Chapter 11. Cancers and palliative care
Performance status and quality of life 349
Lung cancer 350
Breast cancer 353
GI and pancreatic cancers
Colorectal cancer 355
Oesophageal cancer 357
Stomach cancer 359
Pancreatic cancer 360
Gynaecological cancers
Ovarian cancer 361
Cervical cancer 363
Endometrial cancer 364
Urological cancers
Prostate cancer 365
Bladder cancer 367
Renal cancer 368
Testicular cancer 369
Haematological cancers
Leukaemia 370
Lymphoma 373
Myeloma 375
Palliative care 376
PERFORMANCE STATUS AND QUALITY OF LIFE
Performance status
Performance status is a means of stratifying the functional ability of patients with malignant disease. Drawing on the multiple factors that contribute towards a clinician’s overall judgement of a patient, it has been found to be a good predictor of mortality and fitness for therapy. However, it is still largely subjective and can be difficult to interpret in patients with habitually sedentary lifestyles. The two main performance status scales used are the World Health Organization/Eastern Cooperative Oncology Group (WHO/ECOG) and Karnofsky (KPS) scales. Table 11.1 illustrates the WHO/ECOG scale.
| Score | Status |
|---|---|
| 0 | Normal activity, fully active without restriction |
| 1 | Restriction of strenuous activity, can do light work |
| 2 | Ambulatory and capable of self-care, but unable to carry out any work activities: up and about >50% of waking hours |
| 3 | Capable of limited self-care, confined to bed/chair >50% of waking hours |
| 4 | Completely disabled, cannot undertake any self-care, totally confined to bed or chair |
Quality of life
Quality of life (QoL) is a multidimensional characteristic of an individual’s existence. It encompasses their capacity for physical functioning, their experience of disease and treatment-related symptoms, and their social and psychological well-being. Several tools have been developed to assess quality of life with varying levels of complexity and specificity for specific tumours, e.g. Functional Living Index Cancer (FLIC); European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire (EORTC-QLQ).
In contrast to performance status, quality of life measurements are usually patient self-assessments rather than clinician-performed assessments. Where a cancer cannot be cured it is especially important to evaluate treatments in terms of their impact on overall QoL, rather than whether or not they simply improve control of a specific symptom. Indeed, such treatments can sometimes reduce QoL, through the development of side-effects or complications. Likewise, it should be remembered that the impact on QoL of any cancer intervention is very patient-dependent.
LUNG CANCER
Epidemiology and aetiology
In the UK, lung cancer is the second most common cause of cancer in men and the third most common cause of cancer in women. Unfortunately, mortality rates have changed little over the past 10 years and lung cancer is now the commonest cause of cancer-related death.
Tobacco smoking is the principal risk factor for the development of lung cancer, and is thought to contribute to 90% of cases. Other risk factors include a family history in a 1st-degree relative, previous chest radiotherapy, cannabis smoking (more carcinogenic than tobacco) and exposure to asbestos, silica (if in the presence of silicosis), polycyclic hydrocarbons, radon and nitrogen oxides. Genetic abnormalities have also been associated with lung cancer, e.g. chromosome 3p21 deletion, mutation of the p53 gene and altered expression of oncogenes such as c-erb-B2 and N-myc.
Screening
Symptoms of lung cancer often develop late, and patients commonly present with incurable, metastatic disease. Although lung cancer screening seems logical, the results of recent studies have been disappointing. Plain CXR screening has been shown to be insensitive, while CT is limited by low specificity and a high incidence of false positive pulmonary nodules. Various bio-markers have shown promise, but none has been shown to be sufficiently predictive.
Presentation
Common presentations include a new (or changed) cough, haemoptysis, dyspnoea, chest pain, wheeze, a slow to resolve or non-resolving chest infection, fatigue, weight loss and anorexia. Early symptoms may easily be confused with an exacerbation of chronic lung disease, e.g. COPD, mandating a high index of suspicion, careful examination of the CXR and follow-up to ensure complete resolution of symptoms and radiological changes.
Advanced disease is suggested by arm or facial swelling due to superior vena caval obstruction; hoarseness due to tumour involvement of the recurrent laryngeal nerve; cardiac arrhythmias due to pericardial involvement; fits or limb weakness due to cranial metastases; or bone pain due to metastases or pathological fractures.
Investigation, pathology and staging
Investigation
Investigation priorities are three-fold: obtain a tissue diagnosis, stage the disease accurately and assess the patient’s cardiorespiratory fitness and potential operability (see also ‘Performance status’, p. 349). The majority of patients with lung cancer will have significant smoking-related co-morbidity.
Initial investigations should include CXR, FBC, U&E, LFT, Ca, LDH, oxygen saturation and spirometry (see p. 89). If the CXR is concerning or clinical suspicion persists, these should be followed by urgent CT scanning of chest, liver and adrenals. Isotope bone and CT brain scanning are not performed routinely, but undertaken where there is clinical suspicion of metastatic disease.
Since the majority of lung cancers arise centrally from main or segmental bronchi, a histological diagnosis can be obtained by flexible bronchoscopy. Peripheral lesions (about 20% of cases) should be biopsied percutaneously, under CT guidance. This approach carries a significant risk of pneumothorax and, therefore, adequate lung function is essential (FEV1 >1 L). Alternative approaches to tissue diagnosis in difficult cases include:
• fine needle aspiration or biopsy of palpable cervical nodes
• transbronchial lung biopsy: under fluoroscopic guidance where FEV1 >1 L
• transbronchial needle aspiration of mediastinal lymph nodes (TBNA), with or without endobronchial ultrasound (EBUS) guidance
• surgical mediastinoscopy, mediastinotomy, or open lung biopsy
• biopsy of liver metastases.
Pathology
Lung cancer is classified into two main pathological groupings: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). SCLC metastasizes early and is rapidly progressive. NSCLC is further divided into squamous, adenocarcinoma, large cell and undifferentiated NSCLC.
Squamous tumours are more common in older men, often account for cavitating lesions, are slower growing, often appear centrally, but are also usually responsible for Pancoast’s syndrome (Horner’s syndrome and brachial plexus symptoms secondary to an apical tumour). Adenocarcinomas are found peripherally more often than some other types, more commonly affect women and have a greater potential to metastasize early.
Less common forms of lung cancer include broncho-alveolar carcinoma (probably a variant of NSCLC) and the carcinoid tumours. The latter are often polypoid and benign; however, they have a similar neuroendocrine origin to SCLC and some may show malignant features. Carcinoid syndrome is suggested by flushing, diarrhoea and cough. Primary pleural cancers are usually due to adenocarcinoma or asbestos-associated mesothelioma (thickened lobulated pleura on CT).
Staging
Small cell lung cancer (SCLC)
Staging for SCLC is relatively simple:
• limited disease: contained within one hemi-thorax, including pleural effusion, ipsilateral mediastinal nodes and ipsilateral supraclavicular nodes
• extensive disease: any disease beyond this.
Additional markers of an adverse prognosis in SCLC include a low sodium, raised LDH, weight loss and poor performance status.
Non-small cell lung cancer (NSCLC)
The Mountain classification, based on the TNM system, is used. Increasing stage is associated with decreasing 5-year survival (Table 11.2). Patients with stage I and II disease have potentially resectable disease and should be discussed with, or referred to, a cardiothoracic surgeon. Performance status, cardiopulmonary function and the presence of significant weight loss will determine whether the patient is operable.
| Stage | TNM | Description | 5-year survival (%) |
|---|---|---|---|
| Ia | T1 N0 M0 | Tumour <3 cm and surrounded by normal lung/pleura | 75 |
| Ib | T2 N0 M0 | Tumour >3 cm or involves a main bronchus (>2 cm away from the carina), the visceral pleura or associated with localized collapse of the adjacent lung | 55 |
| IIa | T1 N1 M0 | T1 tumour with peribronchial or ipsilateral hilar nodes | 50 |
| IIb | T2 N1 M0 | T2 tumour with peribronchial or ipsilateral hilar nodes | 40 |
| T3 N0 M0 | Tumour involves either the chest wall, mediastinal pleura, diaphragm, pericardium or major bronchi within 2 cm of carina or they are associated with collapse of the entire lung distal the lesion; no nodal involvement | ||
| IIIa | T3 N1 M0 | T3 tumour with peribronchial or ipsilateral hilar nodes | 10–35 |
| T1–3 N2 M0 | T1–3 tumour with ipsilateral mediastinal or subcarinal nodes | ||
| IIIb | Any T4 | Tumour involves the oesophagus, trachea/carina, great vessels or heart, or is associated with a malignant effusion or satellite nodules in the same lobe | <5 |
| N3 disease | Involves contralateral hilar or mediastinal and ipsilateral supraclavicular nodes | ||
| IV | Any M1 | Metastases, including satellite lesions in a separate lobe | <5 |
Survival and management
Lung cancer has one of the worst rates of survival of all cancers: 5-year survival is approximately 7% and many patients die within a few months of diagnosis. Prognosis depends on the type and stage of disease.
Small cell lung cancer treatment
SCLC should be treated with combination chemotherapy, incorporating a platinum-based agent. In limited disease, this is given with curative intent over four cycles. However, the dose and duration of treatment may be limited by performance status and co-morbidity. Only a small proportion of patients will achieve disease remission and, of those, late relapse with cranial metastases is common. Therefore, patients who do achieve an apparently complete response to therapy should be offered consolidative chest radiotherapy and prophylactic cranial radiotherapy to reduce the incidence of relapse.
Non-small cell lung cancer treatment
Radical radiotherapy
Patients with stage I or II disease, not suitable for surgery due to co-morbidity, should be offered radical radiotherapy. This offers a survival advantage, assuming they have sufficient lung reserve and the total tumour volume (including any lymphadenopathy) can be confined within a sufficiently small radiotherapy field.
Chemotherapy
Platinum-based chemotherapy should be offered to patients with advanced NSCLC (stage IIIb or IV) in whom it can improve symptoms, QoL and survival (usually by a number of months rather than years). Chemotherapy may also be offered to patients with stage IIIb disease in some centres, in an attempt to downstage the disease and facilitate surgical resection.
Palliative treatment
When active anti-cancer measures are not feasible, due to poor performance status or significant co-morbidity, or as an adjunct to chemotherapy, palliative (low-dose) radiotherapy may improve symptoms such as pain (e.g. from bone metastases), cough and haemoptysis. Patients with brain metastases should be treated with high-dose steroids (e.g. dexamethasone 8 mg PO 12-hourly) and offered cranial radiotherapy if they have a favourable response.
Recent lung collapse due to an obstructing central tumour can sometimes be palliated with endobronchial laser therapy and stenting. Superior vena caval obstruction (SVCO) is a medical emergency requiring urgent radiotherapy. Stenting is sometimes used beforehand to maintain patency until the radiotherapy effect is established. The effect of steroids in SVCO remains debatable.
Associated COPD, anaemia or pleural effusion should be treated. General measures for the management of breathlessness in advanced malignancy are described in ‘Palliative care’, p. 376.
BREAST CANCER
Epidemiology and aetiology
Breast cancer is the most common cancer in the UK with over 44 000 new cases per year and a life-time risk of the disease in women of 1 in 9. It predominantly affects women over the age of 50 and there is an increased incidence in those with a family history, early menarche and late menopause, nulliparity, a later age of initial child-bearing, use of the oral contraceptive pill or HRT and exposure to chest radiation. There is also an association with alcohol consumption, dietary fat intake, obesity, height and higher social class. Lower incidence is associated with multiple pregnancies, breast-feeding and regular physical exercise.
Certain defective genes are known to be strongly associated with breast cancer, e.g. BRCA (BReast CAncer) 1 and 2. In addition, there are a variety of other genetic factors involved, e.g. over-expression of the epidermal growth factors; amplification of the myc oncogene.
Presentation
Patients may present through the national screening programme or with local symptoms such as a lump or pain in the breast, discharge from the nipple or skin changes such as tethering or ulceration. Symptoms such as axillary swelling, breathlessness or bony pain are concerning and should prompt exclusion of nodal and metastatic disease (present in about 20% of patients).
Investigation, pathology and staging
Investigation
Patients should be seen in a multidisciplinary breast clinic. This allows clinical assessment by a specialist surgeon, review of relevant breast imaging (ultrasound, mammography) and early tissue sampling, by either aspiration or core biopsy. MRI may be used in some centres or in patients with breast implants, in whom ultrasound is less accurate. Routine haematological and biochemical tests should be checked in all patients. A chest X-ray, liver ultrasound or isotope bone scan should be performed if metastatic disease is suspected.
Pathology
Most breast carcinomas are adenocarcinomas; these are subdivided into in-situ carcinomas, invasive lobular cancers and the more common invasive ductal forms. Other, rarer forms of breast cancer include medullary, mucinous and inflammatory tumours, e.g. peau d’orange carcinomas and Paget’s disease of the nipple.
Tumours are graded pathologically into high, intermediate and low grade based on the level of cell differentiation. Oestrogen, progesterone and human epidermal growth factor (HER2) receptor status should also be assessed and used to identify patients for hormone therapy; see below.
Staging
The disease is staged pathologically and requires axilliary node sampling in all but non-invasive cases (stage 0). Staging allows grouping of tumours into early (stage I), locally advanced (stages II and III) and metastatic (stage IV) disease.
• stage 0: non-invasive cancer, i.e. lobular or ductal carcinoma in situ
• stage I: invasive tumours up to 2 cm without further spread
• stage II: invasive tumour 2–5 cm and/or limited axillary node involvement
• stage IIIa: invasive tumour >5 cm or axillary nodes that are clumped together or to surrounding tissue
• stage IIIb: invasive tumour of any size involving skin, chest wall or internal mammary glands, including inflammatory breast carcinoma
• stage IV: metastatic spread.
Survival and management
Combined treatment involving surgery, chemoradiotherapy and hormone treatments achieve 5-year survival rates of around 80% with an estimated 20-year survival rate of about 65%.
Surgery
All patients with invasive disease require axillary surgery and should be considered for postoperative radiotherapy. Patients under 70 years of age with early breast cancer should also be considered for adjuvant chemotherapy.
Hormone therapy
All pre-menopausal women with oestrogen receptor positive disease or unknown oestrogen sensitivity and all post-menopausal women should be considered for hormone therapy in the form of tamoxifen. In post-menopausal women this should be changed to an aromatase inhibitor after 2–3 years and such drugs should be first-line hormonal treatment in post-menopausal women with advanced disease.
Chemotherapy
Patients with advanced disease can be considered for chemotherapy, particularly taxane-based. The monoclonal antibody treatment trastuzumab (Herceptin®) may improve survival in those with advanced disease and HER2 positive status, when given in combination with chemotherapy. In pre-menopausal women with advanced disease, the combination of tamoxifen with ovarian ablation can also be used. Bisphosphonates may be helpful for those with bone pain and megestrol acetate may help control hot flushes.
COLORECTAL CANCER
Epidemiology and aetiology
Colorectal cancer is the second most common cancer in the UK, accounting for over 16 000 deaths per year and 10% of all cancer-related deaths. Risk factors include:
• age >50
• a diet rich in red meat and saturated animal fats and deficient in dietary fibre, fresh fruit and vegetables, calcium and folic acid
• colorectal adenomas or longstanding inflammatory bowel disease
• acromegaly
• previous uterosigmoidostomy or radiotherapy
• obesity and a sedentary lifestyle
• smoking and alcohol use
• genetic factors, e.g. germline mutations in DNA repair genes result in hereditary non-polyposis colon cancer (HNPCC) and inactivation of certain tumour suppressor genes, including APC, K-ras and p53, causes familial adenomatous polyposis (FAP).
Environmental risk factors probably account for 80% of sporadic cases. Genetic factors are particularly important in patients with hereditary cancer syndromes.
Presentation
This varies and is particularly dependent on the site of the primary tumour. Left-sided lesions, in the descending colon, commonly present with fresh rectal bleeding and early bowel obstruction. Right-sided tumours, particularly those in the caecum, are more likely to result in symptoms of anaemia (from occult GI blood loss), altered bowel habit and obstruction (which is a late feature). Anorectal tumours commonly cause early bleeding, mucous discharge and tenesmus (a sensation of incomplete bowel emptying). Other general features include colicky lower abdominal pain, weight loss and fatigue. A small proportion of patients present with complications of obstruction and perforation, including acute peritonitis, local abscess or fistula formation.
Clinical examination may be normal, or there may be evidence of anaemia, iron deficiency, recent weight loss or a palpable abdominal mass. Craggy hepatomegaly suggests metastatic disease. Low rectal tumours may be palpable on PR examination which should be performed in all patients in whom the diagnosis is suspected.
Screening
The NHS Bowel Cancer Screening Programme has recently been introduced. Previous randomized controlled trials have shown that faecal occult blood (FOB) testing every 1–2 years, followed by colonoscopy if necessary, can detect early-stage colorectal cancers and reduces mortality by 16%. The UK screening programme offers FOB testing to all patients aged 60–69. Patients are sent FOB testing kits and instructions for their use and are asked to post them back to a central laboratory. Those with positive results are referred for further assessment ± colonoscopy, if indicated.
Investigation, pathology and staging
Investigation
All patients should have routine haematological and biochemical tests, including Coag. Colonoscopy is the investigation of choice, as rigid sigmoidoscopy will detect less than one-third of all colorectal cancers. Colonoscopy also allows tissue sampling for histological confirmation, screening for synchronous lesions and removal of adenomatous polyps. Barium enema is an alternative in very frail patients, but it is less sensitive and non-specific.
Cross-sectional imaging is essential for staging. CT scanning is sufficient in most cases and will demonstrate intra-abdominal nodes and liver metastases if present. However, pelvic MRI or endoanal ultrasound is necessary to stage rectal cancers accurately. Serum carcinoembryonic antigen (CEA) is elevated in some patients at diagnosis, but is not sensitive enough to be used as a screening test. However, where it is high at diagnosis, it can be used to assess treatment response. It is also used to detect early recurrence during follow-up.
Pathology
Approximately 95% of tumours are adenocarcinomas and most result from malignant transformation of an adenomatous polyp; 65% occur in the rectosigmoid; 15% occur in the caecum and ascending colon. Synchronous tumours are found in 2–5% of patients. Colorectal cancers are usually polypoid or circumferential and they spread by invading outwards through the bowel wall; see ‘Staging’, below.
Staging
Disease stage at diagnosis, using Dukes’ classification, is the principal determinant of survival:
• A: tumour confined within the bowel wall
• B: tumour extending through the bowel wall, but not associated with spread to draining lymph nodes or distant metastases
• C: any tumour associated with spread to draining lymph nodes
• D: any tumour associated with distant metastasis.
Survival and management
Surgical resection is potentially curative and should be performed by a specialist colorectal surgeon. The operation required will depend on the site and size of the primary tumour. All resections involve removal of the tumour surrounded by an adequate resection margin and including all draining lymph nodes. A primary anastomosis of the bowel will be performed, if possible, but all patients should be counselled regarding the risk of being left with a stoma. Patients who present acutely with bowel obstruction or peritonitis will usually require a stoma, at least in the short term. However, a secondary anastomosis can often be performed once the acute illness has resolved. Rectal cancers are particularly prone to early recurrence, even after removal of all visible disease. This risk can be reduced and survival improved by the use of total mesorectal excision.
Patients with pathologically staged Dukes’ A disease do not require adjuvant therapy after surgery. Those with Dukes’ B disease and inadequate resection margins should be offered adjuvant radiotherapy to reduce the chance of local recurrence. Adjuvant chemotherapy with 5-FU improves survival by 4–13% in patients with Dukes’ C disease.
Fit patients with Dukes’ D disease will sometimes be offered surgery to palliate obstruction, pain or bleeding. However, palliative chemotherapy with 5-FU (and irinotecan as second-line) is the more conventional treatment offered and may provide a survival benefit. Other palliative measures include pelvic radiotherapy, endoscopic laser therapy and stenting for rectal symptoms.
OESOPHAGEAL CANCER
Epidemiology and aetiology
In the UK, oesophageal cancer accounts for about 7000 deaths every year. A number of common risks have also been identified. These include excessive alcohol consumption, smoking, obesity and a poor diet. The following factors are associated with an increased risk:
• age (most patients are >60), male sex (twice as common as females) and a family history
• tobacco smoking and heavy alcohol use, especially if taken together
• gastro-oesophageal reflux disease and its consequence, Barrett’s oesophagus (adenocarcinoma)
• obesity, although this may reflect the increased incidence of reflux disease
• dietary nitrosamines, e.g. salted and smoked meats
• previous mediastinal radiotherapy
• coeliac disease (squamous cell carcinoma)
• Plummer–Vinson syndrome (anaemia and oesophageal webbing), tylosis and Howel–Evans syndrome.
Risk reduction has been seen with aspirin or other NSAID use and consumption of fruit and green and yellow vegetables.
Presentation
Symptoms are uncommon in early disease. However, as the tumour enlarges, the patient may present with dysphagia, which may be associated with pain (odynophagia), burning retrosternal discomfort, weight loss, nausea and vomiting, regurgitation of food or haematemesis. Aspiration pneumonia can result from altered oesophageal motility and vomiting. Metastatic disease can lead to presentation with jaundice or respiratory symptoms.
Obvious clinical signs may be absent in many cases, but look for lymphadenopathy, evidence of weight loss and nutritional deficiency and carefully examine the abdomen. Compressive effects in the mediastinum may result in superior vena cava obstruction.
Investigation, pathology and staging
Investigation
Initial investigations should include routine haematological and biochemical blood tests, including LFTs and Coag, and a CXR. Upper GI endoscopy should be performed at an early stage. This allows direct visualization of the tumour and biopsy for histological confirmation and classification. A barium swallow may show an obstructing lesion in the oesophagus, but will need to be followed by endoscopy, unless the patient is extremely frail.
CT scanning of the chest, abdomen and pelvis is routinely performed for staging purposes; see ‘Staging’, below. This allows identification of metastatic disease and suspicious lymph node masses. Because CT tends to under-stage the disease, endoscopic ultrasound (EUS) is now routinely performed in many centres before treatment decisions are made. Positron emission tomography (PET) is an alternative means of identifying metabolically active lymph node (or other) masses if plain CT imaging and EUS are indeterminate.
Pathology
Most tumours are either adenocarcinomas or squamous cell carcinomas. Small cell carcinomas are uncommon and behave similarly to those originating in lung. Adenocarcinomas most commonly occur distally and are closely associated with reflux disease and Barrett’s oesophagus. Squamous cell carcinomas are more common proximally.
Staging
This is based on the TNM stage of the disease and is classified as follows:
• stage I: disease confined to the lamina propria or submucosa (T1 N0 M0)
• stage IIa: disease extends into the muscularis propria (T2 N0 M0) or adventitia (T3 N0 M0), but without nodal or metastatic spread
• stage IIb: T1 or T2 tumour with regional lymph node involvement (T1 or T2 N1 M0)
• stage III: T3 tumour with local lymph node involvement (T3 N1 M0) or any T4 tumour, indicated by local invasion into tissues around the oesophagus, but without distant metastases (T4, any N, M0)
• stage IV; distant metastases, e.g. lung or liver (any T or N plus M1).
Survival and management
Overall 5-year survival is only 6–9%. If the disease in confined to the oesophagus (stage I and IIa disease), oesophagectomy is the treatment of choice, assuming the patient is fit enough. Unfortunately, 5-year survival is disappointing even in these patients (around 30%), but can be improved by the addition of neo-adjuvant chemotherapy with cisplatin or 5-flurouracil (5-FU).
Approximately 70% of patients present with metastatic or locally advanced disease, but palliative treatments may still be worthwhile. These include oesophageal stenting, laser ablation and photodynamic therapy. Palliative radiotherapy can reduce tumour size and improve swallowing, particularly in patients with squamous cell carcinoma, which tends to be radiosensitive.
STOMACH CANCER
Epidemiology and aetiology
The incidence of stomach cancer varies greatly across the world. It is particularly common in Japan, Korea and China, where it is responsible for 11% of all male deaths. In the UK, stomach cancer accounts for about 6000 deaths every year. Risk factors include:
• age >50 and male sex
• H. pylori, which leads to chronic atrophic gastritis
• obesity, smoking and alcohol
• a diet rich in nitrosamines, e.g. salted and smoked meats, and deficient in fresh fruit and vegetables
• pernicious anaemia, adenomatous gastric polyps and previous partial gastrectomy
• genetic factors, including mutations in E-cadherin (associated with hereditary diffuse gastric cancer) and APC (associated with familial polyposis coli, stomach cancer and other malignancies).
Presentation
The majority of patients present with advanced disease. Common symptoms include weight loss (60%) and dyspepsia (50%). Anorexia and nausea occur in approximately one-third. Presentation with acute GI bleeding or anaemia is less common. Occasionally, early stomach cancers may be found on endoscopy performed for dyspepsia alone.
Clinical examination is often normal, but may reveal signs of anaemia, evidence of weight loss, an epigastric mass or palpable supraclavicular lymphadenopathy (Troisier’s sign). Metastatic disease is suggested by jaundice, hepatomegaly or ascites.
Investigation, pathology and staging
Investigation
No sufficiently accurate screening test exists and symptoms are often vague. Therefore, upper GI endoscopy is mandatory in patients with ‘alarm’ features (weight loss, anaemia, vomiting, haematemesis, malaena, dysphagia or a palpable mass). This allows multiple biopsies and brush cytology to be taken from any visible abnormalities. Endoscopic ultrasound can be used to define the extent of tumour spread through the stomach wall. CT scanning is required for staging. If the disease appears resectable this should be followed by laparoscopy to exclude peritoneal seeding.
Pathology
Some of 50% of tumours develop in the antrum, 20–30% in the body, and 20% in the cardia. Of these, 95% are adenocarcinomas and can be further classified into ‘intestinal’ and ‘diffuse’ types. The former is associated with chronic atrophic gastritis and a better prognosis. The latter is often poorly differentiated. Linitis plastica is an uncommon infiltrating, scirrhous cancer which results in a ‘leather bottle stomach’.
Staging
This is based on the extent to which the tumour has invaded through the three layers of the stomach wall (mucosa, muscle layer and serosa), the number of local lymph nodes affected and the presence of metastatic disease.
• stage Ia: tumour confined to the mucosa with no abnormal lymph nodes
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