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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) .
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).
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).
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.
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).
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
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
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).
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.
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
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).
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:
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
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.
c. Management of exudate
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.
3) Attention-diversion 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.
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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