Colon

Harold V. Jamorabon,MD

Embryology
GI tract develop during the 4th week of
gestatation
derived from endoderm and divided into 3
segments
Foregut
Midgut
Hindgut

 Midgut
small intestine, ascending colon, proximal
transverse colon
blood supply: Superior mesenteric artery

Hindgut
distal transverse colon, descending colon,
sigmoid, rectum, proximal 3rd of anus
blood supply: inferior meseteric artery

Anatomy

Disorder of Motility
1. Irritable bowel syndrome
2. Constipation
3. Diarrhea
4. Fecal Incontinence

Irritable bowel syndrome

Abnormal state of intestinal motility modified by psychosocial factors for

which no anatomic cause can be found.

SIGNS AND SYMPTOMS

Episodes of altered bowel function (constipation, diarrhea, or both)
occurring intermittently over a prolonged period of time with or without
abdominal pain.

DIAGNOSIS
History with symptoms exacerbated by physical or emotional stress; must
first exclude organic disease.

TREATMENT

Not a surgical disease

Reassurance, education, and medical treatment

Constipation
Definition
< 3 stools/week while consuming high-fiberr
diet.

Diagnosis:
By history; differentiate between acute
constipation (persistent change in bowel
habits for < 3 months), and chronic
constipation(persistent change in bowel habits
> 3 months).

CAUSES
Diet-related (fluid, fiber)

Lack of physical activity

Medications (especially opiates and anticholinergics)
Medical illness (irritable bowel syndrome, diabetes, hypothyroidism)
Depression
Neurologic disease (Parkinsons disease, multiple sclerosis)
Many other causes

TREATMENT
Short-term: Stool softeners; Fleets enema if suppository fails.
Long-term: After ruling out a treatable cause, encourage dietary
changes such as increasing fiber and fluid consumption.
If dietary changes fail, assess colonic transit time. Defecography or
anometry may prove helpful

Diarrhea

DEFINITION
Passage of > three loose stools/day.

Surgeons are likely to encounter diarrhea in post-op patients.

In the hospitalized patient, a workup may be indicated to rule out
infectious orischemic etiologies.
In the outpatient follow-up setting, diarrhea may occur due to extensive
small bowel resection (short bowel syndrome), due to disruption of
innervation, or even as an expected outcome (gastric bypass).
DIAGNOSIS
Stool sample for enteric pathogens and Clostridium difficile toxin.
Check stool for white blood cells (WBCs) (IBD or infectious colitis), red

blood cells
(RBCs) without WBCs (ischemia, invasive infectious diarrhea, cancer).

Fecal Incontinence

True incontinence:
Complete loss of solid stools

Minor incontinence:
Flatus or occasional soilage of undergarments from seepage

or urgency

SIGNS AND SYMPTOMS

Decreased resting tone and squeeze pressure on rectal examination; rule out

anorectal pathology such as hemorrhoids or rectal prolapse.

ETIOLOGY
Mechanical: Anal sphincter trauma (i.e., secondary to childbirth or
iatrogenic,
s/p fistulotomy for abscess or perianal fistula)
Systemic disease (scleroderma)
Fecal impaction
Neurogenic: Pudendal nerve injury

other

PSEUDOMEMBRANOUS COLITIS
Definition: An acute colitis characterized by formation of an adherent
inflammatory exudate (pseudomembrane) overlying the site of mucosal
injury.
Typically occurs after antibiotics, especially clindamycin, ampicillin, or
cephalosporins.
Due to overgrowth of Clostridium difficile.
Signs and symptoms: Vary from a self-limited diarrheal illness to invasive
colitis with megacolon or perforation as possible complications.
Diagnosis: Detection of C. difficile toxin in stool; proctoscopy or
colonoscopy if diagnosis uncertain.
Treatment: Stop offending antibiotic; give flagyl or vancomycin PO (if
patient unable to take PO, give flagyl IV).
Prognosis: High rate of recurrence (20%) despite high response rate to
treatment.

Radiation Induced
Associated with external radiation therapy (XRT) to pelvis usually for
endometrial, cervical, prostate, bladder, and rectal cancer
Risk factors: Atherosclerosis, diabetes, hypertension, old age,
adhesions from previous abdominal operation
Chance of developing disease is dose dependent:
< 4,000 cGy 0 patients
5,0006,000 cGy Some patients
> 6,000 cGy Most patients

Ischemic Colitis

Acute or chronic intestinal ischemia secondary to decreased intestinal perfusion or

thromboembolism:

INCIDENCE

Ninety percent of cases occur in patients > 60 years of age.

RISK FACTORS

Embolus or thrombus of the inferior mesenteric artery

Poor perfusion of mucosal vessels from arteriole shunting or spasm

Old age
s/p Abdominal aortic aneurysm (AAA) repair
Hypertension
Coronary artery disease
Diabetes
Adhesions from previous abdominal surgery
Underlying obstructive lesion of colon

SIGNS AND SYMPTOMS

Mild lower abdominal pain and rectal bleeding, classically after AAA
repair
Pain more insidious in onset than small bowel ischemia

 DIAGNOSIS
Clinical history; characteristically shows
thumbprinting on barium enema (but contrast
enema is contraindicated in the setting of suspected
bowel gangrene).

TREATMENT
If symptoms mild, observe;
if moderate (with fever and increased WBC), give IV
antibiotics;
if severe (with peritoneal signs), exploratory
laparatomy withcolostomy.

Management of Lower GI Bleeding

Angiodysplasia
most common vascular
lesion of GIT
degenerative lesion of
previously healthy blood
vessels
Loc: Cecum and proximal
ascending colon (75%)
Older population (65 and
above
2nd leading cause of of
lower GI bleeding

Diverticulosis
most common cause
of lower Gi bleeding
Descending colon
and sigmoid

Angiodysplasia vs Diverticulosis

Benign Tumor of the Colon

Colorectal Polyps
HISTOLOGIC TYPES
1. Inflammatory (pseudopolyp): Seen in UC
2. Lymphoid: Mucosal bumps containing intramucosal lymphoid
tissue;
no malignant potential
3. Hyperplastic: Overgrowth of normal tissue; no malignant potential
4. Adenomatous: Premalignant; are classified (in order of increasing
malignant
potential) as tubular (75%), tubulovillous (15%), and villous
(10%)
5. Hamartomatous: Normal tissue arranged in abnormal
configuration;
juvenile polyps, PeutzJeghers polyps

 DIAGNOSIS
Flexible endoscopy (sigmoidoscopy or
colonoscopy)
TREATMENT
Attempt colonoscopic resection if:
Pedunculated, well or moderately
well differentiated, no venous or lymphatic
invasion, invades only into
stalk, margins negative.
Otherwise, a segmental colon resection is
indicated.

Large Bowel Obstruction

Large Bowel Obstruction

Incidence: most commonly occurs in
elderly patients; much less common than
small bowel obstruction.
SIGNS AND SYMPTOMS
Abdominal distention
Cramping abdominal pain
Nausea, vomiting
Obstipation
High-pitched bowel sounds

Large Bowel Obstruction

3 most common causes
Adenocarcinoma (65%)
Stricture sec to diverticulitis (25%)
Volvulus (5%)

Diagnosis
Abdominal Xray upright and supine
Establish 8 to 12 hrs of obstipation
Barium Enema

Large Bowel Obstruction

TREATMENT
Correction of fluid and electrolyte
abnormalities.
NGT for intestinal decompression.
Broad-spectrum IV antibiotics (e.g., cefoxitin).
Relieve obstruction surgically (colonic
obstruction is a surgical emergency since a
nasogastric tube will not decompress the
colon)

Pseudoobstruction (Ogilvies
Syndrome
Massive colonic dilation without evidence
of mechanical obstruction thought to result
from an imbalance between
parasympathetic and sympathetic control
of intestinal motility.
INCIDENCE
More common in older, institutionalized
patients.

RISK FACTORS
Severe infection, recent surgery or trauma.

Pseudoobstruction (Ogilvies
Syndrome
SIGNS AND SYMPTOMS
Marked abdominal distention with mild
abdominal pain and decreased or absent
bowel sounds.

DIAGNOSIS
Abdominal radiograph with massive colonic
distention.
Check for free air under diaphragm with
upright chest x-ray (CXR).

Pseudoobstruction (Ogilvies
Syndrome
Exclude mechanical cause for obstruction with watersoluble contrast
enema and/or colonoscopy.
TREATMENT
1. NGT and rectal tube for proximal and distal decompression,
respectively.
2. Correction of electrolyte abnormalities.
3. Discontinue narcotics, anticholinergics, or other offending
medications.
4. Turn patient frequently and mobilize from bed.
5. Consider pharmacologic decompression with neostigmine (a
cholinesterase inhibitor).
6. If the cecal diameter is > 11 cm or if peritoneal signs develop, the
patient should undergo prompt exploratory laparotomy with
cecostomy or loop colostomy.

Volvulus
Types
Sigmoid Volvulus
Cecal Volvulus
Transverse colon Volvulus

Volvulus
Rotation of a segment of intestine about its
mesenteric axis
INCIDENCE
> 50% of cases occur in patients over 65.

RISK FACTORS
Elderly (especially institutionalized patients)
Hypermobile cecum secondary to incomplete fixation
during intrauterine development (cecal volvulus)

SIGNS AND SYMPTOMS

Same as other causes of large bowel obstruction.

 DIAGNOSIS
Abdominal films: Markedly dilated sigmoid
colon or cecum with a kidney bean
appearance
Barium enema: Characteristic birds beak at
areas of colonic narrowing

 TREATMENT
Cecal volvulus: Right hemicolectomy if vascular
compromise; cecopexy otherwise adequate
(suturing the right colon to the parietal peritoneum)
Sigmoid volvulus:
Sigmoidoscopy with rectal tube insertion to decompress the
volvulus.
Emergent laparotomy if sigmoidoscopy fails or if
strangulation or
perforation is suspected.
Elective resection at a later date to prevent recurrence (40%
of cases recur after nonoperative reduction).

Polyposis Syndrome of the Bowel

Familial Polyposis Syndrome

Polyposis Syndrome of the Bowel

Hereditary, Non polyposis

Colorectal cancer
much more common than FAP
Autosomal dominant
four gene mutation idetified

90% of carriers will develop colon cancer

increase incidence of adenocarcinoma in the ovary,
endometrium, and stomach

Poorly differentiated, highly aggresive mucin

producing adenocarcinoma
Management:
screening for gene mutation in patient with strong
family history

Amsterdam Criteria
Amsterdam I
At least 3 family must have histologically confirmed
colorectal cancer
one must be first degree relative of the two
At least 2 consecutive generations must be affected
At least one of the CRC cases must be diagnosed
before age 50
familial adenomatous polyposis must be excluded

Amsterdam II
At least 3 family members must have a cancer
associated with HNPCC (
colorectal,endometrial,urothelial and small bowel)

Risk factors
Age > 50
Personal history of resected colon
cancer or adenomas
Family history of colon cancer or
adenomas
Low-fiber, high-fat diet
Inherited colorectal cancer
syndrome (familial adenomatous
polyposis
[FAP], hereditary nonpolyposis
colon cancer [HNPCC])
Long-standing UC or Crohns
disease

Diagnosis

Biopsy of the Lesion + Full Colonoscopy

CXR
CT scan to the abdomen and pelvis
CEA level

Treatment
Surgical resection
Goal is to remove primary tumor along with
lymphatics draining involved bowel.
Involves at least a 2-cm margin both proximally and
distally (traditionally requires a 5-cm margin).