Part XV · Supportive care, survivorship, and patient experience · Chapter 85

Rehabilitation and survivorship

Looking harder has never been shown to help. Everything else in this chapter has.

1 · Surveillance after curative treatment and the evidence against intensity

The intuition that more testing finds recurrence earlier, and that earlier detection saves lives, was tested directly. Both halves were examined and only the first survived.

One multicentre trial randomised 1,320 women under 70 years with stage I to III disease. The intensive arm received scheduled bone scan, liver ultrasound, chest radiography and laboratory tests. The control arm kept the same visit schedule with only clinically indicated tests. Both arms received annual mammography. At a median follow-up of 71 months there were 132 deaths in the intensive group and 122 in the control group. Time to detection of recurrence did not differ, and no measure of health-related quality of life differed at any assessment1.

A parallel trial randomised 1,243 patients to periodic chest radiography and bone scan every 6 months or to physical examination and mammography alone. The intensive arm detected more intrathoracic and bone metastases and detected them earlier. Five-year overall mortality was 18.6% and 19.5%2.

The second trial is the more instructive of the two, because it separates the two claims. Intensive imaging does find recurrence earlier. Finding it earlier did not change when patients died. Lead time was gained and nothing was done with it.

Current guidance reflects this. Routine follow-up consists of history, physical examination, and mammography, without routine systemic imaging or tumour markers in asymptomatic patients3. The advice is old. The 1998 update of the ASCO surveillance guideline already recommended against routine blood counts, tumour markers, liver ultrasound and computed tomography4, and the tumour marker guideline weighed each marker against the same outcomes5.

Tamoxifen adds one symptom to the list. Postmenopausal women taking it should have abnormal bleeding evaluated, while premenopausal women have no known increase in uterine cancer and need only routine gynaecological care6.

Caution

This evidence is old and it is not therefore wrong. Both trials predate current imaging and current systemic therapy, so the honest position is that the question was answered under conditions that no longer hold. That is a reason to retest it, not a licence to order scans in the interim. The retesting is happening through molecular residual disease, in SURVIVE and DARE. The unresolved half of the question is whether acting on a lead time improves outcome, and that is the argument in Lead time and the unresolved question of whether acting early helps.

Mammographic surveillance is the exception with a rationale rather than an inherited habit. A new ipsilateral or contralateral primary is potentially curable, so detecting it early changes what can be done. Detecting an asymptomatic distant metastasis does not.

In practice

Give the patient a written schedule and a symptom list. Most recurrences are found by patients between visits, and that is the detection system that actually operates.

Do not order tumour markers or staging scans in an asymptomatic patient because the visit feels empty.

Investigate a new persistent symptom promptly and completely. The evidence is against routine imaging, not against imaging.

2 · Lymphedema and shoulder dysfunction

Reported lymphoedema incidence varies more than the underlying risk does, and the reason is the case definition. A systematic review of 72 studies found that overall more than one in five women who survive breast cancer develop arm lymphoedema. Incidence was 19.9% after axillary lymph node dissection and 5.6% after sentinel node biopsy, and was 28.2% in studies that used more than one diagnostic method. Extensive surgery and being overweight or obese were the risk factors with the strongest evidence7.

The measurement point is worth stating separately. Circumference thresholds, water displacement, bioimpedance, and patient report do not identify the same patients. A study reporting 5% incidence and one reporting 30% may be observing the same population through different instruments. The surgical de-escalation that reduced this risk is in Axillary staging and the long retreat from dissection and Functional morbidity and surgical de-escalation.

Early detection with intervention has been tested. In an interim analysis of 508 patients randomised to surveillance by bioimpedance spectroscopy or by tape measurement, with compression prescribed on a prethreshold trigger, bioimpedance triggered less often and later. Progression to complex decongestive physiotherapy occurred in 4.9% of the bioimpedance group and 14.7% of the tape measurement group, an absolute difference of about 10 percentage points that did not reach conventional significance8. The direction is consistent and the comparison is not yet definitive.

Treatment of established lymphoedema has less support than its routine use suggests. A randomised trial of 103 women found no significant advantage of daily manual lymphatic drainage and bandaging over compression garments alone9. Reviews describe decongestive therapy as effective for symptoms, with surgery for selected patients who do not respond10.

The most useful single result in this area reversed standing advice. Weight lifting had been proscribed for women with lymphoedema. A randomised trial enrolled 141 survivors with stable arm lymphoedema for twice-weekly progressive weight lifting with a fitted compression garment. An increase in limb swelling of 5% or more occurred in 11% of the exercise group and 12% of the control group. The exercise group had fewer exacerbations, less severe self-reported symptoms, and greater upper and lower body strength11.

Shoulder morbidity is separate from lymphoedema and is frequently recorded as if it were the same problem. Restricted range of motion, axillary web syndrome, and post-mastectomy pain syndrome each have their own course. All three respond better to early physiotherapy than to late referral, and the referral is usually late.

3 · Fatigue, cognition, and return to function

Cancer-related fatigue is the most prevalent persistent symptom after treatment and the least investigated, because it generates no abnormal test. Guideline management is screening at intervals, evaluation of contributors, and treatment12. The contributors worth excluding are anaemia, hypothyroidism, depression, sleep disturbance, deconditioning, and endocrine therapy itself. Exercise has the best evidence of any intervention, which is the subject of Exercise, nutrition, and weight management.

Cognitive change has been characterised prospectively rather than anecdotally. In a nationwide longitudinal study, 581 patients with breast cancer and 364 age-matched controls completed a validated cognitive function instrument before chemotherapy, after chemotherapy, and at 6 months. A clinically significant decline was reported by 45.2% of patients against 10.4% of controls from before to after chemotherapy, and by 36.5% against 13.6% at 6 months. Baseline anxiety, depression, and lower cognitive reserve were associated with worse scores. Regimen, hormone therapy, and radiotherapy were not13.

Caution

Self-reported cognitive difficulty and objective neuropsychological testing correlate weakly. The common inference is that one of them must be wrong. Both are valid measurements of different quantities. A patient who performs normally on testing and cannot manage her previous workload has not been shown to be mistaken. She has been shown to have a problem the test does not measure.

Return to function is the outcome patients actually care about and the one least often recorded. It depends on fatigue, cognition, neuropathy, shoulder function, and the flexibility of the job. Work and disability are developed in Work, disability, and social participation, and the financial consequences in Access, affordability, and financial toxicity.

4 · Sexual health and menopausal symptoms

The dominant barrier is that the topic is not raised. Guideline recommendations begin with the clinician initiating the discussion, because patients reliably do not14.

The mechanism after endocrine therapy is oestrogen deprivation acting on the vulvovaginal epithelium, producing the genitourinary syndrome of menopause. Dryness, dyspareunia, urinary symptoms, and reduced arousal follow from a tissue change rather than from a psychological one, and treating it as psychological is the common error.

Non-hormonal measures come first and are more effective than their reputation. Long-acting vaginal moisturisers used on a schedule differ from lubricants used at intercourse, and patients are routinely offered only the second. Pelvic floor physiotherapy and graduated dilators address the pelvic floor hypertonicity that develops secondary to painful intercourse.

Low-dose vaginal oestrogen is the genuinely contested intervention. The concern is measurable systemic absorption in a patient whose treatment aims at near-complete oestrogen deprivation, and the concern is therefore greatest during aromatase inhibitor therapy. The available evidence is observational and does not settle the question in either direction. The defensible position is to name the uncertainty, to reserve it for symptoms that have failed non-hormonal management, and to make the decision jointly. Systemic menopausal hormone therapy after breast cancer is not offered, and the underlying exposure data are in Exogenous hormonal exposure.

Vasomotor symptoms are managed without hormones. Venlafaxine and gabapentin reduce hot flash scores similarly, and in a randomised crossover trial in survivors 68% of those expressing a preference chose venlafaxine15.

Body image, partnership, and identity after mastectomy or reconstruction are not separable from this and are developed in Body image and identity. For young patients, abrupt treatment-induced menopause is a different clinical problem from gradual natural menopause, and that distinction is made in Parenting, relationships, and long-horizon survivorship.

5 · Bone health and cardiovascular risk after treatment

Long-term survivors die of the diseases everyone else dies of. That is the organising fact of this section, and it means the survivorship task is ordinary preventive medicine performed deliberately rather than incidentally.

Bone loss is accelerated by aromatase inhibition and by ovarian suppression, and the management, including the fracture prevention evidence from ABCSG-18 and the adjuvant bisphosphonate data, is set out in Bone, metabolic, and endocrine late effects. The point specific to survivorship is that treatment ends and the deficit does not. Bone density measurement, calcium and vitamin D adequacy, fall prevention, and antiresorptive therapy where indicated all continue after the last prescription.

Cardiovascular risk accumulates from three treatment sources and one background. Anthracycline exposure leaves a fixed reduction in cardiac reserve. Radiation raises coronary event rates in proportion to mean heart dose, with a 7.4% increase per gray and no apparent threshold16. Premature menopause removes a period of relative protection. Against that, conventional risk factors continue to operate and are the only fully modifiable component.

In practice

Hand the cardiovascular and bone tasks to someone by name at the end of treatment. They are not oncology tasks in any narrow sense and they are the ones most often dropped at handover.

Record cumulative anthracycline dose and mean heart dose in the survivorship summary. Nobody can reconstruct them later.

Treat blood pressure, lipids, glucose, and smoking with the seriousness given to the cancer. In a long-term survivor of early breast cancer they are the larger competing risk.

6 · Exercise, nutrition, and weight management

The observational evidence for physical activity is consistent and has a well-known weakness. In a prospective cohort, women with hormone-responsive tumours performing 9 or more MET-hours per week of activity had a relative risk of breast cancer death of 0.50 compared with those doing less. The 95% confidence interval was 0.34 to 0.74. The absolute unadjusted mortality reduction at 10 years was 6 percentage points compared with women doing less than 3 MET-hours per week. Most of the benefit was achieved at the equivalent of walking 3 to 5 hours per week17. The weakness is reverse causation. Subclinical disease reduces activity before it becomes detectable, so some of the association runs backwards.

The observational evidence is not uniform. In one cohort, only the combination of five daily servings of vegetables and fruit with regular activity was associated with better survival, a hazard ratio of 0.5618. Among postmenopausal women with hormone receptor-positive disease in an endocrine trial, physical activity was not associated with survival or recurrence19. In breast cancer itself, an exploratory follow-up of a trial of exercise during chemotherapy found eight-year disease-free survival of 82.7% against 75.6%, a difference that was not statistically significant20. Exercise during treatment improves quality of life, according to a Cochrane review21.

The randomised evidence that structured exercise changes cancer outcomes now exists, and it is not in breast cancer. One trial tested a 3-year structured exercise programme begun after adjuvant chemotherapy for colon cancer. Eight-year overall survival was 90.3% in the exercise group and 83.2% in the health education group. The hazard ratio for death was 0.63, with a 95% confidence interval of 0.43 to 0.9422. That result establishes the principle in a solid tumour. It does not establish the effect size in this disease.

Guideline recommendations during active treatment are for regular aerobic and resistance exercise. The same guideline states that evidence for dietary and weight loss interventions during treatment is very limited23.

Dietary intervention has one long-term randomised result. A dietary modification trial reported extended follow-up at a median of 19.6 years. Deaths after breast cancer were reduced with a hazard ratio of 0.85 and a 95% confidence interval of 0.74 to 0.96. Deaths attributed to breast cancer fell with a hazard ratio of 0.79 and an interval of 0.64 to 0.9724. The intervention was a low-fat dietary pattern with increased vegetable, fruit, and grain intake, and the effect emerged only with very long follow-up.

A randomised trial in women already treated for the disease is shorter and less certain. The Women's Intervention Nutrition Study assigned 2,437 women with resected early breast cancer to a fat-reduction programme or to control25. At an interim analysis after a median of 60 months, relapse had occurred in 9.8% against 12.4%. The hazard ratio was 0.76, with a 95% confidence interval of 0.60 to 0.98, significant in the adjusted Cox model but not on the stratified log-rank test. Mean body weight was 6 pounds lower in the intervention group, and funding for the intervention had ended when the analysis was run.

Weight and metabolic state are prognostic and the interventions that target them have mostly failed to change outcome. Higher body mass index was associated with more recurrences in an exploratory analysis of an adjuvant endocrine therapy trial, and the association was stronger on anastrozole than on tamoxifen26. Metformin was tested directly in MA.32 and did not improve invasive disease-free survival27. The host biology that motivated these trials is in Obesity, insulin signaling, and metabolic dysfunction and Exercise, diet, and modifiable host biology.

Caution

The prognostic association between obesity and recurrence is robust. The inference that losing weight after diagnosis reduces recurrence is not established, and the negative metformin result shows that targeting a plausible mediator is not enough. Recommend exercise because the evidence supports it. Recommend weight loss for function, comorbidity, and symptom burden, and do not promise it will prevent recurrence.

7 · Second primaries and long-term health maintenance

Second cancer risk in this population is modestly elevated and the shape of that elevation matters more than its size. In a population cohort of 476,373 women, by 20 years 13.6% had developed a non-breast primary cancer, 2.1 percentage points more than expected. A contralateral breast cancer had developed in 5.6%, which was 3.1 percentage points more than expected. The contralateral excess was greater in younger women. Contralateral breast cancer accounted for roughly 60% of the overall increase28. The treatment attribution and the therapy-related mechanisms are in Treatment-related second malignancies and clonal hematopoiesis.

Two consequences follow for the survivor rather than for the epidemiologist.

The first is that contralateral surveillance is the surveillance that earns its place, which is the argument already made in Surveillance after curative treatment and the evidence against intensity. Obesity, smoking and alcohol were each associated with contralateral cancer in a population-based study, which gives survivors three modifiable risks29. In carriers of BRCA1 or BRCA2 variants, contralateral risk was 29.5% at 10 years, and lower with tamoxifen or oophorectomy30. After breast conservation, carriers had in-breast recurrence similar to sporadic controls and more contralateral cancers31,32. The second is that a second primary, or a young age at first diagnosis, is an indication for germline testing if it was not already done Inherited susceptibility and familial breast cancer. A pathogenic variant changes the contralateral risk estimate and with it the risk-reducing options in Risk-reducing surgery and the decision calculus.

The broader failure is quieter. Survivors receive intensive cancer-specific follow-up and less general preventive care than comparable people without a cancer history. Colorectal and cervical screening, vaccination, diabetes and hypertension management, and osteoporosis assessment all drift during years of oncology attendance. Naming an owner for each is the remedy, and it belongs to Survivorship care models and transition to primary care.

8 · Survivorship care models and transition to primary care

The question of who provides follow-up has a randomised answer that is rarely acted on. In a trial of 968 patients with early-stage disease who had completed adjuvant treatment, follow-up by the patient's own family physician was compared with follow-up at the cancer centre. Recurrence-related serious clinical events occurred in 17 patients (3.5%) in the family physician group and 18 (3.7%) in the cancer centre group. The difference was 0.19 percentage points, with a 95% confidence interval of minus 2.26 to 2.65. Recurrences numbered 54 and 64 and deaths 29 and

  1. No health-related quality of life measure differed33.

Guideline recommendations set out what follow-up should contain rather than where it happens: surveillance for recurrence, assessment for late and long-term effects, health promotion, and coordination between oncology and primary care34.

The models in use are specialist-led, shared care, primary-care-led, and nurse-led. The evidence above says the setting is not the determining variable. Three things determine whether follow-up works: whether each task has a named owner, whether the primary care clinician knows what the patient received, and whether a defined route back into oncology exists.

Caution

Survivorship care plans were mandated widely on the assumption that a document transfers information and improves outcomes. Randomised evidence that a care plan alone improves patient outcomes is weak. The document is worth producing because the treatment summary it contains cannot be reconstructed later, particularly cumulative anthracycline dose and radiation fields. Producing it and calling the transition complete is the part that does not work.

Risk-stratified follow-up is the direction of travel. A patient with a node-negative T1 tumour and a patient with residual disease after neoadjuvant chemotherapy have different recurrence hazards, described in Annual hazard of recurrence and the long tail of hormone receptor-positive disease. There is no reason for them to attend on the same schedule.

9 · Survivorship in metastatic disease, living long with incurable cancer

Survivorship programmes are built around the end of treatment. For metastatic disease there is no end of treatment, and the result is that a large population is excluded from survivorship care by the structure of the service rather than by any clinical judgement.

The population is not small. Using population-based mortality and survival data, an estimated 154,794 women were living with metastatic breast cancer in the United States at the start of 2017. Three in four of them had initially been diagnosed with stage I to III disease. Median survival and 5-year relative survival for de novo metastatic disease rose across the study period, with the largest gains in younger women35.

What these patients need overlaps with the rest of this chapter and differs in emphasis.

Cumulative toxicity is the dominant problem rather than acute toxicity. Years of sequential therapy leave fixed neuropathy, reduced marrow reserve, and cardiac injury, and each new line is chosen against that accumulated background. Treatment-free intervals and the case for them are in Treatment-free intervals and cumulative toxicity.

Bone health, cardiovascular risk, exercise, sexual health, and cognitive change all apply and are systematically underaddressed, because the clinical encounter is occupied by the scan.

Scan-associated anxiety has a cycle length set by the imaging interval, and it is a predictable recurring event rather than a personality trait.

Employment, insurance, parenting, and fertility remain live issues for people who may live many years. The disease is incurable and the timeframe is not short, and services built for one of those facts usually ignore the other. The visibility problem this creates is developed in Advocacy, peer support, and the metastatic visibility gap.

Caution

Palliative care and survivorship care are frequently treated as alternatives, with referral to one implying the patient is past the other. They answer different questions. Early integration of palliative care improves quality of life and symptom burden36. It should not be argued on survival. The pooled evidence across 43 randomised trials gives a survival hazard ratio of 0.90 with an interval from 0.69 to 1.1737, and the reasoning is set out in Early integration of palliative care and its evidence. Survivorship care asks how to live well for years with treatment continuing. A patient with metastatic disease needs both at the same time, for a long time.

In practice

Run a survivorship review for metastatic patients on a schedule, separate from the response assessment visit. The scan visit will always crowd it out.

Record cumulative exposures as they accrue. Anthracycline dose, taxane cycles, and platinum exposure determine what is available at the fourth line.

Ask about work, dependants, and money. Long survival with continuous treatment produces financial harm that a curative-intent pathway does not, and the mechanisms are in Access, affordability, and financial toxicity.

References

All 37 references
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