CARCINOMA OF

ESOPHAGUS, STOMACH
&
RECTUM

SUBMITTED TO, SUBMITTED BY,

Mrs.ARUL NISHA BIJU. V
TUTOR MSc. NURSIING
COLLEGE OF NURSING COLLEGE OF NURSING
JIPMER
CARCINOMA OF ESOPHAGUS, STOMACH & RECTUM

Introduction
Gastrointestinal (GI) cancer is a term for the group of cancers that affect the digestive system. This
includes cancers of the esophagus, gallbladder, liver, pancreas, stomach, small intestine, bowel (large
intestine or colon and rectum), and anus
Just over 2,000 people are diagnosed with stomach cancer each year. This figure includes a small
number of people diagnosed with gastrointestinal stromal tumors (GIST) or neuroendocrine tumors
(NETs) – relatively rare cancers that are found mostly in the stomach but can occur elsewhere in the
digestive system. Their symptoms and progress vary widely

CARCINOMA OF ESOPHAGUS
Cancer of the esophagus is a relatively uncommon but extremely lethal malignancy

Incidence
Worldwide, esophageal cancer is the eighth most common cancer with an annual incidence of 456,000
new cases. In India, it is the fourth most common cause of cancer-related deaths. There has been a
significant increase in the incidence of esophageal cancer worldwide. Much regional variation exists in
the incidence and pathology of esophageal cancer . It has been reported that in countries with higher
human development index (HDI), there is a higher incidence of adenocarcinoma (AC) of the esophagus.
For example, in the US, the incidence of AC of the esophagus has increased by over 400% over the past
25 years. In contrast, in countries with low HDI, like India, there is a higher incidence of esophageal
squamous cell carcinoma (SCC). Currently, SCC is the most common type of esophageal cancer in the
Indian subcontinent and the most common location is the distal third of the esophagus. Approximately,
47,000 new cases are reported each year and the reported deaths reach up to 42,000 each year in India.
The National Cancer Registry Programme (NCRP) instituted by the Indian Council of Medical
Research (ICMR) periodically publishes cancer statistics from registries across India. The latest
publication is a report from 27 Population‑Based Cancer Registries in the country. This publication has
information on cancer incidence and mortality in the community covering 10% of the country’s
population. Although the coverage is still low, it gives a fair idea of the pattern of cancer incidence
emerging in various regions or parts of the country.“Age‑adjusted incidence rates” or age‑standardized
rate per 100,000 population are the two indices used to compare the incidence of cancer across
registries. The Northeast registry tops the chart in relation to carcinoma of the esophagus, for both men
and women. Cancer of the esophagus is the leading site in the registries in the states of Assam,
Meghalaya, Mizoram, and Nagaland.The Kashmir valley is yet another high incidence area in the
country. Estimates about the expected number of cancers are useful to plan and prioritize health care
services. In a developing country like India, it also aids formulating government policies and
appropriate allocation of resources.

Risk Factors
The major risk factors for Squamous Cell carcinoma esophagus include poor nutritional status, low
intake of fresh fruits and vegetables, consumption of hot beverages, excess tobacco and alcohol
consumption, and possibly human papillomavirus infection. Understanding the etiology of esophageal
cancer could inform interventions for primary prevention of this disease. Published data from different
regions in India have indicated their observations on the local risk factors. ICMR data indicate a very
high incidence of cancers in general and tobacco-related cancers in particular, in the north eastern
region. The proportion of tobacco-related cancers relative to all sites is highest in Assam and
Meghalaya. Pattern of tobacco use in Northeast India is different from the rest of the nation. The bidis
and cigarettes available locally are different from the main land. Another publication from Ludhiana,
Punjab, looked at the risk factors of esophageal SCC in women (who generally neither smoke nor
consume alcohol). Poor nourishment and consumption of hot beverages were found to be linked
The risk factors for Adenoma Carcinoma esophagus include smoking, alcohol, obesity, chronic
gastroesophageal reflux disease, and the presence of Barrett’s esophagus.
Genetic alterations have been consistently observed in esophageal SCC. These include (i) alterations in
tumor suppressor genes, specifically p53; (ii) disruption of the G1 /S cell cycle checkpoint and loss of
cell cycle control; and (iii) activation of proto-oncogenes leading to deregulation of cellular signaling
cascades. The most common gene alterations associated with esophageal SCC

Classification
Epithelial:
• Squamous Cell Carcinoma
• Adeno Carcinoma
• Mucoepidermoid Carcinoma
• Adenoid Cystic Carcinoma
• Small Cell Carcinoma
• Undifferentiated Carcinoma
Non – Epithelial:
• Leiomyosarcoma
• Malignant Melanoma
• Rhabdomyosarcoma
• Malignant Lymphoma

SOME ETIOLOGIC FACTORS BELIEVED TO BE ASSOCIATED WITH ESOPHAGEAL

CANCER
Excess alcohol consumption
Cigarette smoking
Other ingested carcinogens
Nitrates (converted to nitrites)
Smoked opiates
Fungal toxins in pickled vegetables
Mucosal damage from physical agents
Hot tea
Lye ingestion
Radiation-induced strictures
Chronic achalasia
Host susceptibility
Esophageal web with glossitis and iron deficiency (i.e., Plummer-Vinson or Paterson-Kelly
syndrome)
Congenital hyperkeratosis and pitting of the palms and soles (i.e., tylosis palmaris et plantaris)
? Dietary deficiencies molybdenum, zinc, vitamin A
? Celiac sprue Chronic gastric reflux (i.e., Barrett’s esophagus) for adenocarcinoma
Squamous cell carcinomas (SCC)
SCC arise from the squamous mucosa - native to the esophagus - 70% - upper and middle third cancer
in which the tumor cells resemble stratified squamous epithelium. 90% of esophageal cancer
• Most common type of esophageal ca in India (90%)
• Smoking and alcohol are common eitiologic factors (5 fold increase in risk)
• Combined increase risk from 25 - 100 folds
Causes
Dietary
• Nitrosamines (pickled foods , smoked food)
• long term ingestion of hot liquids
• Micronutrient deficiency (Vit. A, B12, C, E).
• Trace Element deficiency (Cobalt, Copper & Selenium).
Acquired
• Cigarette smoking. Alcohol.
• Chronic esophagitis.
• Chronic Dysphagia
• Caustic ingestion
• Radiation exposure
Premalignant conditions :
• Plummer – vinson syndrome
• Tylosis(40%)
• Achalasia (16fold)
• Esophageal strictures and diverticula

Genetic cause
Abnormalities affecting the p16/INK4 tumor suppressor gene and the epidermal growth factor receptors
are frequently present in SCC of the esophagus. Mutation in p53 in 50% of these tumors.

Pathogenesis of SCC
However, esophageal squamous cell carcinoma is also common in some regions where alcohol and
tobacco use is uncommon. Thus, nutritional deficiencies, as well as polycyclic hydrocarbons,
nitrosamines, and other mutagenic compounds, such as those found in fungus-contaminated foods,
must be considered.
Human papillomavirus (HPV) infection has also been implicated in esophageal squamous cell
carcinoma in high-risk areas but not in lowrisk regions
The molecular pathogenesis of esophageal squamous cell carcinoma remains incompletely defined, but
loss of several tumor suppressor genes, including p53 and p16/INK4a, is involved

Clinical Features
•Dysphagia
•Odynophagia
•Obstruction
•Weight loss
•Hemorrhage
•Sepsis

Morphology
• Squamous cell carcinoma begins as an in situ lesion termed squamous dysplasia.
•Epithelial dysplasia
•Carcinoma in situ
•Invasive cancer
Early overt lesions appears as: small, gray-white, plaquelike thickenings or elevation of the mucosa..
In months to years these lesions become tumorous, taking one of three forms:

1. Polypoid fungating type (60%): The most common type. Cauliflower-like friable mass protruding
into the lumen.

2. Ulcerating type (25%): A necrotic ulcer with everted edges that extend deeply and sometimes erode
into the respiratory tree (Pneumonia), aorta (exsanguination)( or elsewhere.

3. Diffuse infiltrative type (15%): appears as annular, stenosing narrowing of the lumen due to
infiltration into the wall of esophagus.
SCC arise about (locations):
20% in the cervical& upper thoracic esophagus
50% in the middle third
30% in the lower third
Most squamous cell carcinomas are moderately to well-differentiated.Intercellular bridges,
Keratinization &Epithelial pearls are commonly seen.
Epithelial nest, Epithelial pearl,
Squamous pearl
Karatin pearl,
Regardless of histology, symptomatic tumors are generally very large at diagnosis and have already
invaded the esophageal wall.
Less common histologic variants include
verrucous squamous cell carcinoma,
spindle cell carcinoma
basaloid squamous cell carcinoma

Prognosis
5-year survival rates are 75% in individuals with superficial esophageal carcinoma but much lower in
patients with more advanced tumors. Lymph node metastases, which are common, are associated with
poor prognosis.

Adenoma carcinoma
almost 70 % - United States and Western countries. Esophageal adenocarcinoma usually occurs in the
distal third of the esophagus and may invade the adjacent gastric cardia. Initially appearing as flat or
raised patches in otherwise intact mucosa, large nodular masses of 5 cm or more in diameter may
develop. Alternatively, tumors may infiltrate diffusely or ulcerate and invade deeply. Nodular, elevated
mass in the lower esophagus

Etiology :
• Increasing incidence of GERD
• Western diet
• Increased use of acid-suppression medications
Histologically it is from :
• Submucosal glands of the esophagus
• Heterotopic islands of columnar epithelium
• Malignant degeneration of metaplastic columnar epithelium (Barrett’s esophagus) – 40 fold incresed
risk

Barrets oesophagus :
• In Barrett's esophagus, normal tissue lining the esophagus the tube that carries food from the mouth
to the stomach changes to tissue that resembles the lining of the intestine.

Symptoms
Early - asymptomatic – mimic GERD
• Dysphagia.
• Weight Loss most common symptoms
• > 2/3rds of lumen has to be obstructed (lack of serosa)
• Vomiting/Regurgitation
• Pain.
• Cough , choking , asp.pneumonia (TEF)
• Hoarseness.( vocal cords)
• Dyspnoea
In high-incidence areas where screening is practice,the most prominent early symptom is pain on
swallowing rough or dry food,Systemic disease – jaundice ,excessive pain ,bone pain, respiratory
symptoms

DIAGNOSTIC AND STAGING INVESTIGATIONS

The clinical utility of a barium contrast study in the diagnosis of dysphagia is questionable. Moreover,
there is a danger of a “normal” barium swallow missing an early esophageal mucosal lesion. However,
it may be useful in a few instances such as to assess the length of the lesion (particularly in stricturing
lesions not allowing passage of a scope) and to assess extraesophageal spread (axis deviation, sinus,
fistula). The upper gastrointestinal (GI) endoscopy remains the preliminary investigation of choice in a
patient with dysphagia. What is the optimal number of biopsies that need to be taken for adequate
diagnosis? In a small study attempting to answer this question, eight biopsies were performed. The first
two specimens were diagnostic in 95.8% cases, and the yield incrementally increased to 100% with
fifth and sixth specimens.A number of Indian studies have been published regarding the cytological
diagnosis of esophageal cancer. Cytopathological correlation was found in about 80% cases, which
raises the possibility of using brush cytology for screening and rapid diagnosis with minimal patient
discomfort.
A contrast‑enhanced computed tomography (CECT) scan of the thorax and upper abdomen is
widely accepted as the preferred modality of staging for cancer of the esophagus in the Indian setting.
It is highly effective in the assessment of the T stage, invasion of surrounding structures, and distant
metastases. However, it is less useful in the assessment of nodal involvement.
Endoscopic ultrasound (EUS) helps to delineate the various layers of the esophagus and can be used
in conjunction with the CT scan. It is very useful in early lesions, in particular early mucosal lesions
that can be resected endoscopically. With regard to locoregional staging of tumor invasion and lymph
nodal involvement, it is superior to CECT scan. However, an EUS may not be technically feasible in
obstructive growths. Therefore, the routine use of EUS is debatable in the Indian setting, because of the
advanced nature of disease at presentation as well as its limited availability in many centers. EUS only
has a limited role in restaging after neoadjuvant therapy, because it cannot reliably differentiate between
fibrosis and residual or recurrent disease.
Positron emission tomography (PET) provides additional staging information, especially when
combined with a CT (PET‑CT) and is the best modality for detecting distant metastasis. In a study by
Duong et al., a PET‑CT changed the clinical management from either curative to palliative or vice versa
in 40% patients

The TNM system

T : the size of the tumour,N: The number of lymph nodes involved,M: whether the cancer has spread
to other parts the bodyEsophageal tumours first grow through the four layers of the esophagus wall, and
then into the rest of the body.
Primary tumor (T)
TX Primary tumor cannot be assessed
T0 No evidence of primary tumor
Tis High-grade dysplasia,* defined as malignant cells confined by the basement membrane
T1 Tumor invades lamina propria, muscularis mucosae, or submucosa
T1a Tumor invades lamina propria or muscularis mucosae
T1b Tumor invades submucosa
T2 Tumor invades muscularis propria
T3 Tumor invades adventitia
T4 Tumor invades adjacent structures
T4a Resectable tumor invading pleura, pericardium, azygos vein, diaphragm, or peritoneum
T4b Unresectable tumor invading other adjacent structures, such as the aorta, vertebral body, and trachea
*High-grade dysplasia includes all noninvasive neoplastic epithelial lesions formerly called carcinoma
in situ; that term is no longer used for columnar mucosae anywhere in the gastrointestinal tract.
Regional lymph nodes (N)
NX Regional lymph node(s) cannot be assessed
N0 No regional lymph node metastasis
N1 Metastasis in 1-2 regional lymph nodes
N2 Metastasis in 3-6 regional lymph nodes
N3 Metastasis in 7 or more regional lymph nodes

Distant metastasis (M)

M0 No distant metastasis
M1 Distant metastasis
 Histologic grade (G)
GX Grade cannot be assessed—stage grouping as G1
G1 Well differentiated
G2 Moderately differentiated
G3 Poorly differentiated or undifferentiated*
*If undifferentiated with glandular component, stage as G3 adenocarcinoma; if
undifferentiated with squamous cell component, or tumor remains undifferentiated after
further testing, group as G3 squamous cell carcinoma.

Squamous cell carcinoma location

X Location unknown
Upper Cervical esophagus to lower border of azygos vein
Middle Lower border of azygos vein to lower border of inferior pulmonary vein
Lower Lower border of inferior pulmonary vein to stomach, including gastroesophageal junction

Stage group pT pN pM Grade Location

Squamous cell carcinoma
0 Tis N0 M0 N/A Any
IA T1a N0 M0 G1, X Any
IB T1b N0 M0 G1–3, X Any
T1a N0 M0 G2–3 Any
T2 N0 M0 G1 Any
IIA T2 N0 M0 G2–3, X Any
T3 N0 M0 Any Lower
T3 N0 M0 G1 Upper/middle
IIB T3 N0 M0 G2–3 Upper/middle
T3 N0 M0 GX Any
T3 N0 M0 Any X
T1 N1 M0 Any Any
IIIA T1 N2 M0 Any Any
T2 N1 M0 Any Any
IIIB T4a N0–1 M0 Any Any
T3 N1 M0 Any Any
T2–3 N2 M0 Any Any
IVA T4a N2 M0 Any Any
T4b N0–2 M0 Any Any
T1–4 N3 M0 Any Any
IVB T1–4 N0–3 M1 Any Any
Adenocarcinoma
0 Tis N0 M0 N/A
IA T1a N0 M0 G1, X
IB T1a N0 M0 G2
T1b N0 M0 G1–2, X
IC T1 N0 M0 G3
T2 N0 M0 G1–2
IIA T2 N0 M0 G3, X
IIB T1 N1 M0 Any
T3 N0 M0 Any
IIIA T1 N2 M0 Any
T2 N1 M0 Any
IIIB T4a N0–1 M0 Any
T3 N1 M0 Any
T2–3 N2 M0 Any
 IVA T4a N2 M0 Any
T4b N0–2 M0 Any
T1–4 N3 M0 Any
T1–4 N0–3 M1 Any
N/A = not applicable; X = not defined

TREATMENT

The approach to cancer treatment is individualized to each patient's situation. Recommended treatments
depend on the stage and health of the patient. A team of physicians will help decide with the patient and
family what might be the best approach to their specific situation. These providers may include
specialists in medical oncology, radiation oncology, and surgery, in addition to the patient's primary
care provider.
Esophageal cancer is often found in older patients who have other underlying illnesses that complicate
treatment. Esophageal cancer is usually diagnosed late in the course of the disease because symptoms
often occur only after a tumor has grown and potentially spread. Most often, if the patient can tolerate
it, treatment consists of a combination of chemotherapy, radiation therapy, and surgery.
The National Comprehensive Cancer Network maintains up-to-date guidelines based upon ongoing
clinical trials that allow cancer specialists to offer treatment advice to patients and family

Surgery

The decision to undergo surgery and the type of surgery that might be appropriate depends upon the
type of esophageal carcinoma (squamous cell or adenocarcinoma), its staging, and the underlying health
of the patient. Some patients are high-risk for surgery and anesthesia because of pre-existing health
conditions like heart or lung disease.
Treatment guidelines are continuously being evaluated and revised, based upon the development of new
treatments and the results of ongoing clinical trials. Decisions about treatment effectiveness often
involve statistical analysis that combines many treatment studies. This meta-analysis helps adjust
treatment options and protocols as more patients are enrolled in studies, more data is obtained, and
hopefully, better survival is achieved.
Surgery may involve esophagectomy or removal of the whole esophagus Some patients are able to
have the removed esophagus replaced with another piece of bowel to connect the mouth to the
stomach. If that is not possible, percutaneous gastrostomy may be required to get food and fluid into
the stomach to be digested. A tube is placed through the skin and anchored into the stomach to allow
tube feedings.

Chemotherapy and radiation

Chemotherapy and radiation therapy (also called external beam radiation) may be administered prior to
surgery to help shrink the tumor. There are a variety of chemotherapy protocols that may be considered.
Surgery may be delayed after the diagnosis is made to allow the chemotherapy and radiation to be
administered.
Chemotherapy and radiation therapy that have been started after surgery have not been shown to
increase survival. However, there may be a benefit to survival when these therapies are continued after
surgery, if they were started before the operation.

Targeted therapy

There are disease-specific genes associated with esophageal cancer. In certain circumstances, the
tumour can be tested to see whether genes like HER2 are present. Targeted medications can attach or
bind to different protein sites on the tumour cells and inhibit tumour growth. This is immunotherapy,
specific cancer-fighting medications that try to kill only tumour cells, unlike chemotherapy, which also
kills normal cells as a side effect.
Endoscopic treatments

If there is high-grade dysplasia confined to the walls of the esophagus with no spread to the lymph
nodes or distant organs (stage I), surgical removal of the tumor may be accomplished via endoscopic
procedure. The gastroenterologist may be able to resect (remove) the damaged tissue using different
techniques.

Photodynamic therapy

Light therapy may be used to treat esophageal cancers that are small in size and have not spread or
metastasized. In this treatment, a photo-sensitizing drug is injected into the body where it is absorbed
by cells, where they can last for two to three days. However, cancer cells seem to keep a concentration
of the drug longer. When the patient is exposed to light from a laser, the drug may kill the cancer cell.

This type of treatment is limited because light cannot penetrate deeply into the body and is effective in
only small tumors. At present, photodynamic therapy is approved for esophageal cancer and non-small-
cell lung cancer.

Approach Considerations

Treatment of esophageal cancer varies according to stage—locoregional (stages I-III) versus metastatic
cancer (stage IV)—and histologic subtype—squamous cell carcinoma (SCC) versus adenocarcinoma.
National Comprehensive Cancer Network (NCCN) treatment recommendations for esophageal cancer
include the following:
 Endoscopic therapy (endoscopic mucosal resection, endoscopic submucosal dissection and/or
ablation) is preferred for high-grade dysplasia (HGD) or T1a tumors ≤2 cm; ablation alone is a
primary treatment option for patients with HGD.
 Select pT1a or pT1b tumors can be treated with endoscopic resection (ER); ablation of residual
Barrett esophagus should follow ER.
 Additional ablation may be needed after ER if multifocal HGD is present elsewhere in the
esophagus but may not be needed for tumors that are completely resected.
 Esophagectomy is indicated for patients with extensive HGD or pT1a adenocarcinoma with
nodular disease that is not adequately controlled by ER with or without ablation; a transhiatal
or transthoracic, or minimally invasive approach may be used; gastric reconstruction preferred;
for postoperative nutritional support, feeding jejunostomy is preferred to gastrostomy.
 Primary treatment options for patients with SCC T1b, N+ tumors and locally advanced
resectable tumors (T2-T4a, any regional N) include preoperative chemoradiation (for non-
cervical esophagus tumors), definitive chemoradiation (recommended for cervical esophagus
tumors) or esophagectomy (for non-cervical esophagus tumors).
 For patients with adenocarcinoma T1b, N+ tumors and locally advanced resectable tumors (T2-
T4a, any regional N) preoperative chemoradiation is preferred; definitive chemoradiation is
indicated only for non-surgical patients; esophagectomy is an option for patients with low-risk,
< 2 cm, well-differentiated lesions.
 Tumors in the submucosa (T1b) or deeper may be treated with esophagectomy.
 For patients with SCC, no postoperative treatment is indicated if no residual disease is present
at surgical margins (R0 resection).
 For patients with adenocarcinoma who have not received preoperative therapy, postoperative
fluoropyrimidine-based chemoradiation (following R0 resection) is indicated for all patients
with Tis, T3-T4 tumors, node-positive T1-T2 tumors, and selected patients with T2, N0 tumors
with high-risk features.
 Chemotherapy following R0 resection is indicated for all patients with adenocarcinoma,
irrespective of the nodal status.
 Chemoradiation may be offered to all patients with residual disease at surgical margins (R1 and
R2 resections).
 Definitive chemoradiation is preferred for all T4b (unresectable) tumors.
  Fluoropyrimidine- or taxane-based regimens are indicated for preoperative and definitive
chemoradiation.
 Two-drug cytotoxic regimens are preferred for patients with advanced disease because of lower
toxicity.
 Trastuzumab should be added to first-line chemotherapy (category 1 for combination with
cisplatin and fluoropyrimidine; category 2B for combination with other chemotherapy agents)
for patients with HER2-overexpressing advanced or metastatic adenocarcinoma (a tumor
immunohistochemistry [IHC] score of 3+ or 2+ with the evidence of HER2 amplification by
fluorescent in situ hybridization [FISH]).
 Ramucirumab, either as a single agent or in combination with paclitaxel, was approved in 2014
by the US Food and Drug Administration (FDA) for the treatment of patients with advanced
esophagogastric junction (EGJ) adenocarcinoma refractory to or progressive following first-
line therapy with platinum- or fluoropyrimidine-based chemotherapy.
Tipiracil/trifluridine:
The FDA approved tipiracil/trifluridine in February 2019 for metastatic gastric or gastroesophageal
junction (GEJ) adenocarcinoma previously treated with at least 2 prior lines of chemotherapy that
included a fluoropyrimidine, a platinum, either a taxane or irinotecan, and if appropriate, HER2/neu-
targeted therapy.

Surgical Indications and Contraindications

Surgery remains the cornerstone of treatment for esophageal cancer. Indications for surgery include the
following:
 Esophageal cancer in a patient who is a candidate for surgery
 High-grade dysplasia in a patient with Barrett esophagus that cannot be adequately treated
endoscopically
Contraindications to surgery include the following:
 Metastasis to N2 nodes (ie, cervical or supraclavicular lymph nodes) or solid organs (eg, liver,
lungs); the treatment of patients with celiac lymph node involvement remains controversial [87]
 Invasion of adjacent structures (eg, the recurrent laryngeal nerve, tracheobronchial tree, aorta,
pericardium)
In addition, the presence of severe, associated comorbid conditions (eg, cardiovascular disease,
respiratory disease) can decrease a patient's chances of surviving an esophageal resection.
Consequently, cardiac and respiratory function must be carefully evaluated preoperatively. A forced
expiratory volume in 1 second of less than 1.2 L and a left ventricular ejection fraction of less than 0.4
are relative contraindications to the operation.

Esophagectomy

Esophageal resection (esophagectomy) remains a critical component of multimodality therapy for

patients with tumors of any stage. Endoscopic mucosal resection is an experimental approach to patients
with T1a disease or high-grade dysplasia that is limited to certain centers and performed only under
protocol. Esophagectomy is no longer is used for palliation of symptoms because other treatment
modalities have become available for relieving dysphagia.
An esophagectomy can be performed by using an abdominal and a cervical incision with blunt
mediastinal dissection through the esophageal hiatus (ie, transhiatal esophagectomy [THE]) or by using
an abdominal and a right thoracic incision (ie, transthoracic esophagectomy [TTE]).
THE offers the advantage of avoiding a chest incision, which can cause prolonged discomfort and can
further aggravate the condition of patients with compromised respiratory function. After removal of the
esophagus, continuity of the gastrointestinal tract is usually reestablished using the stomach.
Some authors have questioned the validity of THE as a cancer operation because part of the operation
is not performed under direct vision and fewer lymph nodes are removed than with TTE. However,
many retrospective studies and 2 prospective ones have shown no difference in survival between the
operations, suggesting that the factor influencing survival is not the type of operation but, rather, the
stage of the cancer at the time the operation is performed.
Morbidity and mortality

Complications from esophagectomy occur in approximately 40% of patients. The morbidity associated
with the surgery consists mostly of respiratory, cardiac, and septic complications, including the
following:
 Respiratory complications (15-20%) - Include atelectasis, pleural effusion, and pneumonia
 Cardiac complications (15-20%) - Include cardiac arrhythmias and myocardial infarction
 Septic complications (10%) - Include wound infection, anastomotic leak (breakdown of the
new connection between the stomach and esophagus), and pneumonia
Anastomotic leaks and stricture may require dilatation (20%). Leaks may be treated with endoscopic
placement of self-expanding, removable plastic stents.
Leak rates vary depending on whether the anastomosis is in the chest (3%-12%) or the neck (10%-
25%). The choice of location for the anastomosis is based mostly on the location of the tumor and the
surgeon’s assessment of the risks and benefits of a thoracic anastomosis. Such anastomoses have a
lower leak rate, but an intrathoracic leak following esophagectomy can lead to sepsis and death.
A retrospective review of 1223 esophagectomies for cancer found that surgical management of
intrathoracic leaks did not increase the patient mortality rate or effect long-term survival.

As with other complex operations (eg, cardiac operations, resection of the pancreas or liver), the lowest
mortality rate with esophagectomy is achieved when the procedure is performed in high-volume centers
by high-volume surgeons. In California from 1990-1994, for instance, 5 high-volume centers had a
mortality rate of 5% or less for esophageal resection for cancer, while the state’s average mortality rate
for this surgery was approximately 18%.
The better results in high-volume centers are due to a team approach. In these facilities, expert surgeons
work with intensivists, cardiologists, pulmonologists, radiologists, and nurses who have experience and
expertise.

Transthoracic esophagectomy

There are two types of TTE, as follows:

 Ivor Lewis esophagectomy (right thoracotomy and laparotomy)
 McKeown esophagectomy (right thoracotomy followed by laparotomy and cervical
anastomosis)
For TTE, the patient is placed supine on the operating room table. An arterial line, a central venous
catheter, a Foley catheter, and a dual-lumen endotracheal tube are placed. Preoperative antibiotics are
administered. An upper midline incision is made.
After exploring the peritoneal cavity for metastatic disease (if metastases are found, the operation is not
continued), the stomach is mobilized. The right gastric and the right gastroepiploic arteries are
preserved, while the short gastric vessels and the left gastric artery are divided.
Next, the gastroesophageal junction is mobilized, and the esophageal hiatus is enlarged. A
pyloromyotomy is performed, and a feeding jejunostomy is placed for postoperative nutritional support.
After closure of the abdominal incision, the patient is repositioned in the left lateral decubitus position
and a right posterolateral thoracotomy is performed in the fifth intercostal space.
The azygos vein is divided to allow full mobilization of the esophagus. The stomach is delivered into
the chest through the hiatus and is then divided approximately 5 cm below the gastroesophageal
junction.
An anastomosis (hand-sewn or stapled) is performed between the esophagus and the stomach at the
apex of the right chest cavity. Then, the chest incision is closed.
McKeown esophagectomy, with an anastomosis in the cervical region, is similar in conduct, but with
the advantage of being applicable for tumors in the upper, middle, and lower thoracic esophagus.
Transhiatal esophagectomy
For THE, the preoperative details are similar to those of TTE, except that a single-lumen, rather than a
double-lumen, endotracheal tube is used. The neck is prepared in the operative field.
The abdominal part of the operation is identical to the TTE; however, dissection of the esophagus is
performed through the enlarged esophageal hiatus without opening the right chest. The esophagus is
mobilized in this fashion all the way to the thoracic inlet.
Then, a 6-cm incision is made in the left side of the neck. The internal jugular vein and carotid artery
are retracted laterally, and the esophagus is identified and isolated posterior to the airway. To prevent
injury to the left recurrent laryngeal nerve, no mechanical retractors are used to retract the trachea.
Next, after resection of the proximal stomach and thoracic esophagus, the remaining stomach is pulled
up through the posterior mediastinum until it reaches the remaining esophagus at the cervical level.
Then, a hand-sewn anastomosis is performed, and a small drain is placed in the neck alongside the
anastomosis. The abdominal and neck incisions are closed. (See the image below.)

Transhiatal esophagectomy in which (a) is the abdominal incision, (b) is the cervical incision, and (c)
is the stomach stretching from abdomen to the neck.

Minimally invasive esophagectomy

The use of laparoscopic and thoracoscopic techniques has revolutionized the treatment of benign
esophageal disorders such as achalasia and gastroesophageal reflux disease (GERD). Advantages of
minimally invasive surgery include a shorter hospital stay, less postoperative discomfort, and much
faster recovery time than with open surgery. Minimally invasive esophagectomy (MIE) is finding a
place in the treatment of esophageal cancer.
In a study of MIE (mainly using thoracoscopic mobilization) in 222 patients, the mortality rate was only
1.4% and hospital stay was only 7 days, which is less than with most open procedures; only 16 patients
(7.2%) required conversion to an open procedure. A report by Luketich et al involving 56 patients also
showed that MIE was comparable to open esophagectomy but the use of neoadjuvant treatment slightly
increased the surgical mortality from 1.5% to 1.8%.
In a randomized French study that compared transthoracic open esophagectomy (n=104) with MIE
(hybrid procedure; n=103), .Mariette et al reported that the incidence of intraoperative and postoperative
major complications, specifically pulmonary complications, was 69% lower with the hybrid procedure,
while 3- and 5-year overall survival and disease-free survival were noninferior. For the hybrid
procedure, the abdominal portion of the operation was performed through five small incisions, rather
than the long abdominal incision used in TTE.
Video-assisted thoracoscopy (VATS) is being used in many centers for the thoracic mobilization of the
esophagus, reducing the size of the chest incision. In addition, laparoscopy can be used to mobilize the
gastric conduit in the abdomen, reducing abdominal incision size as well.
Chemoradiotherapy

The main way chemo is given for esophageal cancer is called systemic chemotherapy. Thedrugs are
injected into your vein or you take them by mouth. These drugs enter your bloodstream and reach most
areas of your body.
Doctors give chemo in cycles, with each period of treatment followed by a period of rest to give the
body time to recover. Chemotherapy cycles generally last about 2 to 4 weeks, and people usually get at
least several cycles of treatment.
Chemo may be used at different times during treatment for esophageal cancer.

Adjuvant chemo: Chemo can be given after surgery. The goal is to kill any cancer cells that may have
been left behind during surgery because they were too small to see, as well as cancer cells that might
have escaped from the main tumor and settled in other parts of the body (but are too small to see on
imaging tests).
Neoadjuvant chemo: For some cancers, chemo is given (often with radiation) before surgery to try to
shrink the cancer and make surgery easier.
Chemo for advanced cancers: For cancers that have spread to other organs, such as the liver, chemo
can also be used to help shrink tumors and relieve symptoms. Although it is not likely to cure the cancer,
it often helps people live longer.
Chemo by itself rarely cures esophageal cancer. It is often given together with radiation therapy (called
chemoradiation or chemoradiotherapy). Chemoradiation is often used before surgery. This can lower
the chance of the cancer coming back and help people live longer than using surgery alone.
Chemoradiation is also sometimes given after surgery, but it isn’t clear that it is as helpful as giving it
before surgery. Drugs used to treat esophageal cancer
Some common drugs and drug combinations used to treat esophageal cancer include:
 Carboplatin and paclitaxel (Taxol) (which may be combined with radiation)
 Cisplatin and 5-fluorouracil (5-FU) (often combined with radiation)
 ECF: epirubicin (Ellence), cisplatin, and 5-FU (especially for gastroesophageal junction
tumors)
 DCF: docetaxel (Taxotere), cisplatin, and 5-FU
 Cisplatin with capecitabine (Xeloda)
 Oxaliplatin and either 5-FU or capecitabine
 Irinotecan (Captosar)
 Trifluridine and tipiracil (Lonsurf), a combination drug in pill form
For some esophagus cancers, chemo may be used along with the targeted drug trastuzumab (Herceptin)
or ramucirumab (Cyramza). For more information on these drugs, see Targeted Therapy for Esophageal
Cancer.
Possible side effects of chemotherapy
Chemo drugs attack cells that are dividing quickly, which is why they work against cancer cells. But
other cells, such as those in the bone marrow (where new blood cells are made), the lining of the mouth
and intestines, and the hair follicles, also divide quickly. These cells are also likely to be affected by
chemo, which can lead to side effects. Side effects depend on the specific drugs used, their dose, and
the length of treatment. Common side effects of chemo include:
 Nausea and vomiting
 Loss of appetite
 Hair loss
 Mouth sores
 Diarrhea or constipation
 Low blood counts
 Increased chance of infection (from having too few white blood cells)
 Easy bleeding or bruising (from having too few blood platelets)
 Fatigue (from having too few red blood cells)
Along with these, some side effects are specific to certain drugs. For example:
 Hand-foot syndrome. During treatment with capecitabine or 5-FU (when given as an
infusion), this can start out as redness in the hands and feet, and then progress to pain and
 sensitivity in the palms and soles. If it worsens, blistering or skin peeling can occur, sometimes
leading to painful sores. It’s important to tell your doctor right away about any early symptoms,
such as redness or sensitivity, so that steps can be taken to keep things from getting worse.
 Neuropathy (nerve damage). This is a common side effect of oxaliplatin, cisplatin, docetaxel,
and paclitaxel. Symptoms include numbness, tingling, and even pain in the hands and feet.
Oxaliplatin can also cause intense sensitivity to cold in the throat and esophagus (the tube
connecting the throat to the stomach) and the palms of the hands. This can cause problems
swallowing liquids or holding a cold glass. If you will be getting oxaliplatin, talk with your
doctor about side effects beforehand, and let him or her know right away if you develop
numbness and tingling or other side effects.
 Allergic or sensitivity reactions. Some people can have reactions while getting the drug
oxaliplatin. Symptoms can include skin rash, chest tightness and trouble breathing, back pain,
or feeling dizzy, lightheaded, or weak. Be sure to tell your nurse right away if you notice any
of these symptoms while you are getting chemo.
 Diarrhea. This is a common side effect with many of these drugs, but can be particularly bad
with irinotecan. It needs to be treated right away — at the first loose stool — to prevent severe
dehydration. This often means taking drugs like loperamide (Imodium). If you are on a chemo
drug that is likely to cause diarrhea, your doctor will give you instructions on what drugs to
take and how often to take them to control this symptom

Nursing Management

Intervention is directed toward improving the patient’s nutritional and physical condition in preparation
for surgery, radiation therapy, or chemotherapy. A program to promote weight gain based on a high-
calorie and high-protein diet, in liquid or soft form, is provided if adequate food can be taken by mouth.
If this is not possible, parenteral or enteral nutrition is initiated. Nutritional status is monitored
throughout treatment. The patient is informed about the nature of the postoperative equipment that will
be used, including that required for closed chest drainage, nasogastric suction, parenteral fluid therapy,
and gastric intubation. Immediate postoperative care is similar to that provided for patients undergoing
thoracic surgery. After recovering from the effects of anesthesia, the patient is placed in a low Fowler’s
position, and later in a Fowler’s position, to assist in preventing reflux of gastric secretions. The patient
is observed carefully for regurgitation and dyspnea. A common postoperative complicationis aspiration
pneumonia. The patient’s temperature is monitored to detect any elevation that may indicate aspiration
or seepage of fluid through the operative site into the mediastinum. If jejunal grafting has been
performed, the nurse checks for graft viability hourly for at least the first 12 hours. To make the graft
visible, the surgeon usually brings a portion of the jejunum to the exterior neck by way of a small
incision. Moist gauze covers the external portion of the graft. The gauze is removed briefly to assess
the graft for color and to assess for the presence of a pulse by means of Doppler ultrasonography.
If an endoprosthesis has been placed or an anastomosis has been performed, a functioning
continuum will exist between the throat and the stomach. Immediately after surgery, the nasogastric
tube should be marked for position, and the physician is notified if displacement occurs. The nurse does
not attempt to reinsert a displaced nasogastric tube, because damage to the anastomosis may occur. The
nasogastric tube is removed 5 to 7 days after surgery, and a barium swallow is performed to assess for
any anastomotic leak before the patient is allowed to eat. Once feeding begins, the nurse encourages
the patient to swallow small sips of water and, later, small amounts of pureed food. When the patient is
able to increase food intake to an adequate amount, parenteral fluids are discontinued. If an
endoprosthesis is used, it may easily become obstructed if food is not chewed sufficiently. After each
meal, the patient remains upright for at least 2 hours to allow the food to move through the
gastrointestinal tract. It is a challenge to encourage the patient to eat, because appetite is usually poor.
Family involvement and home-cooked favorite foods may help the patient to eat. Antacids may help
those with gastric distress. If radiation is part of the therapy, the patient’s appetite is further depressed
and esophagitis may occur, causing pain when food is eaten. Liquid supplements may be more easily
tolerated. Often, in either the preoperative or the postoperative period, an obstructed or nearly obstructed
esophagus causes difficulty with excess saliva, so that drooling becomes a problem. Oral suction may
be used if the patient is unable to handle oral secretions, or a wicktype gauze may be placed at the corner
of the mouth to direct secretions to a dressing or emesis basin. The possibility that the patient may
aspirate saliva into the tracheobronchial tree and develop pneumonia is of great concern. When the
patient is ready to go home, the family is instructed about how to promote nutrition, what observations
to make, what measures to take if complications occur, how to keep the patient comfortable, and how
to obtain needed physical and emotional support.

NURSING PROCESS:

Assessment

Emergency conditions of the esophagus (perforation, chemical burns) usually occur in the home or
away from medical help and require emergency medical care. The patient is treated for shock and
respiratory distress and transported as quickly as possible to a medical facility. Foreign bodies in the
esophagus do not pose an immediate threat to life unless pressure is exerted on the trachea, resulting in
dyspnea or interfering with respiration, or unless there is leakage of caustic alkali from a battery.
Educating the public to prevent inadvertent swallowing of foreign bodies or corrosive agents is a major
health issue. For nonemergency symptoms, a complete health history may reveal the nature of the
esophageal disorder. The nurse asks about the patient’s appetite. Has it remained the same, increased,
or decreased? Is there any discomfort with swallowing? If so, does it occur only with certain foods? Is
it associated with pain? Does a change in position affect the discomfort? The patient is asked to describe
the pain. Does anything aggravate it? Are there any other symptoms that occur regularly, such as
regurgitation, nocturnal regurgitation, eructation (belching), heartburn, substernal pressure, a sensation
that food is sticking in the throat, a feeling of becoming full after eating a small amount of food, nausea,
vomiting, or weight loss? Are the symptoms aggravated by emotional upset? If the patient reports any
of these symptoms, the nurse asks about the time of their occurrence, their relationship to eating, and
factors that relieve or aggravate them (eg, position change, belching, antacids, vomiting). This history
also includes questions about past or present causative factors, such as infections and chemical,
mechanical, or physical irritants; the degree to which alcohol and tobacco are used; and the amount of
daily food intake. The nurse determines whether the patient appears emaciated and auscultates the
patient’s chest to determine whether pulmonary complications exist.

Nursing Diagnosis

Based on the assessment data, the nursing diagnoses may include the following:

• Imbalanced nutrition, less than body requirements, related to difficulty swallowing

• Risk for aspiration related to difficulty swallowing or to tube feeding
• Acute pain related to difficulty swallowing, ingestion of an abrasive agent, tumor, or frequent episodes
of gastric reflux
• Deficient knowledge about the esophageal disorder, diagnostic studies, medical management, surgical
intervention, and rehabilitation

Planning and Goals The major goals for the patient may include attainment of adequate nutritional
intake, avoidance of respiratory compromise from aspiration, relief of pain, and increased knowledge
level.

Nursing Interventions

ENCOURAGING ADEQUATE NUTRITIONAL INTAKE

The patient is encouraged to eat slowly and to chew all food thoroughly so that it can pass easily into
the stomach. Small, frequent feedings of nonirritating foods are recommended to promote digestion and
to prevent tissue irritation. Sometimes liquid swallowed with food helps the food pass through the
esophagus. Food should be prepared in an appealing manner to help stimulate the appetite. Irritants such
as tobacco and alcohol should be avoided. A baseline weight is obtained, and daily weights are recorded.
The patient’s intake of nutrients is assessed.

DECREASING RISK OF ASPIRATION

The patient who has difficulty swallowing or difficulty handling secretions should be kept in at least a
semi-Fowler’s position to decrease the risk of aspiration. The patient can be instructed in the use of oral
suction to decrease the risk of aspiration further.

RELIEVING PAIN
Small, frequent feedings are recommended, because large quantities of food overload the stomach and
promote gastric reflux. The patient is advised to avoid any activities that increase pain, and to remain
upright for 1 to 4 hours after each meal to prevent reflux. The head of the bed should be placed on 4- to
8-inch (10- to 20cm) blocks. Eating before bedtime is discouraged. The patient is advised that excessive
use of over-the-counter antacids can cause rebound acidity. Antacid use should be directed by the
primary care provider, who can recommend the daily, safe dose needed to neutralize gastric juices and
prevent esophagea lirritation. Histamine2 antagonists are administered as prescribed to decrease gastric
acid irritation.

PROVIDING PATIENT EDUCATION

The patient is prepared physically and psychologically for diagnostic tests, treatments, and possible
surgical intervention. The principal nursing interventions include reassuring the patient and discussing
the procedures and their purposes. Some disorders of the esophagus evolve over time, whereas others
are the result of trauma (eg, chemical burns, perforation). In instances of trauma, the emotional and
physical preparation for treatment is more difficult because of the short time available and the
circumstances of the injury. Treatment interventions must be evaluated continually; the patient is given
sufficient information to participate in care and diagnostic tests. If endoscopic diagnostic methods are
used, the patient is instructed regarding the moderate sedation that will be used during the procedure. If
procedures are being performed on an outpatient basis with the use of moderate sedation, the patient is
instructed to have someone available to drive him or her home after the procedure. If surgery is required,
immediate and long-term evaluation is similar to that for a patient undergoing thoracic surgery.

PROMOTING HOME AND COMMUNITY-BASED CARE

Teaching Patients Self-Care

The self-care required of the patient depends on the nature of the disorder and on the surgery or
treatment measures used (eg, diet, positioning, medications). If an ongoing condition exists, the nurse
helps the patient plan for needed physical and psychological adjustments and for follow-up care. Special
equipment, such as suction or enteral or parenteral feeding devices, may be required. The patient may
need assistance in planning meals, using medications as prescribed, and resuming activities. Education
about nutritional requirements and how to measure the adequacy of nutrition is important. Elderly and
debilitated patients in particular often need assistance and education in ways to adjust to their limitations
and to resume activities that are important to them.

Continuing Care

Patients with chronic esophageal conditions require an individualized approach to their management at
home. Foods may need to be prepared in a special way (blenderized foods, soft foods), and the patient
may need to eat more frequently (eg, four to six small servings per day). The medication schedule is
adjusted to the patient’s daily activities as much as possible. Analgesic medications and antacids can
usually be taken as needed every 3 to 4 hours.

Evaluation

EXPECTED PATIENT OUTCOMES

Expected patient outcomes may include:

1. Achieves an adequate nutritional intake

a. Eats small, frequent meals
b. Drinks water with small servings of food
c. Avoids irritants (alcohol, tobacco, very hot beverages)
d. Maintains desired weight
2. Does not aspirate or develop pneumonia
a. Maintains upright position during feeding
b. Uses oral suction equipment effectively
3. Is free of pain or able to control pain within a tolerable level
a. Avoids large meals and irritating foods
b. Takes medications as prescribed and with adequate fluids (at least 4 ounces), and remains
upright for at least 10 minutes after taking medications
c. Maintains an upright position after meals for 1 to 4 hours
d. Reports that there is less eructation and chest pain
4. Increases knowledge level of esophageal condition, treatment, and prognosis
a. States cause of condition
b. Discusses rationale for medical or surgical management and diet or medication regimen
c. Describes treatment program d. Practices preventive measures so injuries are avoided

GASTRIC CANCER(CARCINOMA OF STOMACH)

Introduction

The geographic incidence of gastric cancer has changed dramatically over the last few decades. Prior
to 1950, it was the most common cause of cancer death in men, and the third leading cause of cancer
death in women in the U.S. Mortality from gastric cancer in the United States has declined, perhaps due
to dietary changes. This cancer is twice as common in men than women, twice as common in blacks
than whites, and more common with advancing age. Gastric cancer is also seen in higher rates in Latin
America, Northern Europe and the Far East. It remains the second leading cause of cancer death
worldwide.
Gastric cancer peaks in the seventh decade of life. Often, a delay in diagnosis may account for the poor
prognosis. Fortunately, dedicated research into its pathogenesis and identification of new risk factors,
treatment, and advanced endoscopic techniques have led to earlier detection of gastric cancer.
Recognition that Helicobacter pylori infection causes most gastric ulcers has revolutionized the
approach to gastric cancer today. Gastric tumors include adenocarcinoma, non-Hodgkin’s lymphoma,
and carcinoid tumors.

What is Gastric Cancer?

Gastric cancer consists of two pathological variants, intestinal and diffuse. The intestinal-type is the
end-result of an inflammatory process that progresses from chronic gastritis to atrophic gastritis and
finally to intestinal metaplasia and dysplasia. This type is more common among elderly men, unlike the
diffuse type, which is more prevalent among women and in individuals under the age of 50. The diffuse-
type, characterized by the development of linitis plastica, is associated with an unfavorable prognosis
because the diagnosis is often delayed until the disease is quite advanced. Gastric H. pylori infection is
highly associated with this type as with the intestinal-type.

Adenocarcinoma

Adenocarcinomas arising from gastric epithelium are the most common malignancies of the stomach
(90% of cases). Malignancies arising from connective tissue (sarcoma) and from lymphatics
(lymphoma) are less common. Adenocarcinomas (Figures 2 and 3) are most often found in the gastric
cardia (31%), followed by the antrum (26%), and body of the stomach (14%).

Adenocarcinomas are classified according to histology and location. Histologically, these malignancies
may be divided into well-differentiated and poorly differentiated types, depending on the degree of
gland formation and ability to secrete mucus. Most tumors are heterogeneous in histological
appearance; therefore, classification is made by noting the predominant structures. Thus, well-
differentiated tubular and poorly differentiated signet-ring cell carcinoma make up the majority of
tumors. Less common types are mucinous, papillary and undifferentiated carcinoma.

Early Gastric Cancer

Early gastric cancers, where tumor cells are confined to the mucosa (the most superficial layer of the
stomach), have been identified in Japan where there is active screening of patients at high-risk for gastric
cancer. In these patients, early gastric cancer may appear as a subtle lesion, usually less than 2 cm in
diameter. The identification of early gastric cancer is important because it is potentially amenable to
endoscopic therapy and accompanied by an excellent prognosis

Hereditary (Familial) Gastric Cancer

The term, familial gastric cancer, has been used to describe families in which several members under
the age of 40 have had the diffuse type of gastric cancer. The criteria for diagnosis, as established by
the International Gastric Cancer Linkage Consortium (IGCLC), are: two or more cases of diffuse gastric
cancer in first- or second-degree relatives, with at least one diagnosed before the age of 50 years; OR
three or more pathologically documented cases of diffuse gastric cancer in firstor second-degree
relatives of any age. One third of these families have been found to have a germline mutation of the
CDH1 gene. Affected family members are also at increased risk for breast and colon cancer

Lymphoma

Primary gastrointestinal lymphoma may be of B- or T-cell type, with primary Hodgkin’s disease being
extremely uncommon. Most low-grade B-cell gastrointestinal lymphomas are of mucosal associated
lymphoid tissue (MALT) and arise primarily in the stomach. These lymphomas usually have a favorable
clinical course, but may undergo high-grade transformation.

Symptoms

Most patients are asymptomatic in early stages of gastric cancer and have advanced disease by the time
of presentation. In a review of over 18,000 patients, the most common presenting symptoms included
weight loss and abdominal pain. Epigastric fullness, nausea, loss of appetite, dyspepsia, and mild gastric
discomfort may also occur. Dysphagia may be a prominent symptom for patients with tumors in the
cardia or gastroesophageal junction. In patients with pyloric tumors and tumors located in the antrum,
vomiting and gastric outlet obstruction may occur. Unusual presentations may include acute
appendicitis, musculoskeletal pain, and the sudden appearance of seborrheic keratosis and freckles,
accompanied by pruritis and dermatomyositis. Gastrointestinal bleeding is uncommon, and only seen
in about 20% of cases.
Abdominal pain occurs in most patients with gastric lymphoma; however, symptoms may vary from
those suggesting peptic ulcer disease to advanced gastric cancer. Patients may complain of weight loss,
nausea and vomiting. They may also present with overt gastrointestinal bleeding. Gastric lymphoma is
more often found in younger females when compared to the incidence of gastric cancer

Causes

Environmental Risk Factors

The continued identification of risk factors for gastric cancer may one day lead to the global
development of early detection programs that will change the clinical history of this disease.
Environmental factors appear to be related to the intestinal type of gastric cancer. Socioeconomic status
is inversely correlated with the incidence of this disease. Factors associated with low socioeconomic
status, such as poor sanitation, poor nutrition, and inadequate handling and preservation of food and
water, are involved. Diets high in fresh fruit, leafy vegetables, ascorbic acid, and beta-carotene are
associated with reduced risk. The literature also reports that decreased use of nitrites in prepared foods
has also resulted in a decreased incidence. Though cigarette smoking may increase pre-malignant
lesions and gastric dysplasia, a clear relationship has not been demonstrated. Similarly, the relationship
between alcohol consumption and gastric cancer is inconclusive
Adenocarcinoma of the stomach arises in the setting of atrophic gastritis, a condition in which there is
loss of stomach glands and infiltration of mononuclear cells into the lamina propria. As the disease
process advances and inflammatory processes destroy stomach glands, the ability of the stomach to
secrete acid diminishes. In the most severe cases, histology of the gastric mucosa reveals the patchy
presence of goblet cells and villous formation, features that characterize a pre-cancerous lesion known
as intestinal metaplasia. It is important that a highly trained pathologist review the gastric histology,
because not all forms of intestinal metaplasia are believed to be pre-cancerous. Intestinal metaplasia
that demonstrates marked cell differentiation and production of a sulfated acid mucin is associated with
gastric cancer. The identification of this lesion suggests that an endoscopic surveillance program be
considered, though exact guidelines do not currently exist in the United States. Atrophic gastritis may
arise in response to: 1) chronic infection with Helicobacter pylori, 2) antibodies to the acid-secreting
parietal cells, as seen in pernicious anemia, and 3) surgical resection of the antrum, the portion of the
stomach that releases the parietal cell-stimulating hormone gastrin. Gastric carcinoma may develop in
as many as 9% of patients with atrophic gastritis.

Helicobacter pylori
The most important risk factor identified in the development of gastric cancer is infection of the stomach
with the bacterial organism Helicobacter pylori. Studies with the Mongolian gerbil show that when
infected with H. pylori, the gerbil develops gastritis that progresses to gastric cancer. Epidemiological
studies further support the link between H. pylori and cancer of the distal stomach (i.e., antrum). The
risk of developing gastric cancer is about 1 in 97 in infected individuals, compared to 1 in 750 in
uninfected individuals, over a 30-year period. Thus, the risk of developing gastric cancer in H. pylori-
infected individuals is about 8 times higher than in uninfected individuals. Despite this, the 1996 NIH
consensus panel on H. pylori recommended that treatment not be initiated in asymptomatic infected
individuals

Treatment of asymptomatic individuals remains a controversial issue, particularly because it takes

more than 30 years before one-third of these individuals develop atrophic gastritis. The matter of
treatment is even more confusing, because recent data suggest the eradication of H. pylori predisposes
individuals to cancer of the proximal stomach (cardia) and esophagus. The overall incidence of gastric
cancer is diminishing in western countries, but the incidence of proximal gastric cancers compared to
distal is rising, and coincides with the widespread treatment of H. pylori. Some have proposed that H.
pylori exerts a protective effect in the proximal stomach and esophagus by inducing achlorhydria and
atrophic gastritis. Eradication of H. pylori restores gastric acid production and, in individuals
predisposed to gastroesophageal reflux, could possibly contribute to cancers of the distal esophagus
and cardia. Additional data is needed before treatment recommendations can be made in
asymptomatic individuals. H. pylori leads to atrophic gastritis through direct and indirect mechanisms
(Figure 10). The organism itself induces a host-inflammatory response within the gastric mucosa. This
in turn leads to the production of reactive oxygen species, which can induce DNA damage and
alterations to the genetic controls of normal cell proliferation. The host-immune response leads to the
T-cell release of cytokines, such as interferon-gamma and interleukin-8, which recruit more
inflammatory cells.
H. pylori also appears to play a role in the pathogenesis of gastric MALT lymphomas, which arise as a
reaction to infection of the stomach. Eradication of this organism has demonstrated complete or partial
regression of low-grade lymphoma lesions.

Gastric Polyps
Gastric polyps may evolve into gastric cancer. Conversely, gastric cancer may present as a polypoid
lesion. Commonly found polyps include hyperplastic, adenomas and early adenocarcinoma.
Hyperplastic polyps are the most common and comprise about 80% of all gastric polyps. Their
malignant potential significantly increases when their size is greater than 0.5 cm in diameter.
Adenomatous polyps have a significant risk of cancer as well, and require endoscopic follow-up after
removal.

Hereditary (Familial) Gastric Cancer

The study of familial gastric kindreds has led to the identification of a germline mutation of the CDH1
gene in one third. CDH1 encodes E-cadherin, a cell adhesion molecule that participates in normal cell
differentiation and tissue architecture. Mutation of CDH1 diminish the availability of normal E-
cadherin protein, thus perturbing normal cell differentiation and cell adhesiveness. Mutations of CDH1
in gastric cancer families may occur anywhere throughout the gene, in contrast to CDH1 mutations
occuring almost exclusively in exons 7-9 in individuals with sporadic gastric cancer. A germline
mutation of CDH1 has a 70% penetrance, increasing the susceptibility to gastric cancer. CDH1 is a
tumor suppressor gene, since mutation of the second CDH1 allele, perhaps as the result of
environmental influences such as H. pylori infection or diet, is required for full penetrance. Affected
female family members are at higher risk for breast cancer as well and should be screened accordingly.
How affected family members should be screened for gastric cancer remains a dilemma. Since familial
gastric cancer is the diffuse type, superficial endoscopic mucosal biopsies lack sufficient sensitivity to
identify dysplasia or early gastric cancer. Further studies are needed to determine the role of endoscopic
ultrasound and PET scanning surveillance of family members. Occult gastric cancer has been found in
the surgical specimens of asymptomatic family members with negative endoscopic screening who
elected to undergo prophylactic total gastrectomy. Whether all affected family members should
consider prophylactic gastrectomy remains unclear, but with a 70% chance of developing gastric cancer
and limited surveillance methods, many individuals may opt for this radical procedure.

Molecular Biology

The development of gastric cancer is thought to occur through a multi-step process, in which the earliest
lesion is atrophic gastritis, followed by the development of dysplasia, adenoma, and then
adenocarcinoma. Progression from the preceding lesion to the next developmental stage is accompanied
by molecular genetic events.
Abnormalities in protein-encoding genes that regulate normal cell growth have been detected in gastric
cancers. Alterations to growth factor receptors like c-met and K-sam are often over-expressed in gastric
cancers of the scirrhous type. Proteins such as cyclin E that regulate the cell cycle, critical for the control
of normal cell proliferation, are also over-expressed. Mutation to p53, a tumor suppressor gene, is found
in 64% of gastric cancers. The detection of replication errors in microstellate loci is an indication that
genetic instability is involved.
As stated elsewhere, only one third of families with hereditary gastric cancer possess germline
mutations in the CDH1, indicating that other gene abnormalities contribute to the development of
gastric cancer. CDH1 mutations are also found in indiviuals with sporadic gastric cancer, in addition to
other genetic aberrations. Some of these genetic perturbances are found exclusively in one gastric
variant or the other
Gastric Cancer: Diagnosis

Physical Examination

Physical examination may provide clues to diagnose gastric cancer. The presence of anemia, occult
blood in the stool, and weight loss may suggest a malignancy. A midepigastric palpable mass or nodular
liver may be helpful in localizing the process to the abdomen.
The patient may appear completely healthy on physical exam. Additional findings may include:
abdominal mass, liver metastases, gastric distention, weight loss, supraclavicular adenopathy
(Virchow’s node), rectal mass (Blumer’s shelf), enlarged ovary (Krukenberg’s syndrome), or umbilical
metastases (Sister Mary Joseph’s node). Migratory phlebitis (Trousseau’s syndrome), seborrheic
keratosis and freckles (Leser-Trélat sign), muscle weakness, splenomegaly, ascites, obstructive
jaundice, and peritoneal carcinomatosis may be noted in more advanced disease.
Immunohistochemical techniques are used to differentiate low-grade lymphomas of MALT from
benign reactive lymphoid hyperplasia. Lymphomas show monoclonality of the lymphoid proliferation.
Clinicians should be aware of the possibility that non-Hodgkin’s lymphoma of the stomach may be
linked to acquired immunodeficiency syndrome (AIDS).

Genetic Screening
Genetic screening has been advocated in family members of young patients with the diffuse-type of
gastric cancer. There are no mutational hotspots, so screening for CDH1 mutations requires a survey of
the entire gene. Prophylactic gastrectomy has been performed on carriers of truncating germ-line CDH1
mutations. Remarkably, even asymptomatic individuals who had normal upper endoscopies have
demonstrated malignant cells in their surgical resection specimens, suggesting that this could be a viable
therapeutic option for highly selected individuals. Genetic counseling is necessary for all family
members considering genetic testing and prophylactic gastrectomy. Women in these families who have
a germline mutation of CDH1 are at an increased risk for developing lobular breast cancer and should
be screened accordingly.

Radiological Diagnosis

Radiography has limited diagnostic value in the diagnosis of gastric cancer. Although better studies
(using state-of-the-art techniques performed by practiced technicians) suggest a high sensitivity of x-
rays (80–95%), there are limitations. Upper gastrointestinal series may show thickened or enlarged
gastric folds, filling defects that correspond to a mass or ulcer, or may demonstrate a failure of the
stomach to distend normally to air and instilled barium (Figure 11). These contrast studies do not aid in
accurate disease staging and do not allow differentiation of benign from malignant lesions
Abdominal computed tomography (CT) has been used in gastric cancer tumor staging. The CT scan
can demonstrate the size and location of the cancer, wall thickness, presence or absence of fat between
the mass and adjacent organs, as well as nodal, vascular, or visceral spread of tumor. The CT scan is
unable to distinguish different layers of the gastric wall; hence, it cannot differentiate early from more
advanced lesions. Additionally, CT scanning does not provide tissue confirmation for grading and
typing. The ability to distinguish carcinoma from lymphoma is crucial to provide therapy in a timely
fashion
Transabdominal ultrasonography may be useful in providing information about metastatic disease,
particularly that which affects the liver. Transabdominal ultrasound is largely operator-dependent and
has more limited usefulness than CT scanning because of its low sensitivity.

Endoscopic Diagnosis

Endoscopy provides the most specific and sensitive means of diagnosis of gastric cancers.
Gastrointestinal endoscopy allows the physician to visualize and biopsy the mucosa of the esophagus,
stomach, duodenum, and most of the jejunum During these procedures, the patient is situated in the left
lateral position and may be administered a topical anesthetic to help prevent gagging. Pain medication
and a sedative may also be administered prior to the procedure.
The endoscope (a thin, flexible, lighted tube) is passed through the mouth and pharynx and into the
esophagus. It transmits an image of the esophagus, stomach, and duodenum to a monitor visible to the
physician. Air may be introduced into the stomach through the scope to expand the folds of tissue and
enhance examination More than 90% of gastric cancers are detected by upper endoscopy and biopsy.
Endoscopy facilitates accurate visualization, histological confirmation and typing. Tumor staging,
localization and extent of tumor, and associated local complications may also be established during the
procedure In cases of known gastric cancer, endoscopy is helpful to establish treatment goals (cure or
palliation), TNM stage, and assessment of response to previous therapeutic approaches. Biopsy leads
to correct diagnosis in virtually 100% of cases when at least 7 specimens are obtained. The increasing
use of endoscopy has resulted in detection of “early gastric cancer”, which is amenable to endoscopic
therapy.
Survival in patients with gastric cancer is largely dependent upon the tumor stage and histological type
at the time of initial diagnosis. Correct staging is critical to determining appropriate treatment and
course of action. The TNM staging system considers the depth of tumor invasion (T), lymph node
involvement (N), and distant metastatases to lymph nodes outside specified regional nodes or to other
organs (M) not involved in direct extension from the primary site. Several different methods are used
in the staging of gastric cancer, including endoscopic ultrasound (EUS), computed tomography (CT)
transabdominal ultrasound, endoscopy, and tumor markers.
Endoscopic ultrasound accurately delineates the depth of tumor invasion through the layers of the
gastric wall and lymph node involvement. However, evaluation of distant metastases is limited and
requires additional information from chest x-ray and other abdominal cross imaging, such as CT scan.
EUS is performed after the initial esophagogastroduodenoscopy (EGD). The tip of the echoendoscope
is advanced into the stomach, air is aspirated, and water is injected. The patient is
positioned to achieve optimal visualization. The EUS image reveals a five-layer structure, which
includes the interface between the transducer and mucosa (layer 1), the muscularis mucosa (layer 2),
the submucosa (layer 3), the muscularis propria (layer 4), and the serosa (layer 5) The ability to delineate
specific wall layers allows assessment of depth of penetration and classification of T in TNM staging.
EUS is not useful in the definitive differentiation of benign from malignant ulcers, nor is it useful in
separating infiltrating adenocarcinoma from lymphoma. Histology is essential in making these
distinctions. Endoscopy also plays a critical role in the diagnosis of patients with gastric lymphoma. It
identifies the specific area and extent of the tumor. It can provide a visual diagnosis in many patients
and may also identify associated lesions (H. pylori-related gastritis). Other findings may include
infiltrative and polypoid patterns. Gross endoscopic appearance has led to diagnosis in the majority of
patients with high sensitivity. However, noninvasive studies and endoscopy may understage primary
gastric lymphoma compared to surgery.

Staging

The most significant prognostic factor is depth of tumor invasion at the time of diagnosis. There are
three classifications of gastric tumors. The Boorman classification is based on the macroscopic
appearance of the tumor; the Lauren classification divides tumors into intestinal and diffuse types; and
the TNM classification reflects the depth of tumor infiltration (T) node involvement (N) and the
presence of distant metastases (M). Advanced TNM stages are associated with worse prognoses. Most
patients present with stage III and IV disease, though the number of patients with stage IV disease at
presentation at some U.S. centers has declined during the past 30 years. The five-year survival rate for
patients without nodal involvement is about 40%, and is only 10% for those with metastatic disease.
These figures are unchanged over the past several decades despite advances in medical and surgical
therapy
Definitions:
Primary tumor (T):
Tis = carcinoma in situ: intraepithelial tumor without invasion of lamina propria
T1 = tumor invades lamina propria or submucosa
T2 = tumor invades muscularis propria or subserosa
T3* = tumor penetrates serosa (visceral peritoneum) without invasion of adjacent structures
T4**,*** = tumor invades adjacent structures

*A tumor may penetrate the muscularis propria with extension into the gastrocolic or gastrohepatic
ligaments or into the greater or lesser omentum without perforation of the visceral peritoneum.
**Structures adjacent to the stomach include the spleen, transverse colon, liver, diaphragm, pancreas,
abdominal wall, adrenal gland, kidney, small intestine, and retroperitoneum.
***Intramural extension to the duodenum or esophagus is classified by the depth of greatest invasion
in any of these sites, including the stomach).

Regional lymph nodes (N):

Include the perigastric nodes along the lesser and greater curvatures, and the nodes along the left gastric,
common hepatic, splenic, and celiac arteries.
N0 = no regional lymph node metastasis
N1 = metastasis to 1–6 regional lymph nodes
N2 = metastasis in 7–15 regional lymph nodes
N3 = metastasis in more than 15 regional lymph nodes
Distant metastasis (M):
M0 = no distant metastasis
M1 = distant metastasis

Worse prognoses are associated with tumors of the cardia, shorter duration of symptoms prior to
diagnosis, tumor unresectability, and poorly differentiated histology. Studies are underway to correlate
genetic abnormalities found in tumors to overall prognosis.
One of the most important prognostic factors in gastric cancer is the depth of infiltration. Endoscopic
ultrasound (EUS) has proven to be a very useful tool in staging and assessment of malignancy. EUS
can accurately determine depth of penetration and, with the use of fine-needle aspiration cytology, can
also assess lymph node status. EUS has been shown superior for locoregional staging of gastric cancers.

Laparoscopic Staging

Adenocarcinoma of the stomach may grow by direct extension into adjacent organs such as the colon,
liver, pancreas and spleen. Distant metastases to the lung, as well as to the lymph nodes of the celiac
axis, greater and lesser omentum, and retroperitoneal space, may occur. Metastases may present as a
“Sister Mary Joseph's node” at the umbilicus, a “Virchow’s node” in the left supraclavicular fossa, or a
"Krukenberg's tumor" in the ovary

Laparoscopy has been demonstrated to be a sensitive method for establishing a definitive diagnosis of
liver and other abdominal metastases in the presence of gastric adenocarcinoma. Laparoscopy may be
helpful in patients with positive CT or EUS findings for which no histological confirmation of
metastasis has been shown. The overall accuracy of laparoscopy for metastatic gastric cancer is
96.5%, 5–20% superior to the results obtained from imaging methods Abdominal lavage with
cytologic examination increases the sensitivity of laparoscopy.

Gastric Cancer: Therapy

Overview
There are essentially three modes of therapy for the treatment of gastric cancer. Curative resection,
including endoscopic resection, appears the most effective. Surgical resection entails the removal of the
primary tumor and regional lymph nodes with resection margins free of tumor. Gastric cancer has not
been shown to respond successfully to radiation alone. Chemotherapy has demonstrated limited success
with multi-drug regimens.
Surgical Therapy
The prognosis following surgical resection depends on the stage at presentation. Early tumors confined
to the stomach lining have higher cure rates than cases in which disease has already spread to distant
sites or regional lymph nodes. Cure rates have improved in the past 30 years, particularly in Japan.
These improvements can be attributed mainly to an increase in early detection rates.
The type of surgery performed depends on the extent and location of tumor; therefore, preoperative
evaluation is critical. Initial staging may be established by endoscopy with biopsy. Endoscopic
ultrasound should follow. Endoscopic Ultrasound (EUS) has a sensitivity of 85% in assessing depth of
tumor invasion and detecting nodal involvement prior to surgery. Laparoscopic staging prior to surgical
resection is also advocated and has impacted preoperative treatment decisions.
There are two principle types of gastric resection—the subtotal gastrectomy and the total gastrectomy.
Determination of the type of resection depends on various factors including:
1) the location of the tumor, 2) the size and the extent of the tumor, and 3) the histology pattern.
In addition to removal of the stomach, resections with curative intent generally include
lymphadenectomy, or removal of regional lymph nodes. Controversy remains as to the extent of the
lymphadenectomy required. Some advocate removal of nodes adjacent to the stomach (D1
dissection,)while some centers, particularly in Japan, advocate more radical lymphadenectomy
Occasionally, adjacent organs may need to be removed, including the spleen, omentum and liver.
Following gastrectomy, intestinal continuity is restored using a variety of reconstruction techniques.
When only the distal stomach is removed, reconstruction can be achieved by a Billroth II
gastrojejunostomy
Endoscopic Therapy
Therapeutic endoscopy may be curative for early gastric cancer or palliative for more advanced disease.
The decision to use endoscopic treatment as opposed to surgical resection is affected by tumor stage,
location, morphology, prognosis of the disease, risk factors, assessment of resectability versus cure, and
the associated morbidity with each procedure. The role of adjuvant systemic or regional therapy is also
of importance. EUS provides valuable information regarding the stage and the feasibility of endoscopic
therapy. Patients with more superficial lesions may be candidates for endoscopic (or surgical) resection,
while patients with more advanced disease may require palliative therapy. Tissue resection or ablation,
dilation of strictures, stent placement, palliation of bleeding, and the placement of feeding or
decompression tubes may all be accomplished endoscopically.
Endoscopic Mucosal Resection Endoscopic mucosal resection has been advocated for early gastric
cancers, those that are superficial and confined to the mucosa. Endoscopic mucosal resection may be
attempted in patients without evidence of nodal or distant metastases, with differentiated tumors that
are slightly raised and less than 2 cm in diameter, or indifferentiated tumors that are ulcerated and less
than 1 cm in diameter. The most commonly employed methods of endoscopic mucosal resection include
strip biopsy, double-snare polypectomy, resection with combined use of highly concentrated saline and
epinephrine, and resection using a cap. The prognosis after treatment is comparable to that of surgical
resection for early gastric cancer. Five-year survival rates for individuals undergoing endoscopic
mucosal resection of early gastric cancers have been reported to be as high as 95%.
The strip biopsy method is performed with a double-channel endoscope equipped with grasping forceps
and snare. After marking the lesion border with an electric coagulator, saline is injected into the
submucosa below the lesion to separate the lesion from the muscle layer and force its protrusion. The
grasping forceps are passed through the snare loop. The mucosa surrounding the lesion is then grasped,
lifted, strangulated , and resected by electrocautery
The endoscopic double-snare polypectomy method is indicated for protruding lesions. Using a double-
channel scope, the lesion is grasped and lifted by the first snare and strangulated with the second snare
for complete resection Endoscopic resection with injection of concentrated saline and epinephrine is
carried out using a double-channel scope. The lesion borders are marked with a coagulator. Highly
concentrated saline and epinephrine are injected (15–20 ml) into the submucosal layer to force the
protrusion of the area containing the lesion and elucidate the markings The mucosa outside the
demarcated border is excised using a high-frequency scalpel to the depth of the submucosa. The resected
mucosa is lifted and grasped with forceps, trapping and strangulating the lesion with a snare , and then
resected by electrocautery
A fourth method of endoscopic mucosal resection employs the use of a clear cap and prelooped snare
positioned inside the cap. After insertion, the cap is placed on the lesion and the mucosa containing the
lesion is drawn inside the cap by aspiration. The mucosa is caught by the snare, strangulated, and finally
resected by electrocautery. Using this method, it is possible to retain the resected specimen in the cap
for histological examination.
The major complications of endoscopic mucosal resection include postoperative bleeding and
perforation of the gastric wall. According to the Japanese Society of Gastroenterological Endoscopy,
the complication rate is 0.382 percent. Bleeding is usually discovered several days after the procedure.
During the procedure, an injection of 100,000 times diluted epinephrine into the muscular wall, along
with high frequency coagulation or clipping, may be applied to the bleeding point for hemostasis. It is
important to administer acid-reducing medications to prevent postoperative hemorrhage. Perforation of
the gastric wall may be prevented withsufficient saline injection to raise the mucosa containing the
lesion. The “non-lifting sign” and complaints of pain with snare strangulation of the lesion are
contraindications to endoscopic mucosal resection. When perforation is recognized immediately after a
procedure, clips should be applied to close the perforation, followed by abdominocentesis and aspiration
of air from the abdominal cavity. Surgery should be considered in cases of endoscopic closure failure.
Endoscopic Palliation Tumor ablation may be achieved by endoscopic resection of an exophytic mass
or polyp using a diathermic snare, alcohol injection, or thermal or non-thermal destruction. Tumor
traction and elevation from the wall with secondary snare resection using a double-channel endoscope
has been proposed. Because the resected base is larger, there is a greater probability of obtaining clear
margins.
Thermal photodestruction may be induced by laser. The Nd:YAG laser generating an infrared beam in
a continuous or pulse mode, is applied through direct contact with tumor tissue or in a non-contact
fashion. This method provides focal tumor destruction and is well suited for exophytic masses to regain
lumen or to control bleeding. The Nd:YAG is best suited for soft, non-constricting, non-circumferential
cancers; however, its use is limited because of expense and the need for frequent treatment sessions.
Tumor destruction may also be achieved by non-thermal methods with photodynamic therapy (PDT).
Following the oral or intravenous administration of a photosensitizing drug, the tumor area is exposed
to low-power red light (dye laser emitting 630 nm). Currently, PDT is applied to small tumors 1–2 cm
thick because penetration is only a few millimeters into the tissue. Moreover, PDT is associated with
the risk of delayed hemorrhage following the partial necrosis of large lesions. PDT may also be used as
complementary therapy with other techniques. For example, if the majority of a cancer is removed
surgically, PDT may be used to destroy any remaining small areas. Thorough understanding of the
biology involved is essential before the potential of PDT can be realized in treating gastrointestinal
tumors.
Pure ethanol injection into a tumor induces immediate necrosis. Aliquots of 0.2 ml injection of pure
alcohol are safe and effective. Care must be taken with regard to the amount of alcohol injected, because
the depth of penetration is not predictable. Like laser therapy, over zealous treatment may result in
perforation.
Intratumoral injection of cytotoxic agents has also been used preoperatively or as palliative treatment.
Injection with OK-432 causes degeneration of cancer tissue in carcinoma of the stomach. Studies have
demonstrated that preoperative intratumoral injection of OK-432 improved five-year survival rates in
patients with stage III cancer.
Chemotherapy
Adenocarcinoma of the stomach is relatively sensitive to chemotherapy. Fluorouracil (5-FU) is the most
commonly used drug in the treatment of gastric cancer, with a response rate around 21%. In an attempt
to improve this rate, drug combinations have been tried; the most common is 5-FU, doxorubicin, and
mitomycin C (FAM) with a response rate of 33% and an acceptable degree of toxicity. Other drug
combinations have been tried, although the response duration and overall survival, when compared with
5-FU alone, were not significantly different. In addition, the combination groups had a higher toxicity
rate. Newer investigational modalities employ tumor antigen-specific immunochemotherapy.
Antibodies to tumor antigens are conjugated with chemotherapeutic drugs; in this way, the drugs can
be delivered to the tumor directly.
Bleeding Bleeding may be controlled by endoscopic thermal techniques such as laser and multipolar
electrocoagulation. After resuscitation and stabilization of the patient, endoscopy is the preferred
procedure for treating hemorrhage . Gastric lavage is usually performed to remove blood from the
stomach prior to endoscopy. The goal of endoscopic therapy is to stop the bleeding and/or oozing from
the surface of the tumor. This may be achieved using laser, MPEC, or cauterization

Gastric Outlet Obstruction

Gastric outlet obstruction is commonly associated with malignancy. CT scans and oral contrast
radiographs are useful in diagnosis of this complication. The findings of a large gastric silhouette, gas
bubble, and little or no air in the small intestine or the colon are consistent with gastric outlet
obstruction.
Surgery and/or endoscopy may be used for palliation of gastric outlet obstruction. Surgical procedures,
especially for recurrent disease, carry a high risk of complications and have limited potential for long-
term survival. Patients who have undergone tumor resection and then present with symptoms suggestive
of recurrence should be evaluated endoscopically. Endoscopy is the best procedure for evaluating
gastric outlet obstruction after a 12–24 hour suctioning of the stomach. Non-surgical approaches should
be the principal considerations in these patients.
Endoscopic Therapy Endoscopic dilation of the gastric outlet obstruction is a reasonable palliative
course. Balloon dilation can usually improve the acute problem by producing radial forces on the
strictured segment. Through-the-scope balloons are usually the first choice (over guide wire balloons),
using the largest balloon that can be safely passed into the segment. A well-lubricated balloon is passed
through the endoscopic biopsy channel and carefully positioned in the stricture. The balloon is inflated
with contrast, water, or air, and pressure is maintained for the desired time. Dilation may also be
performed over a guide wire that is passed through the stricture. Sequential balloon dilation is performed
with fluoroscopy and endoscopic evaluation. In the presence of a malignant gastric outlet obstruction,
self-expanding stents have been placed endoscopically for the treatment of obstruction
Good palliation of obstructive symptoms allows patients to consume liquid diets, preventing
dehydration and frequent hospital admissions. Stent migration and occlusion are possible
complications. These problems may be successfully resolved by implantation of a second stent or
electrocoagulation of tumor overgrowth.
Percutaneous endoscopic gastrostomy (PEG) has been used for decompression of gastrointestinal tract
obstructions and most commonly for enteral feeding (Figure 31). In a study of 53 patients with gastric
or small-bowel obstruction, endoscopic gastrostomies were performed for decompression.
Decompression was successful in 89% of these cases with low complication rates.
Surgical Therapy The goal of surgical therapy for the treatment of gastric outlet obstruction is to
remove the obstruction. Gastric outlet obstruction resulting from gastric cancer should be resected by
distal partial gastrectomy or subtotal gastrectomy with lymphadenectomy.

Nursing Intervention

1. Monitor nutritional intake and weigh patient regularly.

2. Monitor CBC and serum vitamin B12 levels to detect anemia, and monitor albumin and
prealbumin levels to determine if protein supplementation is needed.
3. Provide comfort measures and administer analgesics as ordered.
4. Frequently turn the patient and encourage deep breathing to prevent pulmonary complications,
to protect skin, and to promote comfort.
 5. Maintain nasogastric suction to remove fluids and gas in the stomach and prevent painful
distention.
6. Provide oral care to prevent dryness and ulceration.
7. Keep the patient nothing by mouth as directed to promote gastric wound healing. Administer
parenteral nutrition, if ordered.
8. When nasogastric drainage has decreased and bowel sounds have returned, begin oral fluids
and progress slowly.
9. Avoid giving the patient high-carbohydrate foods and fluids with meals, which may trigger
dumping syndrome because of excessively rapid emptying of gastric contents.
10. Administer protein and vitamin supplements to foster wound repair and tissue building.
11. Eat small, frequent meals rather than three large meals.
12. Reduce fluids with meals, but take them between meals.
13. Stress the importance of long term vitamin B12 injections after gastrectomy to prevent
surgically induced pernicious anemia.
14. Encourage follow-up visits with the health care provider and routine blood studies and other
testing to detect complications or recurrence.

Documentation Guidelines

 Physical findings related to gastric cancer:Epigastric discomfort,dyspepsia,anorexia,nausea,

sense of fullness, gas pains, unusual tiredness, abdominal pains, constipation, weight loss,
 vomiting,hematemesis,blood in the stool,dysphagia,jaundice,ascites,bone pain
 GI decompression data: Irrigation and patency of tube, assessment of bowel sounds and passage
of gas,complaints of nausea,amount and description of gastric fluid output
 Presence of postoperative complications: Hemorrhage, obstruction, anastomotic leaks,
infection,peritonitis
 Presence of postoperative dumping syndrome and associated patient symptoms

Discharge and Home Healthcare Guidelines

 Teach the patient the importance of compliance with palliative and follow-up care. Be sure the
patient understands all medications, including the dosage, route, action, and adverse effects.
 Teach the patient the signs and symptoms of infection and how to care for the incision. Instruct
the patient to notify the physician if signs of infection occur.
 Encourage the patient to seek psychosocial support through local support groups (e.g.,I Can
Cope),clergy,or counseling services. If appropriate,suggest hospice services.
 Teach the patient methods to enhance nutritional intake to maintain ideal body weight. Several
small meals a day may be tolerated better than three meals a day. Take liquid supplements and
vitamins as prescribed. Refer the patient to the dietitian for a consultation. Teach family
members and friends prevention strategies. Strategies include increasing the intake of fresh
fruits and vegetables that are high in vitamin C; maintaining adequate protein intake; and
decreasing intake of salty, starchy, smoked, and nitrite- preserved foods.
 CARCINOMA OF RECTUM OR COLON

Definition
A malignant epithelial tumour of the colon or rectum. Only tumours that have penetrated through
muscularis mucosae into submucosa are considered malignant at this site. The presence of scattered
Paneth cells, neuroendocrine cells or small foci of squamous cell differentiation is compatible with the
diagnosis of adenocarcinoma.

ICD-O codes

Adenocarcinoma 8140/3
Mucinous adenocarcinoma 8480/3
Signet-ring cell carcinoma 8490/3
Small cell carcinoma 8041/3
Squamous cell carcinoma 8070/3
Adenosquamous carcinoma 8560/3
Medullary carcinoma 8510/3
Undifferentiated carcinoma 8020/3

Epidemiology

An estimated 875,000 cases of colorectal cancer occurred worldwide in 1996, representing about 8.5%
of all new cancers. The age-standardized incidence (cases/100,000 population) varies greatly around
the world, with up to 20fold differences between the high rates in developed countries of Europe, North
and South America, Australia/New Zealand, and Asia and the still lower rates in some recently
developed countries (Malaysia, Korea) and in developing countries of Africa, Asia and Polynesia.
Significant differences also exist within continents, e.g. with higher incidences in western and northern
Europe than in central and southern Europe. Among immigrants and their descendants, incidence rates
rapidly reach those of the adopted country, indicating that environmental factors are important.
According to the U.S. SEER database, the incidence rate for adenocarcinoma of the colon is
33.7/100,000 and increased by 18% during the period from 1973 through 1987 while the incidence of
rectal adenocarcinoma (12.8/100,000) and mucinous adenocarcinoma in the colon and rectum (0.3 and
0.8, respectively) remained relatively constant. During the last decade of the 20th century, incidence
and mortality have decreased. By contrast, the incidence in Japan, Korea and Singapore is rising rapidly,
probably due to the acquisition of a Western lifestyle. Incidence increases with age: carcinomas are rare
before the age of 40 years except in individuals with genetic predisposition or predisposing conditions
such as chronic inflammatory bowel disease.
Incidence rates in the 1973-87 SEER data for colonic and rectal adenocarcinoma for males were higher
than those for females; whites had higher rates than blacks for rectal adenocarcinoma, but blacks had
higher rates for colonic adenocarcinoma. During 1975-94, a decrease in incidence in whites was evident,
while the incidence of proximal colon cancers in blacks still increased.

Aetiology

Diet and lifestyle

A high incidence of colorectal carcinomas is consistently observed in populations with a Western type
diet, i.e. highly caloric food rich in animal fat combined with a sedentary lifestyle. Epidemiological
studies have indicated that meat consumption, smoking and alcohol consumption are risk factors.
Inverse associations include vegetable consumption, prolonged use of non-steroidal anti-inflammatory
drugs, oestrogen replacement therapy, and physical activity. Fibre may have a protective role, but this
has been questioned recently. The molecular pathways underlying these epidemiological associations
are poorly understood, but production of heterocyclic amines during cooking of meat, stimulation of
higher levels of fecal bile acids and production of reactive oxygen species have been implicated as
possible mechanisms Vegetable anticarcinogens such as folate, antioxidants and inducers of detoxifying
enzymes, binding of luminal carcinogens, fibre fermentation to produce protective volatile fatty acids,
and reduced contact time with colorectal epithelium due to faster transit may explain some of the inverse
associations

Chronic inflammatory Bowel diseases

These are significant aetiological factors in the development of colorectal adenocarcinomas. The risk
increases after 8-10 years and is highest in patients with early-onset and widespread manifestation
(pancolitis). Ulcerative colitis. This chronic disorder of unknown aetiology affects children and adults,
with a peak incidence in the early third decade. It is considered a premalignant disorder, with duration
and extent of disease being the major risk factors.
Crohn disease.
Development of carcinoma is seen both in the small intestine and the large intestine
Modifying factors.
Non-steroidal anti-inflammatory drugs and some naturally occurring compounds block the biochemical
abnormalities in prostaglandin homeostasis in colorectal neoplasms. Some of these agents cause a
dramatic involution of adenomas but their role inthe chemoprevention of adenocarcinoma is less clear.
Polymorphisms in key enzymes can alter other metabolic pathways that modify protective or injurious
compounds, e.g. methylenetetrahydrofolate reductase, N-acetyltransferases, glutathione-S-transferases
Irradiation.
A rare but well recognized aetiological factor in colorectal neoplasia is therapeutic pelvic irradiation
Localization
Most colorectal carcinomas are located in the sigmoid colon and rectum, but there is evidence of
changing distribution in recent years, with an increasing proportion of more proximal carcinomas
Molecular pathology has also shown site differences: tumours with high levels of microsatellite
instability (MSI-H) or ras proto-oncogene mutations are more frequently located in the caecum,
ascending colon and transverse colon.

Clinical features

Signs and symptoms

Some patients are asymptomatic, especially when their neoplasm is identified by screening or
surveillance. Haematochezia and anaemia are common presenting features due to bleeding from the
tumour. Many patients experience change in bowel habit; in the right colon, the fluid faeces can pass
exophytic masses, whereas in the left colon the solid faeces are more often halted by annular tumours
so that constipation is more common. There may be associated abdominal distension. Rectosigmoid
lesions can produce tenesmus. Other symptoms include fever, malaise, weight loss, and abdominal pain.
Some patients present with the complications of obstruction or perforation.
Bleeding
Bleeding is often slight and occurs at end of defaecation,resembling haemorrhoids. Haemorrhoids can
coexist with carcinoma
Sense of incomplete defaecation
The bowels open, but there is a sensation that there is more faeces to be passed. Patient tries to empty
the bowel several times a day, often with passage of flatus and a little blood-stained mucus (‘bloody
slime’).
Alteration of bowel habits
Annular carcinoma leads to constipation. Growths in the middle and lower parts give rise to early
morning diarrhoea mixed with blood.
Pain
Pain is a late feature. Colicky pain is associated with advanced growths of rectosigmoid region due to
some degree of intestinal obstruction. When a deep-seated carcinoma of the rectum erodes the prostate
or bladder, severe pain occurs. Pain in the back or sciatica occurs when the growth invades the sacral
plexus Imaging
 Staging

The classification proposed by C. Dukes in 1929-35 for rectal cancer serves as the template for many
staging systems currently in use. This family of classifications takes into account two
histopathological features: depth of penetration into the wall and the presence or absence of metastasis
in regional lymph nodes. The TNM classification is replacing the Dukes classification

Histopathology
The defining feature of colorectal adenocarcinoma is invasion through the muscularis mucosae into the
submucosa. Lesions with the morphological characteristics of adenocarcinoma that are confined to the
epithelium or invade the lamina propria alone and lack invasion through the muscularis mucosae into
the submucosa have virtually no risk of metastasis. Therefore, ‘high-grade intraepithelial neoplasia’ is
a more appropriate term than ‘adenocarcinoma in-situ’, and ‘intramucosal neoplasia’ is more
appropriate than ‘intramucosal adenocarcinoma ’. Use of these proposed terms helps to avoid
overtreatment.
Most colorectal adenocarcinomas are gland-forming, with variability in the size and configuration of
the glandular structures. In well and moderately differentiated adenocarcinomas, the epithelial cells are
usually large and tall, and the gland lumina often contain cellular debris.

Mucinous adenocarcinoma This designation is used if > 50% of the lesion is composed of mucin. This
variant is characterized by pools of extracellular mucin that contain malignant epithelium as acinar
structures, strips of cells or single cells. Many high-frequency micro-satellite instability (MSI-H)
carcinomas are of this histopathological type.
Signet-ring cell carcinoma This variant of adenocarcinoma is defined by the presence of > 50% of
tumour cells with prominent intracytoplasmic mucin . The typical signet-ring cell has a large mucin
vacuole that fills the cytoplasm and displaces the nucleus. Signet-ring cells can occur in the mucin pools
of mucinous adenocarcinoma or in a diffusely infiltrative process with minimal extracellular mucin.
Some MSI-H carcinomas are of this type.
Adenosquamous carcinoma These unusual tumours show features of both squamous carcinoma and
adenocarcinoma, either as separate areas within the tumour or admixed. For a lesion to be classified as
adenosquamous, there should be more than just occasional small foci of squamous differentiation. Pure
squamous cell carcinoma is very rare in the large bowel.

Medullary carcinoma
This rare variant is characterized by sheets of malignant cells with vesicular nuclei, prominent nucleoli
and abundant pink cytoplasm exhibiting prominent infiltration by intraepithelial lymphocytes {856}. It
is invariably associated with MSI-H and has a favourable prognosis when compared to other poorly
differentiated and undifferentiated colorectal carcinomas.
Undifferentiated carcinoma
These rare tumours lack morphological evidence of differentiation beyond that of an epithelial tumour
and have variable histological features . Despite their undifferentiated appearances, these tumours are
genetically distinct and typically associated with MSI-H.
Other variants Carcinomas that include a spindle cell component are best termed spindle cell carcinoma
or sarcomatoid carcinoma. The spindle cells are, at least focally, immunoreactive for cytokeratin. The
term carcinosarcoma applies to malignant tumours containing both carcinomatous and heterologous
mesenchymal elements. Other rare histopathological variants of colorectal carcinoma include
pleomorphic (giant cell), choriocarcinoma, pigmented, clear cell, stem cell, and Paneth cell-rich (crypt
cell carcinoma). Mixtures of histopathological types can be seen.
Carcinosarcoma
Carcinomas that include a spindle cell component are best termed sarcomatoid carcinoma or spindle
cell carcinoma. The spindle cells are, at least focally, immune reactive for cytokeratin. The term
carcinosarcoma applies to malignant tumours containing both carcinomatous and heterologous
mesenchymal elements.
 BENIGN TUMOURS
Rectum and sigmoid colon are the most frequent sites of polyps. All neoplastic polyps have a tendenc
y to become malignant. This tendency is more in sessile and large polyps. Hence, polyps must be rem
oved totally to exclude carcinoma in situ and to prevent recurrence. A proximal carcinoma should alw
ays be ruled out prior to removal of a polyp, as local implantation of cancer cells may occur in thedist
ally situated rectal wound.

Juvenile polyp
Bright red glistening pedunculated spherical lesions found in infants and children. They have no tende
ncy to turn malignant. If symptomatic, they can be removed by an endoscopic snare

Metaplastic polyps: Small pinkish, sessile polyps and frequently multiple. Harmless.
Inflammatory polyps or pseudopolyps: They are oedematous thickening of mucous membrane associ
ated with colitis

Villous adenomas
Sometimes very large, they have a characteristic frond‐like appearance. They have a tendency to
become malignant. Profuse mucous discharge from these tumours, which is rich in potassium, can cause
electrolyte and fluid loss.
They can be removed through the anus or from above. When malignant change is suspected, the rectum
has to be excised totally

Familial adenomatous polyposis

Multiple rectal and colonic polyps develop around puberty. Genetically transmitted. This condition is
premalignant and requires total colectomy and replacement of the rectum with a ‘pouch’ of folded
ileum.
Bilharzial papilloma Common in Egypt. Can resemble carcinoma.
Benign lymphoma
Circumscribed movable nodules, firm in consistency, greenish white to pink in colour. Complete local
excision is the management
Endometrioma
Constricting lesions at recto sigmoid junction or tumours invading the rectum from the rectovaginal se
ptum. Dysmenorrhoea and rectal bleeding are common symptoms. Can be controlled with oral contr
aceptives or cured by bilateral oophorectomy.
Haemangioma
Uncommon. Can cause serious or even fatal haemorrhage. They have to be treated by excision of the
portion of the anorectum bearing the lesion

CARCINOMA
Second most common variety of malignant tumour in men and fourth common malignant tumour in w
omen.
Origin
Adenomas and papillomas are precarcinomatous conditions. Most rectal carcinomas start as adenoma
Pathological Histology
Three types are recognized.
•Well differentiated adenocarcinoma
•Moderately differentiated adenocarcinoma
•Anaplastic, highly undifferentiated adenocarcinoma
More malignant varieties contain large numbers of mucin producing cells.
Ulcerative types are the usual ones, but papuliferous and infiltrating types are common.

Spread
Local spread
Local spread occurs circumferentially rather than in a longitudinal direction. A period of 18‐24 months
is required for complete encirclement. Annular variety is common at the rectosigmoid junction.
Anteriorly, spread occurs in male to the prostate, seminal vesicles, or the bladder. In the female, the
vagina or the uterus is involved. Posteriorly, sacrum and sacral plexus are involved. Lateral spread
involves the ureters.

Lymphatic spread

Lymphatic spread occurs in an upward direction in cases of carcinoma occurring above the peritoneal
reflection. Below the peritoneal reflection to within 1‐2 cm of the anal orifice, the lymphatic spread is
still upwards, but the first halting place is in the pararectal nodes of Gerota. Primary lateral spread can
occur if the growth occurs in the field of the middle rectal artery. Atypical and widespread lymphatic
permeation can occur in anaplastic growths.
Venous spread
Venous spread is late. Liver, lungs and adrenals are the most common sites.
Peritoneal dissemination may follow penetration of the peritoneal coat in a high placed rectal carcinoma

Dukes staging

A.The growth is limited to the rectal wall. (15%). Prognosis is excellent.

B.The growth has extended to the extrarectal tissues, but no metastasis to the regional nodes.(35%).
Prognosis reasonable.
C.There are secondary deposits in the regional lymph nodes.(50%)
C1 – Local pararectal nodes alone are involved.
C2 –Nodes near the main supplying vessels are involved. Prognosis is poor.
D.Presence of widespread metastasis, usually hepatic

INVESTIGATIONS

Abdominal examination
it is negative in early cases. Annular growth of rectosigmoid junction may present as intestinal
obstruction. Metastases in the liver may be palpable. When the peritoneum is studded with secondary
depositsascites may be found

Rectal examination
In 90% of patients, the neoplasm can be felt digitally as an indurated nodule. If central ulceration
occurs, a shallow depression will be found, the edges of which are raised and everted. On bimanual
examination, it may be possible to feel the lower end of a carcinoma situated in the rectosigmoid
junction. After the finger has been withdrawn, if it has been in contact with a carcinoma, it is smeared
with blood or mucopurulent material tinged with blood. Sometimes, lymph nodes can be felt as one or
more hard, oval swellings in the extra rectal tissues posteriorly or posterolateral. In females, a vaginal
examination is done. When the tumour is situated in the anterior wall of the rectum, it can be palpated
accurately with one finger in the vagina and another in the rectum

Modern imaging techniques permit non-invasive detection and clinical staging. Conventional barium
enema detects large tumours, while air-contrast radiography improves the visualization of less
advanced lesions. Cross-sectional imaging by CT, MRI imaging and transrectal ultrasonography permit
some assessment of the depth of local tumour invasion and the presence of regional and distant
metastases. Scintigraphy and positron emission tomography are also used.

Procto‐sigmoidoscopy
will show a carcinoma if the rectum is emptied of faeces.Biopsy is taken from the edge of the tumour.
It will confirm the diagnosis and to some extent permit grading

Endoscopy The development of endoscopy has had a major impact on diagnosis and treatment.
Colonoscopy allows observation of the mucosal surface of the entire large bowel with biopsy of
identified lesions. Chromoendoscopy employing dyes to improve visualization of non-protruding
lesions and magnification, have been developed. The flat neoplastic lesions
Colonoscopy is done to exclude a synchronous tumour,whether an adenoma or carcinoma. If an aden
oma is found, it can be snared and removed via the colonoscope. If a full colonoscopy is not possible
, a barium enema should be done.
Carcinoembryonic antigen

Treatment
•Some form of excision is essential if at all possible, because of the extreme suffering if the neoplasm
remains.
•Prior to surgery, it is necessary to assess the fitness of the patient for operation and the extent of spre
ad of the tumour.

A) Ultrasound, CT, Xray of the chest and CT of the chest are done to exclude distant metastasis.

B)Transluminal ultrasound, where a probe is placed in the rectal lumen can be used to assess the local
spread of the tumour. CT and MRI are also useful to assess local spread.

Principles of surgical treatment

•Radical excision of the rectum together with the mesorectum and associated lymph nodes should be
the aim. Even in the presence of metastases, a rectal excision should be considered, as this is often the
best means of palliation.
•Solitary metastatic deposits in liver have been resected with good long-term survival.
•When a tumour is locally advanced, a course of preoperative radiotherapy may be given to reduce its
size and make it more amenable for radical excision.
•For patients who are unfit for radical excision or who have widespread metastases, a lesser local
procedure such as trans anal excision, laser destruction or interstitial radiation should be considered.
When a rectal excision is possible, the aim should be to restore the continuity of the bowel and preserve
the anal sphincter.
•A sphincter saving procedure (Anterior Resection) is usually possible for tumours of the upper two‐
thirds of the rectum.
•Removal of the rectum with a permanent colostomy (Abdomino Perineal Excision) is required for
tumours of the lower one‐third.
•Anterior resection is now applied to at least two‐thirds of patients presenting with carcinoma of the
rectum. Here, the neoplasm is excised radically with at least 2 cm. margin of normal bowel below the
lower edge of the tumour, removal of all the mesorectum and high ligation of the inferior mesenteric
lymphovascular pedicle.
•Once the rectum has been mobilized, it is removed and the remaining bowel ends are washed well.
Continuity is restored by direct end to end anastomosis, either manually or with stapler.
Preoperative preparation
•Bowel is prepared by diet and use of purgatives.
•Prophylactic systemic antibiotics are given (usually Cefuroxime 750mg. and Metronidazole 500mg
IV) an hour prior to surgery.
•All patients are seen preoperatively by a stoma care nurse and counseled regarding the colostomy and
possible complications of operation like pelvic autonomic nerve damage resulting in bladder and
sexual dysfunction.
•Anaemia and electrolyte deficiencies are corrected.
•An indwelling bladder catheter is passed prior to surgery

Abdominoperineal resection
•AP resection is done as a synchronous transabdominal and perineal procedure with two operative
teams.
•Position : Modified lithotomy
•Technical points:
•The locoregional and distant spreads are evaluated and mobility of the lesion is assessed.
The lateral peritoneum is incised and the sigmoid mobilized, identifying the left ureter.
•The inferior mesenteric artery is ligated below the left colic branch.
•Posterior mobilization is done carefully preserving the presacral nerves and without breaching the
presacral fascia. Damage to the presacral fascia can lead to severe haemorrhage from the presacral
veins.
•The anterior plane is just behind the seminal vesicles.
•The permanent end colostomy is through the rectus sheath to minimize subsequent hernia

Anterior resection

•The rectum is mobilized to the level of the levators through the abdomen. The colon is anastomosed
to the anus with an intraluminal circular stapler or by hand suture.
•The same procedure can be done through a laparoscope

Hartmann’s operation

Ideal procedure for an old and feeble patient who will not tolerate a lengthy anterior resection or an
abdominoperineal resection The rectum is excised through the abdomen, anorectal stump is transect
ed and closed. A terminal colostomy is done

Palliative colostomy

It is done for patients presenting in an advanced stage with intestinal obstruction

Pelvic exenteration (Brunschwig’s operation)

Here, the aim is to remove all the pelvic organs,together with the internal iliac and obturator group of
lymph nodes. Urine has to be diverted through an ileal conduit.

Radiotherapy

Some adenocarcinomas respond to megavoltage cobalt therapy or neutron beam irradiation. RT can
be used as an adjuvant alone or with chemotherapy. RT can be given for inoperable primaries and lo
cal recurrences. Intracavity radiation can be applied through the anal route

Immunotherapy
Monoclonal antibodies to CEA combined with cancericidal agents are used for management of disse
minated disease

Prognosis
Survival rates are influenced by Dukes’ stage, with stage C patients doing worse than those with stage
A and B.Fixed lesions and poorly differentiated tumours have poor prognosis.
Overall, 5‐year survival rate is about 50% in advanced centres

Local recurrence
Local recurrence is mostly due to inadequate removal. It is managed by RT.
Neodymium: yttrium‐aluminium‐garnet (Nd: YAG)
laser can be used for an obstructing or bleeding lesion. Intraluminal stent can be
inserted endoscopically in high stenosing rectal cancers to palliate a tumour that is causing obstruction
Nursing Intervention

 Administer chemotherapy agents as ordered, provide care for the client receiving chemotherapy.
 Provide care for the client receiving radiation therapy.
 Provide care for the client with bowel surgery.
Documentation Guidelines

 Response to diagnosis of colorectal cancer,diagnostic tests,and treatment regimen

 Description of all dressings, wounds, and drainage collection devices: Location of drains; color
and amount of drainage; appearance of the incision; color of the ostomy stoma; presence,
amount,and consistency of ostomy effluent
Discharge and Home Healthcare Guidelines
PATIENT TEACHING
 Teach the patient the care related to the abdominal incision and any perineal wounds. Give
instructions about when to notify the physician (if the wound separates or if any redness,
bleeding, purulent drainage, unusual odor, or excessive pain is present).
 Advise the patient not to perform any heavy lifting (&#x10fc00;10 lbs),pushing,or pulling for 6
weeks after surgery.
 If the patient has a perineal incision, instruct her or him not to sit for long periods of time and to
use a soft or “waffle”pillow rather than a rubber ring whenever in the sitting position.
 Teach the patient colostomy care and colostomy irrigation.
 Give the following instructions for care of skin in the external radiation field:Tell the patient to
wash the skin gently with mild soap,rinse with warm water,and pat the skin dry each day; not to
wash off the dark ink marking that outlines the radiation field; to avoid applying any lotions,
perfumes,deodorants,and powder to the treatment area; to wear nonrestrictive soft cotton cloth-
ing directly over the treatment area; and to protect skin from sunlight and extreme cold.
 Explain the purpose, action,dosage,and side effects of all medications prescribed by the
physician.
FOLLOW-UP
 Stress the need to maintain a schedule for follow-up visits recommended by the physician.
Encourage patients with early-stage disease and complete healing of the bowel to eat a diet
consisting of a low-fat and high-fiber content with cruciferous vegetables (Brussels
sprouts,cauliflower,broccoli,cabbage). Most colorectal tumors grow undetected as symptoms
slowly develop. Survival rates are best when the disease is discovered in the early stages and
when the patient is asymptomatic. Unfortunately,50% of patients have positive lymph node
involvement at the time of diagnosis. Participation in procedures for the early detection of
colorectal cancer needs to be encouraged. Suggest follow-up involvement with community
resources such as the United Ostomy Association and the American Cancer Society.

THEORETICAL APPLICATION
CASE
The patient is male, 80 years old, born and raised in Caucaia/CE. He is married, has eight children, is
literate and lives in his own house with his wife and children. He is Christian and he reported spiritual
well-being. He is an ex-smoker (exposure for 50 years) and a former alcoholic (exposure for 45 years).
Clinical background: diabetes mellitus (DM) and systemic arterial hypertension (SAH). He was
diagnosed with moderately differentiated rectal adenocarcinoma in the first quarter of 2014 and has
undergone eight sessions of chemotherapy (CT) with 35 mg leucovorin and 160 mg fluorouracil scheme
and 28 sessions of radiotherapy (RT). He reported that during the period of this treatment he felt much
physical and mental fatigue. After the completion of the CT and RT neoadjuvant he was admitted to
the surgical clinic to undergo the surgical procedure rectosigmoidectomy with colorectal anastomosis
and the preparation of ileostomy. The elderly patient and his companion (son) were aware of the rectal
neoplasia. In the study’s first contact with the patient, on the second day after surgery (2 October 2014),
the patient was conscious and he was able to communicate. He had lost 8 kg in the last six months, was
pale, hydrated with exudate dirtiness in the abdomen from leakage through the collection bag laminar
drain (penrose) and was maintaining a full liquid diet with good acceptance and physiologic serum with
five ampoules of short-stay hypertonic glucose through central venous access (CVA) located in the right
jugular vein (RJV). The insertion site showed no signs of infection.

Nursing
callista Roy Nursing Diagnoses Nursing Outcomes
Interventions (NIC
adaptation modes (NANDA-I code) (NOC code)
code)

Physiological mode: Electrolyte balance and acid- Electrolytes control

Electrolyte imbalance risk (00195), base (0600) (1160)
Complex needs -
due to the high loss of water and
fluids and
electrolytes by ileostomy. Hydroelectrolyte
electrolytes.
control (2080)
Impaired skin integrity risk (00047) Ostomy self-care (1615) Ostomy Care (0480)
due to the presence of ileostomy
which can lead to contact Skin supervision
Physiological mode: Risk Control (1902)
dermatitis, because it contains (3590)
basic needs -
enzymes that can irritate the skin.
protection.
Impaired tissue integrity (00044),
evidenced by destroyed tissue
(stoma and laminar drain

Risk of infection (00004) due to Protection against

Risk Control:
Physiological mode: central venous catheter, urinary infection (6550)
basic needs - catheter, Penrose drain, ileostomy, Infectious process (1924)
protection. surgical incision, hospital
environment, and age.
Acute pain (00132), characterized
Pain level (2102). Pain control (1400)
by reports of pain and protective
Physiological mode: gestures related to a surgical Analgesic
Discomfort level (2109).
Complex Needs - procedure. administration
senses. -2300

Physiological mode: Fall Risk (00155) due to the age of

Knowledge: Fall Prevention Preventing slips and
basic needs - 80, anemia and the hospital
(1828). trips (6490)
protection. environment.

Impaired social interaction (00052), Improved

Communication (0902).
characterized by the familiar story socialization (5100)
of change in the interaction and
Improved body image
Social mode early treatment that caused a lot of Body image (1200).
(5220)
fatigue, related deficiency in terms
of ways to strengthen mutuality Strengthening self-
after cancer diagnosis. Self-Esteem (1205).
esteem (5400)

Social mode Impaired home maintenance Family operation (2602). Advice (5240)
(00098) characterized by reports of
overburdened family members and Active listening
financial crisis and; related to (4920)
rectum neoplasia (disease) and
insufficient finances.

Improved coping
Coping (1302).
Anxiety (00146), characterized by (5230)
expressed feelings that can interfere Teaching: disease
self-concept mode: with the elderly's ability to reach Acceptance: Health
process (5602)
personal self. their highest level of physical well- Anxiety Reduction
being related to chronic disease State (1300)
(5820).
experience.

Physiological mode: Electrolyte balance and acid- Electrolytes control

Electrolyte imbalance risk (00195), base (0600) (1160)
Complex needs -
due to the high loss of water and
fluids and
electrolytes by ileostomy. Hydroelectrolyte
electrolytes.
control (2080)
Impaired skin integrity risk (00047) Ostomy self-care (1615) Ostomy Care (0480)
due to the presence of ileostomy
which can lead to contact Skin supervision
Physiological mode: Risk Control (1902)
dermatitis, because it contains (3590)
basic needs -
enzymes that can irritate the skin.
protection.
Impaired tissue integrity (00044),
evidenced by destroyed tissue
(stoma and laminar drain

Risk of infection (00004) due to Protection against

Risk Control:
Physiological mode: central venous catheter, urinary infection (6550)
basic needs - catheter, Penrose drain, ileostomy, Infectious process (1924)
protection. surgical incision, hospital
environment, and age.

Acute pain (00132), characterized Pain level (2102). Pain control (1400)
Physiological mode:
by reports of pain and protective
Complex Needs - Analgesic
gestures related to a surgical Discomfort level (2109).
senses. administration
procedure.
-2300
Knowledge: Fall Prevention Preventing slips and
(1828). trips (6490)
Physiological mode: Fall Risk (00155) due to the age of
basic needs - 80, anemia and the hospital
protection. environment.
Impaired social interaction (00052), Improved
Communication (0902).
characterized by the familiar story socialization (5100)
of change in the interaction and
Improved body image
Social mode early treatment that caused a lot of Body image (1200).
(5220)
fatigue, related deficiency in terms
of ways to strengthen mutuality Strengthening self-
after cancer diagnosis. Self-Esteem (1205).
esteem (5400)

Social mode Impaired home maintenance Family operation (2602). Advice (5240)
(00098) characterized by reports of
overburdened family members and Active listening
financial crisis and; related to (4920)
rectum neoplasia (disease) and
insufficient finances.

Anxiety (00146), characterized by Improved coping

Coping (1302).
expressed feelings that can interfere (5230)
self-concept mode: with the elderly's ability to reach Teaching: disease
personal self. their highest level of physical well- Acceptance: Health
process (5602)
being related to chronic disease
Anxiety Reduction
experience. State (1300)
(5820).

CONCLUSION
Nursing care, in light of Roy's theory, facilitated dialogue with the patient and his family in the
achievement of goals and the modification of behavior through the implementation of
interventions/activities. Gradually, the elderly patient evolved satisfactorily with adaptive behaviors.
One can also observe that the care implemented with the NP allowed us to act in a targeted way on the
adaptive problems of the elderly patient with rectal cancer and SIT, using a clinical judgment to improve
the patient’s quality of life.
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