A.

Introduction

Colon cancer afflicts more than 135,000 patients per year in America. It kills
more than 55,000 patients per year and many more patients suffer morbidity from
curative colon cancer surgery or chemotherapy. Recently promulgated screening and
surveillance colonoscopy regimens, as recommended by medical professional societies
(including the American Gastroenterological Association, the American Society for
Gastrointestinal Endoscopy, the American College of Gastroenterology, and the
American Cancer Society, and as approved by Medicare and most private medical
insurance companies for reimbursement, can largely avoid this morbidity by
colonoscopic removal of premalignant polyps, and can largely prevent this mortality by
early detection of colon cancer at a curable stage (Jemal 2004).

Yet only about one quarter of eligible patients currently undergo any form of colon
cancer screening. This failure tragically results in tens of thousands of preventable deaths
and even greater morbidity per annum in America. Aside from patient reluctance to
undergo colonoscopy because of the invasiveness, risks, and discomfort of the test, a
major factor in this breakdown is the failure by primary care physicians and internists to
educate their patients and refer them for screening colonoscopy. Contrariwise, primary
care physicians and internists occasionally refer patients who are inappropriate
candidates for screening colonoscopy because of age less than 50 years, a negative
screening colonoscopy within the past decade, or severe medical comorbidity and a poor
prognosis. Education of primary care physicians and internists, who can in turn educate
their patients, should eliminate these barriers to mass screening and optimize referral for
colonoscopyn (Nelson, 2003).

B. Defenition

Colorectal cancer is caused by the abnormal growth of epithelial cells which form
the lining of the colon or rectum. These small growths (known as polyps) are often
benign, although some have the potential to develop and become cancerous. It is
estimated that up to two thirds of colorectal polyps are pre-malignant and associated with
a risk of colorectal cancer (Levin B et al, 2008).

Colon cancer: Cancer that forms in the tissues of the colon (the longest part of the
large intestine). Most colon cancers are adenocarcinomas (cancers that begin in cells that
make and release mucus and other fluids) (National cancer institute, 2014) .

C. Anatomy and physiology

The large intestine is so called because of its ability to distend. It forms a three-
sided frame around the small intestine leaving its inferior area open to the pelvis. It is
designed to absorb water from the contents of the small intestine that pass into it.
Although the small intestine absorbs some water this process is intensified in the large
intestine until the familiar semisolid consistency of faeces is achieved. The large intestine
is approximately 1.5 m in length and extends from the ileum to the anus. Its size
decreases gradually from the caecum, where it is approximately 7 cm in diameter, to the
sigmoid, where it is approximately 2.5 cm in diameter (Keshav, 2003).

The large intestine has four segments: the caecum, colon, rectum and anal canal.
The colon is divided into four sections: the ascending colon, transverse colon,
descending colon and sigmoid colon. The large intestine also houses a variety of bacteria.
These bacteria, known as commensals, live happily in the bowel and generally do not
cause any problems. In fact, they play an important part in digestion they ferment
carbohydrates and release hydrogen, carbon dioxide and methane gas. The bacteria also
synthesise a number of vitamins such as vitamin K and some B vitamins. They are also
responsible for breaking down the bilirubin into urobilinogen, which gives the faeces its
characteristic brown colour.

However, outside the bowel the bacteria can cause illness and even death. The
blood supply to the large intestine is mainly by the superior and inferior mesenteric
arteries. The internal iliac arteries supply the rectum and anus. Venous drainage is mainly
by the superior and inferior mesenteric veins, and the rectum and anus are drained by the
internal iliac veins. The nerves supplying the large intestine are via the sympathetic and
parasympathetic nerves. The external anal sphincter is under voluntary control and is
supplied by motor nerves from the spinal cord (Siegfried 2002; Ellis 2004).

The small intestine terminates at the posteromedial aspect of the caecum. The
caecum is fixed to the right side near the iliac crest. At the opening to the caecum there is
a fold of mucous membrane known as the ileocaecal valve, which allows the passage of
materials from the small intestine into the large intestine and prevents the reflux of
contents from the colon back into the ileum. The contents of the colon are heavily
colonised by bacteria whereas the small intestine is relatively free of microbes. The
caecum is a dilated portion and has been described as a blind pouch approximately 6 cm
in width and 8cm in length. It is continuous with the ascending colon superiorly and has
a blind end inferiorly. Attached to the caecum is a coiled tube closed at one end called the
vermiform appendix. It is usually 813 cm in length although this can vary from 2.5 cm
to 23 cm and has the same structure as the walls of the colon; however, it contains more
lymphatic tissue (Moore & Dalley 1999).

The ascending colon is approximately 15 cm long and joins the caecum at the
ileocaecal junction. The ascending colon is covered with peritoneum anteriorly and on
both sides, however, its posterior surface is devoid of peritoneum. It ascends on the right
side of the abdomen to the level of the liver where it bends acutely to the left. At this
point it forms the right colic or hepatic flexure and then continues as the transverse colon
(Thibodeau & Patton 2002).

Transverse colon, This is a loop of colon approximately 45 cm long that continues

from the left hepatic flexure across to the left side of the abdomen to the left colic
flexure. It passes in front of the stomach and duodenum and then curves beneath the
lower part of the spleen on the left side as the left colic or splenic flexure and then passes
acutely downward as the descending colon (Watson 2000).
 Descending colon, This section of the colon passes downwards on the left side of
the abdomen to the level of the iliac crest. It is approximately 25 cm in length. The
descending colon is narrower and more dorsally situated than the ascending colon.

The sigmoid colon begins near the iliac crest and is approximately 36 cm long. It
ends at the centre of the mid-sacrum, where it becomes the rectum at about the level of
the third sacral vertebra. It is mobile and is completely covered by peritoneum and
attached to the pelvic walls in an inverted V shape.

The rectum is approximately 13 cm in length and begins where the colon loses its
mesentery. It lies in the posterior aspect of the pelvis and ends 23 cm anteroinferiorly to
the tip of the coccyx, where it bends downwards to form the anal canal (Tortora &
Grabowski 2002).

Anal canal, This is the terminal segment of the large intestine and is approximately
4 cm in length opening to the exterior as the anus. The mucous membrane of the anal
canal is arranged in longitudinal folds that contain a network of arteries and veins. The
anus remains closed at rest. The anal canal corresponds anteriorly to the bulb of the penis
in males and to the lower vagina in females and posteriorly it is related to the coccyx.

The internal anal sphincter is composed of smooth muscle and is the lower of the
two sphincters. It is about 2.5 cm long and can be palpated during rectal examination. It
controls the upper two-thirds of the anal canal. The external sphincter is made up of
skeletal muscle and is normally closed except during elimination of faeces. The nerve
supply is from the perineal branch of the fourth sacral nerve and the inferior rectal
nerves (Martini 2004).

D. Etiology and Risk Factors

There are several risk factors that may increase the chance of an individual
developing colorectal cancer (American Cancer Society, 2011).

Risk factors:

Family history:A persons risk doubles if a direct relative has previously had
the disease. There is an even greater risk if more than one relative has had
colorectal cancer.

Genetics:Individuals with inherited disorders such as familial adenomatous

polyposis (FAP), where an individual is prone to polyp formation, have a
higher risk of developing colorectal cancer.

Colorectal polyps or inflammatory bowel diseases:A history of polyps or

inflammatory bowel disease, where the bowel is inflamed for many years,
increases the risk of colorectal cancer.
 Age:Although a person can develop colorectal cancer at any age, the risk
increases greatly with age. Over 90% of colorectal cases are diagnosed in
patients over the age of 50.

Lifestyle: A sedentary lifestyle is associated with a higher risk of colorectal

cancer. Studies have also linked obesity, lack of exercise, smoking and
excessive alcohol consumption to a greater risk of colorectal cancer.

Potential protective agents: Non-steroidal anti-inflammatory drugs (NSAIDs),

such as aspirin, have been associated with a reduced risk of colorectal cancer.
A healthy, fibrecontaining diet and hormone replacement therapy in women
are also possible protective factors.

E. Pathophysiology

Colon cancer arises from mucosal colonic polyps. The critical parameter of
polyps in terms of natural history, particularly malignant potential, is histology. The
two most common histologic types are hyperplastic and adenomatous. Histologically,
hyperplastic polyps contain an increased number of glandular cells with decrease
cytoplasmic mucus, but lack nuclear hyperchromatism, stratification, or atypia (Tsai
CJ, 1995).

Adenomatous nuclei are usually hyperchromatic, enlarged, cigar-shaped, and

crowded together in a palisade pattern. Adenomas are classified as tubular or villous.
Histologically, tubular adenomas are composed of branched tubules, whereas villous
adenomas contain digitiform villi arranged in a frond. Tubulovillous adenomas
contain both elements. Virtually all colon cancers arise from adenomas as
demonstrated by multiple epidemiologic, clinical, and pathologic findings. First,
about one third of operative specimens containing colon cancer contain one or more
synchronous adenomas, a significantly higher rate than in age-matched controls
without colon cancer. Second, the risk of colon cancer markedly increases with
increasing number of adenomatous polyps (Rubin CE, 2003).

Third, adenomatous tissue is frequently found contiguous to frank carcinoma.

Fourth, patients with familial adenomatous polyposis (FAP), who have hundreds or
thousands of adenomatous colonic polyps, inevitably develop colon cancer if
colectomy is not performed. Fifth, patients who refuse polypectomy for adenomas
develop colon cancer at a rate of about 4% after 5 years and 14% after 10 years. This
adenoma-to-cancer sequence is supported by recent findings about the molecular basis
of colon cancer, as described later. A relationship between hyperplastic polyps and
colon cancer is controversial. Hyperplastic polyps may increase slightly the risk of
colon cancer, but the effect is small (Higuchi, 2004).

Risk factors for malignancy in hyperplastic polyps include large polyp size (>1
cm diameter); location in the right colon; a focus of adenoma within the polyp (mixed
hyperplasticadenomatous polyp); occurrence of more than 20 hyperplastic polyps in
the colon; a family history of hyperplastic polyposis; and a family history of colon
cancer. Serrated polyps sometimes previously classified as a type of hyperplastic
polyp may, like adenomas, be a significant risk factor for colon cancer. Serrated
polyps, unlike ordinary hyperplastic polyps, tend to be large and to occur in the right
colon . The colonocytes in these polyps frequently have BRAF genetic mutations and
DNA methylation (Wynter CV, 2004).

Molecular pathogenesis

History of recent molecular advances Colon cancer is probably the best

understood complex (multistep) cancer in terms of molecular genetics. A brief history
helps summarize and place in perspective the recent, revolutionary advances in the
molecular basis of colon cancer. Investigation of the pathogenesis of two uncommon
familial colon cancer syndromes, FAP and hereditary nonpolyposis colon cancer
(HNPCC), led to dramatic breakthroughs in understanding the molecular basis of the
more common sporadic (nonsyndromic) form of colon cancer. The clinical genetics
and clinical phenotype of FAP was described during the last two centuries: patients
with FAP develop hundreds or thousands of adenomatous polyps throughout the colon
beginning after puberty and inevitably develop colon cancer (Wynter CV, 2004)

This syndrome is inherited as a classic mendelian autosomal-dominant single

gene. During the past two decades FAP was shown to be caused by germline mutation
of the adenomatous polyposis coli (APC) gene located on chromosome 5q. A patient
with FAP carries this germline mutation in one allele in all somatic cells, including
colonocytes. This mutation underlies the development of hundreds of adenomatous
polyps throughout the colon; colonic adenomas form when the second APC allele is
damaged or lost in a colonocyte. The clinical genetics and clinical phenotype of
HNPCC were characterized during the twentieth century.

In HNPCC multiple cases of colon cancer, without gastrointestinal polyposis,

occur within a family. Colon cancer typically occurs in the right colon beginning as
sessile polyps in middle age. The Amsterdam Criteria, as recently modified by the
Amsterdam II Criteria, are used clinically to diagnose HNPCC. These criteria include
all the following: three or more relations with colon cancer, one of whom is a
firstdegree relative of the other two; colon cancer involving at least two generations in
the family; and at least one colon cancer diagnosed before age 50 years. During the
past 15 years, HNPCC was shown to be caused by mutations of one of the mismatch
repair genes, including hMSH2, hMSH6, hMLH1, hMLH3, hPMSI, and hPMS2.
Germline mutations of the hMLH1 and hMSH2 genes account for most of the cases.
Mismatch repair enzymes, encoded for by mismatch repair genes, normally recognize
errors in nucleotide matching of complementary chromosome strands and initiate
segmental excision of the newly synthesized strand to ensure faithful strand
replication.

Cells with mismatch repair gene mutations cannot repair spontaneous DNA
errors and progressively accumulate mutations throughout the genome with
succeeding DNA replications. This progressive accumulation leads to genetic
hypermutability and chaos; mutations accumulate in oncogenes and tumor suppressor
genes that can result in colon cancer. Mismatch repair gene mutation is detected as
microsatellite instability, in which errors occur in simple DNA repetitive sequences,
such as in poly-A or CA-tandem repeating sequences (Robbins DH, 2002).

Molecular biology

These breakthroughs provided not only the molecular basis of syndromic

hereditary colon cancer but also of sporadic colon cancer. Colon cancer is believed
caused by a cascade of genetic mutations leading to progressively disordered local
DNA replication and accelerated colonocyte replication. The progressive
accumulation of multiple genetic mutations results in the transition from normal
mucosa to benign adenoma to severe dysplasia to frank carcinoma .

Mutations of the mismatch repair genes are believed to account for about 15%
of sporadic colon cancers. APC mutation is believed to account for about 80% of
sporadic colon cancers. Spontaneous somatic APC mutation in colonocytes is
believed to underlie, the development of sporadic adenomatous polyps. APCgene
mutations occur early in adenoma development and are often found in aberrant crypt
foci, the earliest identifiable dysplastic crypts. APC mutations are found in about 50%
of sporadic adenomas (Suraweera N, 2002).

Adenomas usually remain benign.Malignant transformation requires further

genetic alterations. TheDCC(deleted in colon cancer) gene encodes for a neural cell
adhesion molecule receptor and normally promotes apoptosis and suppresses tumors.
Loss of the normalDCCgene is believed to be important in the transition from an
intermediate to a late adenoma. Its role in this transition is supported by its frequent
allelic deletion during this transformation.

The normalp53gene product arrests the cell cycle following DNA injury to
permit either DNA repair if the damage is correctable, or apoptosis if the damage is
too severe. The wild-type p53 protein product is up-regulated after cell stress from
radiation exposure, DNA injury, or other noxious events to prevent new DNA
synthesis and halt cell division. Loss of p53 function can promote genomic instability
as genetic errors are replicated without check, resulting in loss of heterozygosity.
Mutation of thep53geneis believed to be important in the transition from late adenoma
to frank carcinoma. About 50% of lesions with high-grade dysplasia and about 75% of
frank cancers exhibit loss of normalp53function, usually from a missense point
mutation of one allele and deletion of the other, wild-type, allele (Brenner DA, 2004).

The K-rasgene encodes for a protein involved in signal transduction from the
cell membrane to the nucleus. Specific mutations of this gene result in constitutive
activation of this signal pathway and increased colonocyte replication. These
mutations are associated with exophytic growth of adenomas in the transition to
carcinoma. About 50% of colon cancers have K-rasmutations (Yashiro M, 2001).
 The accumulation of genetic mutations leads to genetic instability, manifested
by loss of heterozygosity. Loss of heterozygosity accelerates carcinogenesis. Cells
with loss of heterozygosity have one, instead of thenormal two, alleles of some genes
because of loss of individual chromosomes during mitosis. A tumor suppressor gene is
more likely to lose normal function when only one allele is present after loss of
heterozygosity. Only one, rather than two, allelic mutations are then required for loss
of its function. DNA methylation at the promotor region can terminate and silence
gene expression without DNA mutation.

In particular, DNA methylation can inactivate suppressor genes, thereby

promoting cancer. Colon cancer is sometimes associated with methylation and
inactivation of p14, normally an upstream inducer of thep53tumor suppressor
pathway. This occurs in about 25% of colon cancers. The inactivation produces the
same cancer henotype as mutation of the tumor suppressor genep53. Methylation of
the tumor suppressor genep16, designatedCDKN2A, occursin about 35% of colon
cancers (Kanazawa, 2002)

F. Symptoms and diagnosis

Early diagnosis of colorectal cancer has the potential to improve survival rates;
however early symptoms (such as abdominal pain) may be confused with other
diseases, meaning many patients have advanced disease when diagnosed. Almost
85% of patients referred to hospital have one or more of the following high-risk
symptoms(John SKP, 2011; Henley SJ et al, 2010) :

Rectal bleeding

A mass in the abdomen or rectum

Change in bowel habit

Perianal symptoms, such as abscesses or lesions

As the cancer becomes more advanced, other symptoms can develop. For
example, excessive bleeding from the colon can cause anaemia, which leaves the
patient feeling breathless and tired. If the cancer begins to obstruct the colon, further
symptoms include bloating, constipation and vomiting (NHS UK bowel cancer
symptoms, 2011).

Methods of diagnosis vary from country to country but typically if a patient

presents high-risk symptoms to their doctor they will be given a physical examination.
If this raises any concerns, a number of additional tests may be performed:

Colonoscopy the entire length of the colon is viewed using a colonoscope.

Sigmoidoscopy a small tube (sigmoidoscope) is used to view the lower colon.

 Double contrast barium enema x-rays of the colon and rectum. Barium lines the
colon allowing an outline to be viewed in an x-ray.A biopsy, where sample tissue is
removed during a colonoscopy or sigmoidoscopy, is required to confirm the
diagnosis of colorectal cancer and determine how advanced the disease is (staging)
(eMedicine, 2011).

Staging determines how advanced the cancer is and whether it has spread to
other parts of the body. It helps to identify the most appropriate treatment options for
the patient. Staging in colorectal cancer can be confirmed by:

Blood tests to look for tumour markers

Biopsies, analysing tissue samples taken during a colonoscopy or sigmoidoscopy

Imaging tests (CT scans, chest x-rays, ultrasound, MRI scans)

Surgery. The most common staging for colorectal cancer is defined by the tumour,
node, metastasis (TNM) staging system, which classes a patient into stages I-IV
according to the level of invasion or spread of the tumour to other organs
(metastasis). Using the TNM staging, the progression of the original primary tumour
is denoted by the letter T (tumour); N (node) indicates whether the tumour has
spread to lymph nodes; M (metastasis) represents whether the tumour has
metastasised to distant organs in the body, most commonly the liver or lungs. T, N
and M are followed by numbers giving further information on the stage of the
disease: increasing numbers signify later stages. Early-stage disease (stage I and II)
describes a tumour that has not yet spread to the lymph nodes or other distant areas
in the body. With early-stage disease there is the chance of cure if the tumour can be
successfully surgically removed. When cancer spreads from the original site,
affecting the lymph nodes (stage III) or other parts of the body (stage IV), treatment
becomes more difficult(AJCC, 2010; Frederick LG et al, 2010; American Cancer
Society Colorectal Cancer Guide, 2011).

G. Treatment

Treatment options for patients vary and are assessed taking into account the
following variables: Tumour size, Stage of diagnosis, The location of the tumour in
the colon or rectum, The risk of the cancer returning, The physical health of the
patient. In general the current treatment options for colorectal cancer are surgery,
chemotherapy, and biological therapies. Radiotherapy is not often used to treat
metastatic colorectal cancer due to sideeffects, although it can be used after surgery to
destroy any residual cancer cells (American Cancer Society Colorectal Cancer Guide,
2011).

Surgery
 The majority of patients with early-stage colorectal cancer will undergo
surgery to remove as much of the tumour as possible in a procedure known as
resection. Any areas surrounding the cancerous tissue and nearby lymph nodes will
also be removed to reduce the risk of the cancer spreading. Resection is also a
treatment option for some patients with later stage disease, particularly when the
cancer has metastasised to the liver. A less invasive procedure known as laparoscopic
resection, where the affected area of the colon is removed through keyhole surgery,
can also be performed on patients with early-stage colorectal cancer (Labianca R et al,
2010).

Chemotherapy

Patients diagnosed with advanced disease are usually treated with

chemotherapy after surgery, known as first-line treatment. Bevacizumab was
approved by the FDA in February 2004 for use in metastatic colorectal cancer when
used with standard chemotherapy treatment (as first-line treatment) and with 5-
fluorouracil-based therapy for second-line metastatic colorectal cancer. This
recommendation was based on the E3200 trial addition of bevacizumab to
oxaliplatin/5-FU/leucovorin (FOLFOX4) therapy. Bevacizumab is a recombinant
humanizedmonoclonal antibody that blocks angiogenesis by inhibiting vascular
endothelial growth factor A(VEGF-A).VEGF-A is a chemical signal that stimulates
angiogenesis in a variety of diseases, especially in cancer (Los, M., 2007).

Bevacizumab administered in combination with 5-fluorouracil/leucovorin-

based chemotherapy 2860 days after primary cancer surgery caused no increased risk
of wound healing complications compared with chemotherapy alone. While wound
healing complications were increased in patients who had major surgery during
bevacizumab therapy, the majority of bevacizumab-treated patients experienced no
complications (FRANK A, 2005).

Wound cancer management

Literature on the treatment of malignant wounds focuses on controlling

infection and odor, managing exudate and protecting surrounding skin, minimizing
bleeding, reducing pain, and optimizing the emotional welfare of the patient and
family ( Wilson, 2005).

a. Wound cancer irigation

For irigation cancer wound, practicioner can use lavage with an antibiotic
solution, including gentamicin (240 mg) and clindamycin (600 mg) dissolved in
500 mL normal saline. During this lavage, the solution allowed to sit in the
abdominal cavity for 3 minutes.

b. Infection and odor control.

 Infection and odor control is achieved by managing local bacterial colonization
with wound cleansing and debridement and the use of local antimicrobial agents.
Wound cleansing reduces odor by removing necrotic debris and decreasing
bacterial counts. If the lesion is not friable and the patient is able, the wound may
be cleansed in the shower. You can using mesalt dressing or metronidazole gel
0.75-0.8%. Topical therapy is available by crushing metronidazole tablets in
sterile water and creating either a 0.5% solution (5 mg/cc) or a 1% solution (10
mg/cc

c. Management of exudate

Because inflammation and edema are commonly present in these wounds,

there tends to be significant exudate. Dressings should be chosen to conceal and
collect exudate and odor. It is essential to use dressings that contain exudate
because a patient who experiences unexpected drainage on clothing or bedding
may experience significant feelings of distress and loss of control. Seaman
suggests nonadherent contact layers, such as Vaseline gauze, for the primary
dressing on the wound bed, covered with soft, absorbent dressings, such as gauze
and abdominal pads, for secondary dressings to contain drainage. Dressings are
changed one to two times daily based on the amount of exudate and odor
(Seaman, 2002).

d. Control of bleeding

The viable tissue in a malignant wound may be very friable and bleed with
minimal manipulation. In addition, cancer patients may have coagulation defects
related to their disease and or treatments that increase their risk of bleeding
Prevention is the best method for controlling bleeding. This involves gentle
dressing removal and the use of nonadherent dressings or moist wound products.
When dressings adhere to the wound on removal, they should be soaked away
with normal saline to lessen trauma. If bleeding does occur, applying direct
pressure for 10 to 15 minutes is the first intervention. Local ice packs may also
assist in controlling bleeding. Gauze saturated with topical vasoconstrictors such
as epinephrine or cocaine may control bleeding, but the patient should be
monitored for systemic effects of these drugs.

e. Pain management

There are several types of pain associated with malignant wounds: deep pain,
neuropathic pain, and superficial pain related to procedures.

1) Psychological approaches to pain management

Personal beliefs and appraisals, emotional reactions, coping behaviours and

social contextual factors are the primary targets of psychological interventions.

2) Coping skills training

 Coping skills training teaches patients cognitive and behavioural skills to
manage pain, reduce distress, enhance their perceptions of control over pain
and promote an active self-management approach. Coping skills can be
broadly grouped into attention-diversion techniques and cognitive coping
strategies.

3) Attention-diversion strategies

Attention-diversion involves redirecting attention to competing external or

internal stimuli, and strategies may include relaxation training, diaphragmatic
breathing, guided imagery, self-hypnosis, mindfulness meditation and
distracting thoughts and activities. Engaging in meaningful and stimulating
activities, for example talking to friends, listening to music and going out, can
reduce awareness of pain. (Hanson, 1990)

4) Cognitive coping strategies

Using methods drawn from cognitive therapy, patients are taught how to
identify and change unhelpful or negative thoughts (cognitive restructuring)
that contribute to psychological distress and facilitate more adaptive coping
thoughts that reduce distress and enhance other coping efforts.

5) Pain Management Programmes

Pain Management Programmes (PMPs) based on cognitive and behavioural

principals are the treatment of choice for people whose persistent pain
adversely affects their quality of life. A PMP aims to improve the physical,
psychological, emotional and social dimensions of a persons quality of life,
working towards achieving optimal functioning and self-reliance in managing
persistent pain. Pain relief is not a primary goal, although improvements in
pain have been reported . PMPs consist of education and guided practice.
Education includes information on on the principles and rationales of
treatment, pain physiology, the psychological aspects of pain, exercise and
improving function, and self-management of pain problems. The emphasis,
however, is upon guided practice in the use of physical, psychological and
practical methods to improve quality of life (e.g. exercise to improve fitness
and mobility, a gradual return to goal-defined activities, cognitive therapeutic
methods to identify and challenge appraisals, beliefs and processing biases,
relaxation and distraction techniques, and communication skills). (The British
Pain Society, 2007; Morley, 1999; Van Tulder, 2000; Guzman, 2001)

H. Client Prognosis

Now, client had colorectal cancer stadium 4 with no blader and part of colon.
Cancer cel has metastase until lung its means metastasic cancer cannot be treated with
surgery (unrectable cancer). The treatment possible to do for patient is consist for
debridement surgery, woun toilet, cemotherapy, taregeted terapy or combination of
 these techniques. Client ever underwent chemotherapy and rediation but not have
result and know client had prescription for fluorouracil (5-FU). This is standard
treatment for metastatic stage IV colorectal cancer. 5-FU is typically administered
with leucovorin, a drug that is similar in structure and function to the essential vitamin
folic acid. If 5-FU LV cant help to kill cancer cel maybe we can suggest to addition
target therapies like as bevacizumab c to blocking VEGF. Know client has show sign
of side effect of the treatment like anemia, hair loss, pain and weight loss so the
treatment is for improve quality of life.

I. Summary

In this case, client has shows sign and symptom about cancer colorectal. First
sign that patient felt is abdominal pain and uterus inflamation. That is not uterus
inflamation but metastation of cels cancer to uterus so total histerectomy should
performed. Metastasis in this client body very quick, 1 year later patient should
underwent blader and part of colon operation.

Problem that client have now is spreading metastasis to all organs. The
metastasis made wound isnt healing, pain still felt, discharge still out. So, nursing
management and treatment just for supporting quality of life patient such as
controlling infection and odor, managing exudate and protecting surrounding skin,
minimizing bleeding, reducing pain and treatment side effect of chemoterapy. Medic
treatment is just chemoterapy with target cell.

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