CHAPTER 31 Nursing the patient with cancer

Introduction

Cancer remains one of the top priorities in health care alongside heart disease, stroke and diabetes. It can profoundly affect every aspect of life, encompassing physical, psychological, social or spiritual aspects. Cancer care is changing rapidly with advances in technology and emerging treatments improving survival rates. Nurses are now at the forefront of care for cancer patients and their families.

Despite improvements in survival, the term ‘cancer’ impacts on the attitudes and beliefs of practitioners and patients, instilling thoughts about pain, uncertainty and death (Box 31.1). Government policy in prevention and predictions about the nature and cause of cancer can appear controversial and contradictory. This creates misinformation and inconsistency surrounding the disease.

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Cancer is a serious social problem, costing much in human and financial terms. One in three people in the UK risk developing cancer in their lifetime. One in four deaths are attributable to cancer (Cancer Research UK 2009). The incidence of different cancers and the death rate associated with them can vary both within the UK and globally. (See Useful websites Cancer Research UK, World Health Organization.)

Oncology as a specialty

The UK political and health care agenda has recognised cancer as a high priority area for over a decade. The first important documentation to drive organisational change in cancer services across the country was initiated by the publication of the Calman–Hine/Calman Report (Department of Health 1995). The Calman Report focused around the patient and their family, care being delivered in specific designated cancer centres and cancer units in partnership with each other. The report recommended a seamless service integrating primary, secondary and tertiary care, with real commitment to psychosocial as well as medical needs. It also provided the opportunity to think about cancer control, early screening and detection programmes.

Subsequent policy documents have influenced the progression of cancer services and, following devolution, England, Wales and Scotland have set out their own policy directions for health (Department of Health 2004, Scottish Government 2008). Comprehensive long-term strategies are continually being developed to shape cancer services, focusing on all aspects of the patient’s cancer journey, ensure equity of care and invest in equipment and the cancer workforce. Nursing plays a key role in this development and both student nurses and newly qualified health care professionals need to understand the multidisciplinary nature of cancer management within and outside the hospital, appreciating the roles of all those providing patient care.

The fundamental process of cancer

The formation of cancer is a very complex process which involves the disruption of the regulation of growth of normal cells in the body. The process is called carcinogenesis. Any organ within the body has the potential to become cancerous, however some cancers are more common and potentially linked to a known carcinogen exposure.

In recent decades, molecular biology has made great progress in unravelling the steps involved in this process of cell transformation and is improving our ability to understand, classify, diagnose and treat cancer. A critical component in understanding the cancer process and rationale for treatment is a knowledge of the structure and function of cells, the role of deoxyribonucleic acid (DNA) and the cell cycle. (See Further reading, e.g. Martini & Nath 2009 and Useful websites, e.g. Cancerquest.)

To maintain functional cells through cell division the normal regulatory function of the cell will employ chemical signals to drive and halt growth; this is controlled by genetic components of the cell. The chemical signals are protein components of growth factors, receptors, and messenger and regulatory proteins. The chemical signals act within individual cells and are also utilised when communicating with neighbouring cells in regulating growth. Damage to the genetic components of the cells can result in loss of function and ability to regulate growth. As the scientific evidence for the chemical signals is complex this text will concentrate on the key genetic components involved.

During scientific research on viruses and how they propagate and reproduce within their host, scientists discovered extremely important genes involved in regulation of cell growth. These genes were called proto-oncogenes and had the ability to promote cell growth (switch on). When one of these genes becomes damaged and permanently switched on it is referred to as an oncogene. The ability of the cell to inhibit (switch off) growth is regulated by a tumour suppressor gene, the activity of which was revealed when investigating the childhood hereditary cancer retinoblastoma. When this gene is damaged the function is lost and the cell can no longer switch growth off. Another gene implicated in the replication repair process is called the mismatched repair gene. This gene repairs damaged DNA after replication. When this gene is damaged the cell accumulates lots of mismatched DNA which in turn promotes cell growth. The last essential gene controls the process of apoptosis (programmed cell death) – when the cell has divided a certain number of times it commits cell death. Therefore damage in this gene results in an inability to programme the cell to die. Such damage may occur from either error in DNA replication during mitosis or exposure to environmental agents. In the transformation to a cancerous growth, there is a progressive series of mutations of genes regulating cell division and differentiation.

Cancers develop when the cell can no longer regulate its own growth, resulting in the cells being able to divide rapidly. To survive within the host the forming tumour seeks out a new blood supply to maintain its growth which results in small fragments of tumour splitting off and travelling to distant sites to form secondary tumours (metastases); the cancer is said to have metastasised.

Tumours grow by repeated cell divisions; their rate of growth is often defined in terms of doubling time. Tumours vary greatly in their doubling time but, contrary to popular belief, their growth is not as rapid as that of normal tissues. For a tumour growth to exceed 1 or 2 mm, it requires a blood supply for survival; therefore the formation of a capillary network from the surrounding host tissue is initiated by proteins or angiogenic factors, e.g. fibroblast growth factor (FGF) and tumour necrosis factor (TNF).

Tumour pathology

A tumour may be benign or malignant. ‘Cancer’ is a general term used to describe all malignant neoplasms, i.e. a new growth of tissue, or tumour.

Usually benign tumours are:

• well differentiated – still closely resemble the host tissue

• slow growing

• enclosed in a capsule

• non-invasive – do not invade locally or metastasise.

Once removed, benign tumours rarely recur. However, a benign tumour can cause problems or even death in certain sites. For example, a benign brain tumour can cause pressure on the brain (see Ch. 9) and some benign tumours cause problems in other ways, such as bleeding or secreting excess hormones.

Malignant tumours grow at the expense of the host. They are characterised by:

• various degrees of cell differentiation – well differentiated to totally undifferentiated

• variable growth rate – may be uncoordinated; some are slow growing

• having no enclosing capsule

• their invasive nature – locally by infiltration and by metastatic spread to other sites.

Malignant tumours destroy vital structures, cause severe weight loss and debility (cancer cachexia syndrome) and result in death without effective treatment. It is, however, important to remember that as survival times continue to improve many more people will be ‘living with cancer’.

Understanding the molecular biology of cancer is very important to identify and obtain a definitive cancer diagnosis and thus predict prognosis. Increasing knowledge about newer biological factors such as HER2/neu receptors and proliferative index (rate of cell division in the tumour) has altered the way adjuvant treatments (see p. 812) are prescribed and these indicators are increasingly used to predict prognosis. The HER-2/neu receptor belongs to the epidermal growth factor receptor family which is one of the receptors critical in controlling the pathway for epithelial cell growth and differentiation, and possibly angiogenesis (Karunagaran et al 1996). Overexpression of the HER-2/neu protein is observed in 15–20% of breast cancers (Slamon et al 1989), and it is now accepted that high levels of expression of HER-2/neu identify those patients most likely to respond to trastuzumab in both the adjuvant and metastatic disease setting.

Identification of the steps involved in carcinogenesis has led directly to the discovery of molecular tumour markers (Table 31.1). Among the cancers for which molecular diagnostics has had an impact is chronic myeloid leukaemia (CML). The marker of this disease is the Philadelphia chromosome, which is detectable in 95% of cases. This additional information enhances the ability to accurately diagnose and determine prognosis.

Table 31.1 Examples of molecular genetic markers used in cancer diagnosis and prognosis

Cancer	Genetic Marker	Principal Application
Chronic myeloid leukaemia	Philadelphia chromosome t(9;22)(q34;q11) [BCR/ABL]	Primary diagnosis, detection of residual disease after treatment
Non-Hodgkin’s lymphoma
Follicular	t(14;18)(q32;q21) [BCL2/IGH]	Primary diagnosis, detection of residual disease after treatment
Burkitt’s	t(8;14)(q24;q32)	As above
Neuroblastoma	MYCN amplification	Prognosis
Breast cancer	HER2-neu/ERB2 amplification	Prognosis
Familial cancers
Breast	BRCA1, BRCA2	Diagnosis of hereditary predisposition
Colon	APC, MSH2, MLH1	As above
Wilms’ tumour	TP53 mutation	As above
Retinoblastoma	RB mutation	As above

Tumours may be classified not only by their biological behaviour but also traditionally by their tissue of origin. Most tumours retain sufficient characteristics of the normal differentiated cell to allow recognition of the type of tissue from which they were derived, which is the basis for the classification of tumours by tissue type (Table 31.2).

Table 31.2 Classification by tissue type of malignant tumours

Tissue of Origin	Malignant Tumour
Epithelial	‘Carcinoma’
Squamous: surface epithelium, cell lining covering body cavities, organs and tracts	Squamous cell carcinoma, e.g. lung, skin, stomach
Glandular: glands or ducts in the epithelium	Adenocarcinoma, e.g. breast, lung, colon
Transitional cells: bladder lining	Transitional cell carcinoma, e.g. bladder
Basal cells: skin layer	Basal cell carcinoma (BCC), ‘rodent ulcer’
Liver	Hepatocellular carcinoma
Biliary tree	Cholangiocarcinoma
Placenta	Choriocarcinoma
Testicular epithelium	Seminoma, teratoma, embryonal carcinoma
Endothelial cells	Angiosarcoma
Mesothelial: covering the surface of serous membranes	Mesothelioma, e.g. pleura, peritoneum

Connective tissue	‘Sarcoma’
Bone	Osteosarcoma
Cartilage	Chondrosarcoma
Fatty tissue	Liposarcoma
Fibrous tissue	Fibrosarcoma
Lymphoid tissue	Lymphomas
Bone marrow	Leukaemias, e.g. ALL, CML

Muscle	‘Myosarcoma’
Smooth muscle	Leiomyosarcoma
Striated muscle	Rhabdomyosarcoma
Cardiac muscle	Cardiac sarcomas

Neural
Meninges	Meningeal sarcoma
Glia	Glioblastoma multiforme
Neurones	Neuroblastoma, medulloblastoma

Germ cells
Testes or ovary	Teratoma, germ cell

ALL, acute lymphoblastic leukaemia; CML, chronic myeloid leukaemia.

Epidemiology of cancer

Epidemiological studies provide data about possible causes of different forms of cancer and inform the strategies for cancer prevention and screening. The most commonly diagnosed cancers in the UK are breast, lung, colorectal and prostate; together these four cancers make up over 50% of all new cancers each year (Cancer Research UK 2009). The 20 most commonly diagnosed cancers are shown in Figure 31.2.

Figure 31.2 The 20 most commonly diagnosed cancers (ex NMSC), UK, 2006 (Cancer Research UK, http://info.cancerresearchuk.org/cancerstats/incidence/commoncancers/ June 2009). CNS, central nervous system; NHL, non-Hodgkin’s lymphoma.

Cancer is associated with increasing age. Around 75% of people diagnosed with cancer are aged 60 years and over (Cancer Research UK 2009). Cancer is very rare in children; approximately 1% of cancers are diagnosed in children, teenagers and young adults (Cancer Research UK 2009). (See Further reading, e.g. Baggott et al 2002.)

The incidence of cancer in the UK is one of the highest in the northern hemisphere. Predominantly, cancer is a disease of well-resourced countries but it is clear that patterns of cancer are set to increase in developing countries over the next decade (Ferlay et al 2007). The greater incidence in the northern hemisphere may be partly attributed to the availability of screening, diagnostic and reporting procedures, improved overall life expectancy and diet. Geographical variations across the world in the incidence of cancer provide clues to the lifestyles of different populations.

In Mozambique a high incidence of liver cancer is thought to have been associated with aflatoxin from mould found on stored peanuts. Since the introduction of more appropriate storage practices, the incidence of liver cancer has been falling. The Japanese have a low incidence of breast cancer in comparison to the UK and USA but a high incidence of stomach cancer.

Epidemiological investigation of genetic predisposition to cancer is growing rapidly as developments in molecular biology make it possible to study genetic markers in large populations. The completion of the Human Genome Project is accelerating the discovery of such markers (see Useful websites).

Aetiology of cancer

The cause of cancer is the combined interaction of genetic and environmental factors and it is difficult to separate the two completely. Although all cancers have a genetic origin at the cellular level, this does not mean that all cancer is inherited. Genetic changes or mutations may be either somatic (acquired) or germline (inherited).

• Germline mutations are those present in the gamete (oocyte or spermatozoon) of a parent that can be passed to the offspring. The mutation is present in every cell of the body.

• Somatic mutation is when an individual body cell, post conception, acquires a gene alteration. If not repaired, the mutation is passed on to all future cells through mitosis. These clonal changes are unique to the cells in that particular tissue and are not inherited.

Many questions remain to be answered regarding the exact mechanisms involved in the cellular mutations that lead to cancer. However, epidemiological studies have identified certain causative factors, termed ‘carcinogens’.

Carcinogens are factors that both initiate and promote changes in the cell which lead to cancer. Both are required to cause the cancer:

• Initiation – a mutagenic event occurs in the DNA of a single cell.

• Promotion – repeated exposure to carcinogenic agents may or may not cause this initiated cell to proliferate to form a tumour.

Carcinogenic factors and substances can be either intrinsic or extrinsic.

Intrinsic factors

Heredity

Inherited cancers constitute 5–10% of all cancers. Several genes have now been identified that are responsible for predisposing individuals to develop certain cancers. Cancers that occur with increased frequency in families are components of various hereditary cancer syndromes, e.g. hereditary non-polyposis colon cancer (HNPCC).

Cancer susceptibility genes such as BRCA1 and BRCA2 have been identified in breast and ovarian cancer. Women who inherit a mutation in these genes may face a 50–85% lifetime risk of developing breast cancer including an increased risk for ovarian cancer (Calzone & Biesecker 2002). Testing for these particular genes and others is now available commercially.

Hormones

Certain hormones are thought to promote some tumours. Early menarche, late menopause and nulliparity are associated with an increased lifetime risk of breast cancer. The Million Women Study (2003) found that the use of combined oestrogen plus progesterone hormone replacement therapy (HRT) also increases the risk of breast cancer. High testosterone levels have been related to increased risk of prostate cancer (Ross et al 2003).

Immunity

Individuals with impaired immunity are more susceptible to cancer; for example, people with HIV disease have a higher incidence of Kaposi’s sarcoma than the normal population (see Ch. 35). It is the prolonged immunosuppression that may predispose these patients to cancer rather than the infectious agent per se.

Pre-existing disease

Any tissue subjected to constant irritation or to a disease process has an increased susceptibility to malignant change.

Extrinsic factors

At least 70% of cancers occur in epithelial cells which are constantly exposed to external, ingested or inhaled substances. Extrinsic factors related to lifestyle and the environment are important in the process of carcinogenesis. These factors include physical agents, chemical agents, viruses and diet.

Physical agents

Radiation

is known to cause cellular mutations and cancer. Survivors of the atomic bomb explosions in Hiroshima and Nagasaki in Japan experienced a high incidence of leukaemia and skin cancer. Early research has shown an apparent increase in the incidence of leukaemia among the children of fathers working in the nuclear industry, possibly due to germ cell mutations (Gardner et al 1990). Repeated exposure to therapeutic doses of radiation is not thought to be harmful, although stringent precautionary regulations must be followed for the protection of all exposed workers. Therefore, it is not routine discharge of radioactivity by the nuclear industry that should be feared, but rather the catastrophic event, such as occurred at Chernobyl in 1986.

Ultraviolet light (UVL)

There is overwhelming evidence that repeated exposure to solar UVL is the primary cause of basal and squamous cell carcinoma (see Ch. 12). Data establishing a direct causal relationship with sunlight are more complex, but suggest a promotional role of sunlight in the cause of melanoma. Light-skinned or freckled individuals who are unable to manufacture sufficient protective melanin are particularly at risk (see Ch. 12).

Chemical agents

Tobacco

Ninety per cent of all lung cancers can be attributed to tobacco smoking. The temporal relationship between smoking and lung cancer was defined in the 1950s by studies undertaken by Doll & Hill (1954). Cigarette smoking has now clearly been identified as a major cause of cancers of the mouth, pharynx, larynx, bladder and pancreas, whilst contributing to many others. Risk is more dependent on duration of smoking than on consumption. Smoking 20 cigarettes a day for 40 years is eight times more hazardous than smoking 40 cigarettes a day for 20 years. People who stop smoking even well into middle age avoid most of their subsequent risk of lung cancer, and stopping before middle age avoids more than 90% of the risk attributable to tobacco (Peto et al 2000). It is also evident that non-smokers are at risk from exposure to other people’s smoke: one-quarter of lung cancer cases in non-smokers are estimated to be due to passive smoking (International Agency for Research on Cancer [IARC] 2004).

Alcohol

Excessive alcohol, ingested over long periods of time, contributes to cancers of the mouth, pharynx, oesophagus and liver. Those who drink spirits as opposed to wine and beer and those who smoke as well as drink are particularly at risk.

Viruses

Although cancer is not contagious, some cancers are associated with viral infections. For example, the Epstein–Barr virus (EBV) causes a systemic infection that may precede Burkitt’s lymphoma, a malignant disease common in parts of Africa. Patients with chronic hepatitis B are more susceptible than others to liver cancer. The human papilloma virus (HPV), which may be sexually transmitted, is associated with cervical cancer, and the development of vaccines against some types of HPV has created opportunities to prevent some cases of cervical cancer (see p. 812).

Diet

Epidemiological studies that isolate diet as a causal factor in the development of cancer are extremely problematic to undertake. Nevertheless, dietary factors have been implicated as a major cause of the high incidence of cancer in the West. Countries where the average diet is high in fat and protein appear to have a high incidence of breast cancer, and low-fibre diets are thought to contribute to bowel cancer.

Cancer prevention and screening

Prevention of cancer is a major focus of research and education. The goal of primary prevention is to reduce the risk of the healthy population developing cancer. Secondary prevention aims to detect early-stage, curable cancer. Primary prevention is therefore the most effective and economic method of controlling cancer.

Nurses now have a responsibility to incorporate health promotion, health education and disease prevention in their role as well as the care of those who are ill. This wider role is reflected in their initial and post-registration education. Community health practitioners work in health centres offering a range of health promotion programmes, as well as screening for ill health. Antenatal care, well-woman or well-man clinics, sexual health and family planning centres and other health screening clinics all provide opportunities for the promotion of cancer prevention. Within hospitals, clinical nurse specialists incorporate cancer awareness and prevention in their roles, with many involved in local and national initiatives such as cancer site-specific awareness weeks and health promotion in schools.

Primary prevention

Primary cancer prevention includes activities such as:

• identifying risk factors in individuals or groups

• counselling high-risk individuals to promote behaviour modification

• genetic screening

• implementation of new cancer prevention programmes, e.g. smoking cessation, healthy eating.

Media reporting of cancer risk development requires cautious interpretation and should be put into perspective by reference to the original studies on which it is based. It is important to remember that substances that are carcinogenic in animals are by no means always so in humans. Moreover, everyday exposure to some substances implicated is so minimal as to make risk insignificant. Some media scares do little to promote health; fear of cancer, after all, is one of the most common reasons why people avoid screening or fail to present with symptoms.

Health promotion programmes

Health promotion/education programmes have some measure of success. Several government publications have taken on ‘The Cancer Challenge’, with measures to promote a ‘pro-health’ culture (Department of Health 2000, Scottish Executive Health Department [SEHD] 2004). Projects have been developed to assist smokers to quit, particularly in areas with high levels of deprivation, prisons, the army and working men’s clubs. Political action has included a comprehensive ban on tobacco advertising, a smoking ban in public places and the workplace, the setting up of new stop-smoking clinics and a smokers’ helpline, nicotine replacement patches and bupropion available on prescription, as well as a major health education campaign in schools aimed at preventing youngsters from starting to smoke (Department of Health 2000, SEHD 2004).

Through working partnerships with the community and the food industry, strategies to promote healthy eating include a national ‘Five a Day’ programme, improving accessibility to affordable fresh fruit and vegetables, and advocating five portions of these daily (see Ch. 21) (Box 31.2).

Attitudes

Psychologists have developed a Health Belief Model (Strecher & Rosenstock 1997) to predict an individual’s preventive health behaviour and account for some of the factors which determine attitudes to health and illness. The Health Belief Model states that an individual feels vulnerable to a disease if they believe they are susceptible to developing it and believe the disease to be serious. Preventive action will be taken only after the individual has balanced the benefits of that action against its physical, psychological and financial costs (Smith 2005).

Despite being taught about the risks of smoking, teenage smokers may consider themselves to be young and healthy and therefore not ‘at risk’. Young people in general are motivated by short-term rather than long-term rewards. Smoking in some subcultures and families is associated with attributes such as maturity or rebelliousness, which the young person and their peer group may value. Later, the physical addiction to nicotine becomes a coping mechanism for life’s stresses and social deprivation. For such people, possible avoidance of lung cancer is not worth the cost of surrendering the immediate gratification and social status offered by smoking.

Clearly, consideration of the wider causes of individual behaviour would lead those involved in health promotion to an awareness of the social and political action necessary. The causes of social deprivation need to be considered alongside individual behaviour. Preventive services must be readily accessible, based on the expressed needs of the community and client-centred.

The concepts of health and ill health are open to wide interpretation. An essential aspect of communication is that everyone understands and attaches the same meaning to language used. If adherence to health care programmes is to be achieved, nurses need to understand an individual’s personal health beliefs and how information is interpreted.

Secondary prevention: screening

The prognosis and outcome of patients with cancer is improved considerably if the tumour is detected at an early stage. Complete cure can only be assured if pre-cancerous tissue can be identified and treated, as in the case of cervical intraepithelial neoplasia (CIN).

Cancer screening difficulties

The development of an accurate and cost-effective method of screening at-risk sections of the population is problematic for several reasons. The test must have both a high degree of sensitivity, reducing the risk of false-negative results, and specificity, reducing the psychological trauma and expense of treating false-positive results.

It must be possible to identify an at-risk group; otherwise the cost of screening becomes prohibitive. Finally, and most problematically, it must be determined whether detecting the cancer type at an early stage will prolong life (Segnan et al 2004).

The general cancer screening programmes currently offered (in the UK) are:

• breast cancer screening

• cervical cancer screening

• colorectal cancer screening.

Plus the Prostate Cancer Risk Management.

(See Useful websites NHS Cancer Screening Programmes.)

Breast cancer screening

Despite recent debates about the quality of over 40 years of trials, it is generally agreed that there is a clear benefit and reduction in mortality from breast cancer from screening women over the age of 50 years by mammography every 2 years (IARC 2002). In the UK mammography is routinely offered every 3 years to women aged between 50 and 70 years. However, the age range for routine invitation for screening is to be extended to include women aged 47 to 73. Accepted screening techniques include mammography and clinical breast examination, although Baxter (2001) has concluded that breast self-examination is of no benefit in routine screening. The value of screening women of 40 years or younger remains controversial, consequently professional clinical judgement and a woman’s choice should guide decision-making. The denser breast tissue of premenopausal women makes mammograms difficult to interpret in this age group. In future, genetic screening and new technologies such as digital mammography may be of benefit.

Cervical cancer screening

Cervical cancer is one of the most common female cancers in under-resourced economies. Since the introduction of the Papanicolaou (‘Pap’) smear test in the mid 1960s, there has been a steady decline in mortality rates in the UK. Women in the UK are first offered screening at age 25 years. This continues every 3 years until they reach the age of 49 years. Thereafter the test is offered at 5-year intervals until women reach the age of 64. Women aged 65 or over are only offered a smear test if they have not had a smear since they reached 50 or have recently had an abnormal smear. However, some GPs may offer early screening as part of their consultation with women regarding sexual health.

Uptake of the service by groups at highest risk, i.e. women over the age of 40, of lower socioeconomic status and in minority ethnic groups, could be better. Barriers to cervical screening include lack of sensitivity and trust in health professionals, possible feelings of guilt and embarrassment, judgemental attitudes, and a lack of privacy and supportive care in clinics (Fitch et al 1998). It is important for staff working in screening services to have well-developed interpersonal and communication skills to alleviate any fears or anxieties. In addition, clinic schedules should allow time to provide support.

Intervention strategies based on individual respect, health care provider relationships and inclusion of significant others may increase adherence to cancer screening guidelines (Steven et al 2004).

Colorectal cancer screening

The natural history of colon cancer with the relatively long time from biological onset to the development of cancer makes it a good candidate for screening. A national bowel screening programme based on faecal occult blood (FOB), using a home screening kit, was rolled out in 2006 (England) and 2007 (Scotland). The service became available throughout the UK in 2009.

Screening is routinely offered every two years to people aged 60–69 years (in England) and 50–74 years (in Scotland). However, people aged over 70 years in England can request a screening kit (NHS Cancer Screening Programme 2009a). People with an unclear result will have the FOB test repeated. Where an abnormal result occurs the person is offered an appointment with a specialist nurse to discuss colonoscopy (see Ch. 4). Campaigns by Colon Cancer Concern have been initiated to promote a greater awareness of the early warning signs of colon cancer (see Ch. 4).

Screening options for other cancers

Screening programmes for the cancers below are being reviewed, including:

• prostate cancer

• ovarian cancer

• lung cancer.

Prostate cancer

There is at present no consensus regarding the most appropriate screening method. There are three main screening modalities: digital rectal examination (DRE), serum prostate-specific antigen (PSA) and transrectal ultrasonography (TRUS). There are wide ranges in the estimates of sensitivity and specificity. Interest in PSA (a blood test) emerged in the late 1980s. However, PSA may be elevated in men with non-cancerous conditions. There is currently no evidence that prostatic screening improves clinical outcomes; in fact, there are issues of uncertainty surrounding the appropriateness and type of treatment for men with early-stage prostatic cancer, since it has a long asymptomatic latency period. It is therefore important to consider that there might be an adverse psychological impact as a result of prostate screening although, for those men at risk, it may provide some reassurance (Cantor et al 2002).

A Prostate Cancer Risk Management programme is available to improve men’s understanding of the benefits and limitations of PSA testing (NHS Cancer Screening Programme 2009b).

Ovarian cancer

This cancer is sometimes referred to as the ‘silent killer’ because it often presents late and has the highest mortality rate of all malignant gynaecological cancers. Transvaginal ultrasound and detection of a raised cancer antigen (CA125) in the blood provide two possible techniques for the screening of ovarian cancer. However, as with PSA, CA125 may be elevated in non-malignant conditions. A UK collaborative trial of ovarian cancer screening (UKCTOCS) is underway to answer the question of whether or not early detection will save lives. The effectiveness of different screening technologies is being examined. A report is expected in 2010 and will make recommendations about ovarian cancer screening for the whole population (Menon et al 2009).

Women known to have a high familial risk of developing ovarian cancer are offered annual screening as part of a national familial ovarian cancer screening study.

Lung cancer

It has been shown that low-dose spiral computed tomography (CT) scanning can identify lung cancer in high-risk but asymptomatic individuals (Gohagan et al 2005). Whilst this may be a useful screening test, further evidence is required to see if early detection is linked with a decrease in mortality.

Medical intervention and the nurse’s role

Diagnosis and staging

Patients present with cancer at different stages of the disease and may be asymptomatic or symptomatic.

The staging of a cancer is the process whereby the extent of the disease is established; this involves a variety of tests (see the appropriate chapter for the staging of a particular tumour site). The diagnosis and staging can be long, complex and tedious for the patient and their family, raising many issues of uncertainty. However, accurate staging of the extent of the disease is vital for the following reasons:

• Different forms of treatment are known to be effective for specific tumours and at specific disease stages. For example, thoracic surgery for a patient with disseminated small cell lung carcinoma (SCLC) and metastases in the ribs would be inappropriate given the metastatic spread of the disease. Staging avoids human and financial cost of using inappropriate treatment.

• It provides a better estimation of prognosis.

• It allows clinicians to determine a patient’s eligibility to enter a clinical trial of a new treatment.

The tumour, node (lymph) and metastasis (TNM) system

The most common internationally used method of defining disease stage is the TNM system (Sobin & Wittekind 2002), in which:

• T denotes the size or extent of local invasion of the primary tumour.

• N refers to the spread to local lymph nodes

• M refers to the presence of metastases.

Agreed staging criteria exist for each cancer, such as those staging systems used for lung cancer (Box 31.3), gynaecological, testicular cancers, etc. (see Chs 3, 7). Box 31.4 illustrates the staging system through the experience of a young man with testicular cancer.

Box 31.3 Information

Adapted from Sobin & Wittekind (2002).

Summary of the TNM staging system for lung cancer

T (primary tumour)

TX	Positive cytology only
Tis	Carcinoma in situ
T1	Tumour ≤3 cm in diameter. No proximal invasion
T2	Tumour >3 cm in diameter, within 2 cm from carina or invading the visceral pleura or partial atelectasis
T3	Tumour of any size extending into the chest wall, diaphragm, pericardium, mediastinal pleura or within 2 cm of carina, total atelectasis
T4	Tumour of any size with invasion of mediastinal organs or vertebral body, malignant pleural effusion

N (lymph nodes)

N0	Nodes negative
N1	Positive nodes in ipsilateral hilar nodes
N2	Positive ipsilateral, mediastinal and subcarinal nodes
N3	Positive contralateral mediastinal or hilar nodes, scalene or supraclavicular nodes

M (distant metastases)

M0 No metastases
M1 Metastases present

The disease is then staged using the above information, as follows:

Box 31.4 Reflection

Staging Dan’s testicular cancer

Staging system generally used in the UK

Stage I	Tumour confined to testes
Stage II	Pelvic and abdominal lymph node involvement
Stage III	Mediastinal and/or supraclavicular lymph node involvement
Stage IV	Distant metastases, e.g. lung

Dan, a 22-year-old student, discovered a testicular swelling but chose to ignore it, initially because he misinterpreted it as a sports injury and he was busy with exams, and later because he felt embarrassed and frightened. Nine months later he presented to the student health centre because he was becoming breathless far more readily than usual and suffered a constant backache. These symptoms were due to lung metastases and referred pain caused by metastases in the para-aortic lymph nodes.

Dan was admitted to a surgical ward, where a biopsy under anaesthesia was performed. A frozen section taken for histology showed a testicular teratoma. A left orchidectomy was then performed.

Following postoperative recovery, Dan was transferred to an oncology ward for staging. Dan lived too far away to travel to the department each day; otherwise the necessary tests could have been performed while he was an outpatient. Dan wanted to know why staging was needed and the specialist nurse explained the purpose of staging and outlined the tests that would be necessary. The tests were carried out and their results were as follows:

• chest X-ray: showed multiple lung metastases

• thoracic computed tomography (CT) scan: confirmed lung metastases

• abdominal CT scan: showed a large para-aortic lymph node and no liver metastases

• blood samples for full blood count, urea, creatinine and electrolytes, liver function and tumour markers (alpha-fetoprotein [AFP] and human chorionic gonadotrophin [hCG]).

These tests showed that Dan had stage IV testicular teratoma (see staging system above). Dan asked the specialist nurse to explain the results and treatment options to him and his parents who were extremely concerned.

Even extensive disease is curable with cisplatin-based chemotherapy. Accordingly, this was the treatment course chosen following further discussion with Dan.

Note. Creatinine clearance measures the rate at which the kidneys are able to clear creatinine (a byproduct of metabolism) from the blood. It is calculated from the serum creatinine using an equation that includes age, gender, and lean body weight to establish baseline measurements for subsequent assessment of any nephrotoxicity (damage to kidney tissue or function) induced by platinum compounds.

Activities

• Consider how you would react if you discovered a lump in a testis or a breast. Would you seek medical advice quickly, assume it to be completely innocent and forget it, or would you think it could be cancer but wait and hope the lump goes away?

• Discuss the role of the specialist nurse in supporting patients during the staging phase of a cancer with your mentor.

Some types of cancer – usually those that are disseminated at presentation – cannot be effectively staged with the TNM system and have necessitated the development of other systems.

During the course of their illness, patients may be restaged in order for their response to treatment, or the extent of disease recurrence, to be assessed.

See website Critical thinking question 31.1

Psychological impact of diagnosis and staging

Primary diagnosis

It is very common for patients to be aware that they have cancer before they are told formally of their diagnosis. This awareness derives from their experience of symptoms, tests and, in some cases, surgery and from the non-verbal communication of staff or relatives. How to inform patients in full of their diagnosis, and when this should be done are ongoing issues of ethical debate (Box 31.5).

Box 31.5 Information

Informing patients of their diagnosis: ethical considerations

Two ethical principles are central to the discussion of whether it is always right to tell a patient the whole truth about their diagnosis: these are the principles of autonomy and of beneficence (see further reading, e.g. Thompson et al 2006).

Autonomy

Patients have a right to autonomy, or self-determination. They cannot make decisions about their treatment or the future if they are not fully aware of their diagnosis. However, research has suggested that denial as a coping mechanism is sometimes necessary for the preservation of well-being during a crisis, allowing an individual time to mobilise the resources to cope with the seriousness of their disease (Moyer & Levine 1998). Unlike years ago, patients are now normally told their diagnosis, with a discussion of prognosis – often a medical uncertainty – and the level of information is tailored to the individual’s needs. There is no evidence to suggest that acceptance correlates positively to survival in cancer (Spiegel 2001).

Beneficence

The principle of beneficence obligates health care professionals to prevent harm and ‘do good’ for their patients. It may seem obvious that to tell lies or withhold the truth is wrong. Patients may suffer severe psychological problems if they continue to feel unwell despite the optimistic messages they receive from others, and may even blame themselves for their symptoms. They may also lose trust if and when they discover the ‘conspiracy’.

Discussion

The matter is seldom as simple as the choice between lying and truth-telling, and each case must be considered individually. Relatives may ask that their family member be protected from the whole truth. However, respect for the patient’s autonomy should, whenever possible, override such a request, but the relatives and patient need to be supported when such information is given, and their issues and concerns addressed.

Tension can arise within the health care team when medical staff fail in their responsibility to disclose appropriate information to those patients who clearly wish to know more. Other staff – nurses in particular – who spend more time with patients become frustrated in their attempts to meet the psychological needs of individuals who lack awareness of the reality of their situation. There must be an open staff forum for the discussion of such problems.

In most cancer centres, the issue is not whether, but how and when, to inform patients of diagnosis and prognosis. A study by Schofield et al (2003) showed that clinical practices that are linked to lessening anxiety include preparing the patient for a possible cancer diagnosis, having significant others present at diagnosis, being given as much information as desired in understandable language, having questions answered, talking about feelings and being given reassurance. It would seem appropriate that a nurse is present at such discussions because they can follow up the conversation and help the patient to strike a balance between realistic hope and the acceptance of reality.

Box 31.6 provides an opportunity for you to reflect on patient experiences of being given a diagnosis of cancer.