor's disease 284
Montgomery's gland problems 283
Morbidity 118
Morphine 235, 235b
Mortality 199
screening 4
statistics 1
taxanes 207
Mou predictive model 251–252
Multiple abdominal scars 154
Multiple gene expression assays 209
Muscle twitching 153
Muscle-sparing free TRAM flap techniques 156
Musculoskeletal problems 262–263
Myelodysplasia 205
Myocutaneous flap
implants 136–138
latissimus dorsi (LD) 84, 84f, 85b
Myosubcutaneous latissimus dorsi (LD) miniflap 84b, 85f
N
National Cancer Institute of Canada, Clinical Trials
Group (NCIC CTG) 205
National Cancer Institute (USA), SEER programme
34–35
National Comprehensive Cancer Network 28
National DCIS audit (UK) 193–194
National Institute for Health and Clinical Excellence
(NICE) 2b, 10–11, 192, 230, 248
ductal carcinoma in situ (DCIS) 185–186, 191b
risk groups classification 10b
National Institutes for Health, State-of-the-Science
conference 191b
National Surgical Adjuvant Breast and Bowel Project
(NSABP) 212
B-06 trial 247
B-14 trial 200
B-17 trial 186, 187, 188, 189t, 243
B-20 trial 209
B-24 trial 186, 189t, 192, 192b
B-31 trial 210, 211, 211t
B-32 trial 109, 112–113, 118, 122b
B-34 study 209
B-35 trial 192, 193
B-42 trial 202
B-43 trial 193
P-1 chemoprevention trial 182, 192
STAR trial 140, 140b
Nausea 237, 238t
NEAT (National Epirubicin Adjuvant Trial) 205b
Needle core biopsy 3, 3b, 165
vs fine-needle aspiration (FNA) 12, 289
Neoadjuvant therapy
axillary surgery 220–221
breast-conserving surgery (BCS) 63–64

318
Index
Neoadjuvant therapy (Continued)
chemotherapy 112–114, 220–221, 220f, 221b,
223–225, 224f
endocrine 223, 225–226
locally advanced breast cancer 223–226
Neuroendocrine carcinoma 181
Neuropathic pain 236
NHS (UK National Health Service)
Breast Screening Programme 5, 6t, 9, 9t, 38, 183–184,
258–259, 295
Litigation Authority 294
referrals 298
Trusts 296
Night sweats 261
Nipple adenoma 275, 275f
Nipple discharge 44–50, 272–276, 272f
aetiology 274–275
assessment 45–46
bloody 275
causes 44–45, 45t
investigation 273–274, 274f
surgery 46–47, 275–276
see also Mammary ductoscopy (MD)
Nipple reconstruction 137f, 149f, 158
Nipple-areola complex (NAC)
eczematous changes 172
excision 77
necrosis 134
preservation in surgery 131–132
reconstruction 138, 138f, 158–159
undermining 96–97
Nipple-areola complex (NAC) sparing
mastectomy (NSM) 132, 133–134, 133b,
136–138
incisions 134–135, 134f, 135f
Nipples, supernumerary 268, 269f
Nipple-sharing 158
N-methyl-d-aspartate antagonists 236
Nodal status 199–200, 204–205
Node-positive carcinoma 303
Node-negative carcinoma 303
Non-autologous reconstruction 148–151, 149f
complications 150–151
contraindications 149
indications 148
techniques 149–150
Non-autologous volume replacement with saline/silicone
implants 85
Non-sentinel node metastases 115–118, 115t
Non-steroidal aromatase inhibitors (AI) 233
NOPQRST pain history tool 235, 235b
North Central Cancer Treatment Group (NCCTG),
Intergroup N9831 210, 211, 212
Nortriptyline 236
Notch receptor pathways 180
Nottingham method, tumour grade 24, 24f
Nottingham Prognostic Index (NPI) 34, 303, 304t
Oncotype DX 209
NTPBCS (Nottingham Tenovus Primary Breast Cancer
Study) 21f, 22–23, 34–35
O
Obesity, endocrine therapy 203–204
Ocreotide 238t
Oedema of breast 279–280
Oestrogen 203b, 233
blocking 225, 226
Oestrogen receptor (ER) 25–26, 219, 231, 250, 278
assay interpretation 26
measuring 26
pathway 199
status 205, 289
Oestrogen receptor (ER)-positive disease 32, 203t,
220–221, 223, 233, 261
hormone therapy 231b, 232f
taxanes 207b
Oestrogen receptor (ER)-negative disease 32, 233
growth pathway 183f
taxanes 207b
Oncoplastic surgery (OPS) 16–17
breast-conserving surgery (BCS) 92–93
classification system 94–95, 95t
complications 105
discussion 104–106
evolution 106
general considerations 95
indications 104
level I 95–97
glandular defect, re-approximation 16–17
incisions 95–96
nipple-areola complex (NAC) undermining
96–97
skin undermining 96, 96f
tissue excision 96f, 97
level II 97–104
atlas principles 98–99
lower inner quadrant 100
lower outer quadrant 102–103
lower pole location 99–100
retroareolar location 103–104
upper inner quadrant 100–101
upper outer quadrant 101–102, 102f, 103f
upper pole 101
limitations 105–106
multidisciplinary treatment 105
patient selection 93–94
glandular density 94
tumour location 93–94, 94f
volume 93
role 83
safety 104–105
technique, choice 83–84, 84t
Oncotype DX scoring system 33–34, 188,
191, 209
Ondansetron 238t
One-stop clinics 288–289
Opioid-induced conditions
constipation 237
nausea/vomiting 238t
Opioids 235
common concerns 235, 236b
neuropathic pain 236
Oral contraceptives 270
Ovarian ablation 231–232
postmenopausal patients 233
side-effects 232t
tamoxifen 231–232, 232b
Ovarian cancer 128, 129
Ovarian suppression 203
Overexpansion 150
Oxford Overview see Early Breast Cancer Trialists'
Collaborative Group (EBCTCG)

319
Index
P
Paclitaxel 205, 207–208
PACS 004 trial (France) 211, 211t
Paget's disease of breast 170–172, 171f, 275
clinical presentation 171
diagnosis 171–172
pathology 171
prognosis 172
treatment 172, 172t
Pain
flares 235–236
metastatic disease 235–237, 235b
radiotherapy (RT) 246
PALB2 gene 128t
Palliative care see under Metastatic disease
Palliative Prognostic Index 238, 238t
Papillary carcinoma 181
Papillomas 273, 274–275
Para areola cysts 284
Paraesthesia 116–117
Partial breast irradiation (PBI) 248–249, 249f
Patent blue V 166
Path Vision test 28
Patient information leaflets 295
Patient-reported outcomes (PROs) 263
Pectoral fascia 74, 80
Pedicled myocutaneous flap 269
Pedicles, secondary 103
Perforator flaps 85
Periareolar inflammation 279
Periareolar sepsis 279
Permanent expandable breast implant 148
Pertuzumab 223–224, 234, 234f
PharmDx test 28
Phyllodes tumour 272
Physical examination 298–299
Physician Insurers Association of America (PIAA) 298
Phytoestrogens 276
Platinum agents 233t, 234
Pleural effusions 237
Pneumothorax 302
Poland's syndrome 268–269
Polymerase chain reaction (PCR) 21
Population screening 4
Positive predictive value (PPV) 7t
Positron emission tomography (PET) 120, 165
/computed tomography (CT) 224–225, 231
Post-mastectomy radiotherapy (RT) 147
Postmenopausal women, endocrine therapy 231–233,
232t, 233f
Postoperative management, failure 301
Postoperative seroma 153b
Post-radiotherapy (RT) angiosarcoma 174
Postsurgical infections 279–280
PREDICT model 35
Predictive factors 25–30
defined 20
tools 31–33
Pregabalin 236
Pregnancy, bloody nipple discharge 275
Pregnancy-associated breast cancer (PABC) 164–168
classification 167–168
clinical presentation 164–165
diagnosis 165
pathology 164
Pregnancy-associated breast cancer (PABC) (Continued)
prognosis 167–168
treatment 165–167, 166f
axillary staging 166
local therapy 165–166
locally-advanced/inflammatory cancer 167
systemic therapy 166–167
termination/future pregnancy 167
Pre-litigation protocol 296
Premenopausal women, endocrine therapy 203, 203t,
231–233
Preoperative assessment, failure 301
Primary angiosarcoma 174, 174f
Primary breast lymphoma (PBL) 173–174, 173f
Primary care, delay 297, 304–305
PRIME I trial 247–248
PRIME II trial 247
Progestagens 232, 232t, 233b
Progesterone receptors (PRs) 25–26, 250
Prognostic factors 34–36
defined 20
tools 31–33
Prognostic index
defined 20
International Prognostic Index 174
Nottingham see Nottingham Prognostic Index (NPI)
Van Nuys Prognostic Index (VNPI) 187–188
Prolactin levels 273
Prophylactic mastectomy 112, 139
Protein truncation tests (PTT) 129
Proteomics 32–33
Pseudoangiomatous stromal hyperplasia (PASH) 278
Pseudogynaecomastia 284
Psychoactive agents 286b
Psychosocial issues 258–267
breast cancer surgery (BCS) 259–260
axillary surgery 260
decision-making 259
quality of life (QoL) 259
delay in presentation 258–259
ductal carcinoma in situ (DCIS) 260–261
hormone therapy 261–264
exercise 263–264
gynaecological/sexual problems 262
musculoskeletal problems/arthralgia 262–263
vasomotor problems 261–262, 261t
risk-reducing mastectomy (RRM) 133b, 139
PTEN gene 128t
Purse-string scar 79
Q
Quadrantectomy 53–56, 83t, 104b
Quality assurance, screening 5, 6t
Quality of life (QoL)
ductal carcinoma in situ (DCIS) 260–261
exercise 263–264
radiotherapy (RT) 247–248
Queen's Bench 296
R
RAD51C gene 128t
RAD51D gene 128t
Radial scars 278

320
Index
Radiation see Radiotherapy (RT)
Radioisotope occult lesion localisation (ROLL)
15–16, 15f
Radiotherapy (RT) 242–257
angiosarcoma 174
autologous tissue 148, 151
axillary 118, 251–252, 252t
breast-conserving surgery (BCS) 243–244, 245f, 246f,
247, 247b
capsular contracture 150–151
cardiac morbidity, radiation-induced 252–253
ductal carcinoma in situ (DCIS) 188–191, 189t, 191f,
192b, 242–244
hypofractionated dose 248
intensity-modulated (IMRT) 242
invasive breast cancer (IBC) 242–243, 243b,
244–247
locally advanced breast cancer 221–223, 221b
male breast cancer (MBC) 169
nausea/vomiting 238t
older patients 250–251
palliative 237, 237b
partial breast irradiation (PBI) 248–249, 249f
planning/delivery 242
postmastectomy (PMRT) 249–250
postoperative 222
primary radical 222–223, 223f
quality of life (QoL), impact 247–248
reconstruction 159
side effects 221, 221b
whole-breast 56
Raloxifene 140, 140b
Reconstruction 146–163
complications 159, 159f
contraindications 148
finishing surgery 158–159
contralateral breast 158
flap donor site 158
nipple-areola (NAC) reconstruction 158–159
reconstructed breast 158
implant 78
local recurrence (LR) 159
locally advanced breast cancer 221
radiotherapy (RT) 159
risk-reducing mastectomy (RRM) 135–138, 136b,
136f, 137f, 138f
techniques 148–158
timing 146–148
delayed 147, 147b
delayed-immediate 147, 148
immediate 76–80, 146–147, 147b, 306
tissue-based 77–78
Records, alteration 301
Recreational drugs 286b
Recurrence see Local recurrence (LR)
Reduction, breast, complications 288
Relaxation 262
Replens® 262
Resection 86b
defects 83
Retching 237, 238t
Reverse transcription - polymerase chain reaction (RT-
PCR) 21, 22
Risk-reducing mastectomy (RRM) 130–131, 131b,
132–133
with breast reconstruction 135–138, 136b, 136f,
137f, 138f
Risk-reducing mastectomy (RRM) (Continued)
contraindications 133b
follow-up 138
genetic counselling 131
protocol 131–132
psychosocial issues 133b, 139
sentinel lymph node (SLN) biopsy 139
surgical consultation 132–135
technique, choice 133b
uptake 138–139
Rituximab 174
Round block mammaplasty 101
Royal College of Pathologists 38
S
St Gallen Consensus 208
St Gallen criteria 35, 36
Saline implants, volume replacement 85
SALSA (Secondary Adjuvant Long-term Study with
Arimidex), ABCG-16 trial 202
San Antonio Breast Cancer Symposium 117–118
Sarcoma 272
Scar patterns 76, 77
Sclerosing adenosis 278
Sclerosing lesions 270t, 278
Screening 4–11
adverse effects 9–10
aims 4
effectiveness, factors affecting 5
‘high risk’ women, methods 10–11
‘increased risk’ women 10–11
age 11
methods 10–11, 11f
litigation 304
method/frequency 4–5
population 4
process 5–9, 7t, 8f, 9t
quality assurance 5, 6t
Secondary pedicles 103
SEER (Surveillance Epidemiology and End Results)
(National Cancer Institute (USA)) 34–35, 168–169
Selective norepinephrine reuptake inhibitors (SNRIs)
262, 263
Selective oestrogen receptor modulators (SERMs) 140,
261, 262
Selective serotonin reuptake inhibitors (SSRIs) 262,
263, 277
SENTINA trial 113
Sentinel lymph node (SLN) biopsy 21, 21b, 220–221
axillary irradiation 251–252
vs axillary node dissection 118–119
axillary staging 166, 172
controversies 112–114
glue 80
inframammary fold (IMF) 79
male breast cancer (MBC) 170
mastectomy 78–80, 112
melanoma 173
neoadjuvant chemotherapy 221b
over-dressing 80
pectoral fascia 80
positive 252t
postoperative radiotherapy (RT) 247
preoperative marking 78f, 79
radioisotope occult lesion localisation (ROLL) 16

321
Index
Sentinel lymph node (SLN) biopsy (Continued)
risk-reducing mastectomy (RRM) 139
scar patterns 79
skin stapler 80
studies 113
technique 79–80, 110–112
injection material/location 110–111, 110f
intraoperative evaluation 111–112
lymphoscintigraphy 111, 111f
trials 109, 109b, 110t
Seromas 116–117, 153b, 279–280
Sexual problems 262
SGAP (superior gluteal artery perforator) flap 157
Short transverse scar 78
Shoulder fat 75
SIEA (superficial inferior epigastric artery) flap 154,
156, 157b
Signet cell carcinoma 181
Silicone implants 85, 154
Silver-enhanced in situ hybridisation (SISH) 27
Simple total mastectomy (STM) 133b
Single nucleotide polymorphisms 128t
Skin
care, lymphoedema 120b
erythema 220f
fibrosis 246
stapler 80
undermining 96, 96f
Skin-sparing dissection 134f
Skin-sparing mastectomy (SSM) 76–77, 77t, 133–134,
133b, 146
Sloane Project 193–194
Smear cytology 46
Smoking 80f, 279, 282–283
wound healing 71–72, 76
SNUH predictive model 251–252
SOFT (Suppression of Ovarian Function) trial 203
SOLD (Synergism or Long Duration) study 211
Solid carcinoma 181
Southwest Oncology Group (SWOG) 8814 trial 206, 209
Oncotype DX 209
Specialist referral, delay 298
Spinal cord compression 236, 237
Stanford nomogram 115–116
Staphylococcus aureus 279–280
STAR trial (Study of Tamoxifen and Raloxifene) 140, 140b
START (Standardisation of Breast Radiotherapy)
START A trial 221–222, 248
START B trial 248
Stem cells 180
therapy 194
Stereotactic core biopsy 13, 183–184
Steroidal aromatase inhibitors (AI) 233
STK11 gene 128t
Strattice® 149–150, 150f
Subareolar injection technique 110–111, 111b
Subcutaneous mastectomy technique 146
Superior pedicle mammaplasty
inverted-T scar 99–100, 99f, 100f
therapeutic 102
Support/compression garments 120b, 121
Surgery
axillary see Axillary surgery
clinically occult lesions 13–16
complications 136–138
gynaecomastia 286–287
high-risk women with breast cancer 139
Surgery (Continued)
imaging 13–17
innovative 85
locally advanced breast cancer 219–221
metastatic disease 235
nipple discharge 46–47
oncoplastic see Oncoplastic surgery (OPS)
options 219–220.
see also specific procedures
SWEDCIS trial 188
T
TACT (Taxotere as Adjuvant Chemotherapy
Trial) 207
TAILORx trial 209
Tamoxifen 199–200, 203b, 208, 209
age 203, 203t, 225–226, 233, 233b
vs anastrozole/letrozole 200–201
vs aromatase inhibitors 226b
breast-conserving surgery (BCS) 243b
cosmetic outcome 64
vs danazol 277b
duration 200
extended therapy 202
fibromatosis 278
gynaecological problems 262
gynaecomastia 286, 286b
HER-2 status 29–30, 206
male breast cancer (MBC) 170
mastalgia 277
metastatic disease 233
obesity 203–204
ovarian ablation 231–232, 232b
pregnancy-associated breast cancer (PABC) 167
recommendations 204t
recurrence 57, 226
sequential aromatase inhibitors 201–202
trials 140, 140b, 192, 192b
TARGIT (targeted intraoperative radiotherapy)-A trial
248–249, 249f
Taxanes 167, 207–208, 210, 212, 234
choice/schedule 207–208
side-effects 233t
trastuzumab 234
T-DM1 trials 223–224, 234
TEAM (Tamoxifen, Exemestane Adjuvant Multinational)
trial 202
Technetium-99m 166
Tenon predictive model 115–116, 251–252
Terminal care 230
Tetracycline 279
Thoracodorsal artery perforators (TDAP flaps) 85
Three-dimensional computed tomography
(CT) 242
Tissue
-based reconstruction 77–78
excision 96f, 97
microarrays (TMAs) 33
Tissue expansion 148, 149f, 150, 269
expanders 148, 149–150, 149f
TNM staging system 20–21, 24, 219, 220t
TOP2A gene (topoisomerase II-α) 206–207
Total duct excision/division 276
TP53 gene 127, 127b, 128t, 129
Trainees 301–302

322
Index
TRAM (transverse rectus abdominis myocutaneous) flap
64, 84–85, 136b, 151, 151f
complications 157t
free 72, 154, 155f, 156, 156f
muscle-sparing 156, 157b
pedicled 154–155, 155f
Transmucosal fentanyl 236
TRANS-SUPREMO biological substudy 250
Trastuzumab (Herceptin®) 167, 210–212, 210f, 211t,
223–224, 226–227
cardiotoxicity 212
chemotherapy 211
duration 211
HER-2-positive disease 206, 211–212, 220–221, 223, 234
metastatic disease 234
Triple assessment 297, 299, 300t
Triple-negative breast cancer 212
Triple-negative phenotype cancers (TNP) 30
Tuberous breasts 269
Tubular breasts 269
Tubular fibroadenomas 271
TUG (transverse upper gracilis) flap 157
Tumour(s)
architecture 187
comedo 180, 186
non-comedo 181
cosmetic outcome 60–61
desmoid (fibromatosis) 278
differentiation 23
doubling time 300
extensive in situ component (EIC) 58, 59
grade 24, 24f, 57
granular cell 284
histological type 57, 187
isolated cells 114–115, 114f, 115t
location 61, 61f, 62f, 93–94, 94f
lymphatic/vascular invasion 57–58
multiple 52–53, 58
palpability 187
phyllodes 272
re-excision 63, 66
recurrence 57–58, 57t
size 22–23, 23f, 52, 57, 57t, 187
Turkish predictive model 251–252
Tyrer–Cuzick program, risk estimation 130, 130b
U
UK Coordinating Committee on Cancer Research
(UKCCCR), UK/ANZ DCIS trial 187, 188, 189t,
191f, 192, 243
Ulnar-mammary syndrome 268–269
Ultra-small superparamagnetic iron oxide-enhanced
MRI 120
Ultrasound 2–3, 46
axilla 119–120
breast abscess 280–281
guidance 12–13, 286–287
litigation 299
metastatic disease 230–231
neoadjuvant chemotherapy 224–225
nipple discharge 273
pregnancy-associated breast cancer (PABC) 165
United Kingdom Association of Cancer Registries 38
University of Southern California/Van Nuys Prognostic
Index (USC/VNPI) 187–188
US Oncology phase III trial 207
V
V mammaplasty 100
Vacuum-assisted biopsy (VAB) 12–13, 183–184
Vagifen® 262
Vaginal dryness 262
Vaginal oestrogen preparations 203b
Van Nuys Prognostic Index (VNPI) 187–188
Vascular invasion 25, 25f, 57–58
Vasomotor problems 261–262, 261t
Venlafaxine 262, 264
Vertical mammaplasty (Lejour/Lassus) 100
Vertical scar design 78
Vestibular disease 238t
Vinca alkaloids, side-effects 233t
Vinorelbine 167, 234
Vitamin E 264
Volume displacement 84
techniques see Oncoplastic surgery (OPS)
vs volume replacement 84t
Volume replacement 83–84
future prospects 88
indications 86, 86b
with latissimus dorsi (LD) miniflaps 87
mammographic surveillance 88
perioperative outcomes 87–88, 88f
techniques 84–90
timing 86
vs volume displacement 84t
Vomiting 237, 238t
Vulvo-vaginal atrophy 262
W
Whole-breast radiotherapy (WBRT) 243, 244b
Wide local excision 53–56, 83t
complications 55
technical details 53–55, 53f
Wire-guided excision 13–15, 14f
Wise pattern mastectomy 79
with implant reconstruction 78, 78f
risk-reducing 135f, 137f, 138f
with tissue-based reconstruction 77–78, 78f
Women's Health Questionnaire (WHO) 261–262
Woolf report 296
Working Classification, lymphomas 173
World Health Organization (WHO), International
Agency for Research on Cancer 4b
Wound healing, risk factors 71–72
Wound infections 116–117
X
X-rays 230–231, 234–235
Y
Yoga 262
Z
Zelondronate 236–237
ZO-FAST study 209–210