DEFINITION

Herniation of the mucosa through the muscular layers of the bowel wall at sites where arterioles penetrate, forming small outpouchings or diverticula.

Are generally numerous, collectively referred to as diverticulosis. Diverticulitis refers to the inflammation of diverticula.

INCIDENCE

> 50% of Americans over 70 years of age. Men and women equally affected. Sigmoid colon most commonly involved with progressively

decreasing frequency of involvement as one proceeds proximally.

RISK FACTORS

1. Old age

2. Low-fiber diet

SIGNS AND SYMPTOMS/Diverticulosis

1. 80% of patients are asymptomatic.

2. Massive, painless lower GI bleeding is classic (notably absent in diverticulitis).

SIGNS AND SYMPTOMS/Diverticulitis

1. Persistent abdominal pain initially diffuse in nature that often becomes localized to the left lower quadrant (LLQ) with development of peritoneal signs.

2. LLQ and/or pelvic tenderness.

3. Ileus/abdominal distention.

4. Anorexia, nausea, vomiting, and change in bowel habits (usually constipation).

5. Large bowel obstruction.

6. Fever.

7. Elevated WBC.

DIAGNOSIS/Diverticulosis

1. Characteristic history and physical exam

2. Confirmed by diverticula identified on CT/barium enema and/or colonoscopy.

Treatment:

1. High-fiber diet

2. Stool softeners.

DIAGNOSIS/Diverticulitis1. Characteristic history and physical exam.

2. Elevated WBCs.

3. CT scan (test of choice):

A. Pericolonic inflammation

B. With or without abscess formation.

4. Barium enema and colonoscopy may induce perforation and are contraindicated in the acute setting but should be obtained in follow-up.

5. Abdominal x-ray:

A. Ileus

B. Distention

C. And/or free intraperitoneal air.

TREATMENT

Uncomplicated diverticulitis:

1. Outpatient management:

A. Clear liquid diet

B. PO antibiotics

C. And nonopioid analgesics with close follow-up.

2. Follow-up includes :

A. Colonoscopy

B. Dietary recommendations once acute infection has subsided.

TREATMENT

3. If outpatient therapy fails, admit for:A. IV antibiotics B. IV hydration with bowel rest.C. Nasogastric tube (NGT) is placed when there is evidence of ileus or

small bowel obstruction (SBO), with nausea and vomiting.

TREATMENT The Hinchey staging system is often used to describe the severity of

complicated diverticulitis:

1. Stage I includes colonic inflammation with an associated pericolic abscess.

2. Stage II includes colonic inflammation with a retroperitoneal or pelvic abscess.

3. Stage III is associated with purulent peritonitis.

4. Stage IV is associated with fecal peritonitis. Stage I and II are treated by:

1. IV antibiotics

2. CT-guided aspiration.

TREATMENT

If the abscess is inaccessible to drainage and not responding to antibiotics, then it is treated surgically:

1. Drainage with Hartmann pouch

2. Or sigmoid colectomy. Stage III and IV need operative management:

1. In the emergent setting, a Hartmann’s procedure is usually performed (i.e., resection with proximal colostomy and distal pouch with reversal later—two-stage procedure).

TREATMENT

2. If patient is very unstable, then a diverting colostomy may be performed.

3. Elective resection of affected bowel must be considered in the patient who has recurrent episodes of diverticulitis requiring treatment.

4. All patients with diverticulitis must undergo a full colonoscopy 4–6 weeks after the attack to rule out malignancy, as sometimes colonic malignancy presents as diverticulitis.

PROGNOSIS

One third of patients remain asymptomatic One third have episodic pain One third progress to have a recurrence.

DEFINITION GI bleeding distal to the ligament of Treitz. LGIB is considered massive when the patient requires 3 or more units

of blood within 24 hours. Most common causes are diverticulosis and angiodysplasia. Other causes include:

1. Cancer

2. IBD

3. Ischemic colitis

4. Hemorrhoids Anticoagulation treatment increases the risk for LGIB.

MANAGEMENT

INCIDENCE

Most commonly occurs in elderly patients Much less common than small bowel obstruction.

SIGNS AND SYMPTOMS

1. Abdominal distention

2. Cramping abdominal pain

3. Nausea

4. Vomiting

5. Obstipation

6. High-pitched bowel sounds.

DIAGNOSIS

1. Supine and upright abdominal films:

A. Distended proximal colon

B. Air fluid levels

C. And no distal rectal air.

2. Establish 8- to 12-hour history of obstipation

3. Passage of some gas or stool indicates partial small bowel obstruction, a nonoperative condition.

4. Barium enema: May be necessary to distinguish between ileus and pseudo-obstruction.

TREATMENT

1. Correction of fluid and electrolyte abnormalities.

2. Nasogastric tube for intestinal decompression (as gastric emptying is reflexly inhibited).

3. Broad-spectrum IV antibiotics (e.g., cefoxitin).

4. Relieve obstruction surgically (colonic obstruction is a surgical emergency since a nasogastric tube will not decompress the colon).

DEFINITION

Rotation of a segment of intestine about its mesenteric axis Characteristically occurs in the sigmoid colon (75% of cases) or

cecum (25%).

INCIDENCE

More than 50% of cases occur in patients over 65.

RISK FACTORS

1. Elderly (especially institutionalized patients).

2. Chronic constipation.

3. Pyschotropic drugs.

4. Hypermobile cecum secondary to incomplete fixation during intrauterine development (cecal volvulus).

SIGNS AND SYMPTOMS

See Large Bowel Obstruction.

DIAGNOSIS

1. Clinical presentation.

2. Abdominal films: Markedly dilated sigmoid colon or cecum with a “kidney bean” appearance.

3. Barium enema: Characteristic “bird’s beak” at areas of colonic narrowing.

TREATMENT Cecal volvulus:1. Right hemicolectomy if vascular compromise2. Cecopexy otherwise adequate (suturing the right colon to the

parietal peritoneum). Sigmoid volvulus: 1. Sigmoidoscopy with rectal tube insertion to decompress the

volvulus.2. Emergent laparotomy if sigmoidoscopy fails or if strangulation or

perforation is suspected.3. Elective resection in same hospital admission to prevent recurrence

(nearly 50% of cases recur after nonoperative reduction).

DEFINITION

Massive colonic dilation without evidence of mechanical obstruction.

INCIDENCE

More common in older, institutionalized patients.

RISK FACTORS

1. Severe infection

2. Recent surgery

3. Trauma

SIGNS AND SYMPTOMS

1. Marked abdominal distention

2. Mild abdominal pain

3. Decreased or absent bowel sounds.

DIAGNOSIS

1. Abdominal radiograph with massive colonic distention.

2. Exclude mechanical cause for obstruction with water-soluble 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. Consider pharmacologic decompression with neostigmine (a

cholinesterase inhibitor).5. If peritoneal signs develop, the patient should undergo prompt

exploratory laparotomy to treat possible perforation.6. Refractory cases may need total colectomy.

Hemorrhoids

Prolapse of the submucosal veins located in the left lateral, right anterior, and right posterior quadrants of the anal canal.

Classified by type of epithelium:

1. Internal if covered by columnar mucosa (above dentate line)

2. External if covered by anoderm (below dentate line)

3. And mixed if both types of epithelia are involved. Incidence: Male = female.

Hemorrhoids

Risk factors:

1. Constipation

2. Pregnancy

3. Increased pelvic pressure (ascites, tumors)

4. Portal hypertension. Diagnosis:

1. Clinical history

2. Physical exam

3. Visualize with anoscope.

Anal Fissure

Painful linear tears in the anal mucosa below the dentate line Induced by constipation or excessive diarrhea.

SIGNS AND SYMPTOMS

1. Pain with defecation.

2. Bright red blood on toilet tissue.

3. Markedly increased sphincter tone and extreme pain on digital examination.

4. Visible tear upon gentle lateral retraction of anal tissue.

DIAGNOSIS

1. History 2. Physical exam.

TREATMENT

1. Sitz baths.

2. Fiber supplements, bulking agents.

3. Increased fluid intake.

4. If nonsurgical therapy fails, options include:

A. lateral internal sphincterotomy

B. Or forceful anal dilation.

Anorectal Abscess

Obstruction of anal crypts with resultant bacterial overgrowth and abscess formation within the intersphincteric space.

RISK FACTORS

1. Constipation/diarrhea

2. IBD.

3. Immunocompromise.

4. History of recent surgery or trauma.

5. History of colorectal carcinoma.

6. History of previous anorectal abscess.

SIGNS AND SYMPTOMS

1. Rectal pain, often of sudden onset

2. With associated fever

3. Chills

4. Malaise

5. Leukocytosis

6. Tender perianal swelling with erythema and warmth of overlying skin.

TREATMENT

Surgical drainage.

Anorectal Fistulas

Tissue tracts (abnormal connections between two areas) originating in the glands of the anal canal at the dentate line that are usually the chronic sequelae of anorectal infections, particularly abscesses.

CLASSIFICATION OF ANORECTAL FISTULAS

1. Intersphincteric (most common): Fistula tract stays within intersphincteric plane.

2. Transsphincteric: Fistula connects the intersphincteric plane with the ischiorectal fossa by perforating the external sphincter.

3. Suprasphincteric: Similar to transsphincteric, but the fistula loops above the external sphincter to penetrate the levator ani muscles.

4. Extrasphincteric: Fistula passes from rectum to perineal skin without penetrating sphincteric complex.

SIGNS AND SYMPTOMS

Recurrent or persistent perianal drainage that becomes painful when one of the tracts becomes occluded.

DIAGNOSIS

1. Bidigital rectal exam.

2. Anoscopy.

3. If the internal opening cannot be identified by direct probing, it should be identified by probing the external opening or by injecting a mixture of methylene blue and peroxide into the tract.

TREATMENT

1. Intraoperative unroofing of the entire fistula tract

2. With or without placement of setons (heavy suture looped through the tract to keep it patent for drainage and to stimulate fibrosis).

Pilonidal Disease

Definition: A cystic inflammatory process generally occurring at or near the cranial edge of the gluteal cleft.

Incidence: Most commonly seen in young men in their late teens to the third decade.

SIGNS AND SYMPTOMS

1. Can present acutely as an abscess (fluctuant mass)

2. Or chronically as a draining sinus with pain at the top of the gluteal cleft.

TREATMENT

1. Incision and drainage under local anesthesia

2. With removal of involved hairs.

ANAL CANCER

Neoplasms of the anorectal region That are classified into:

1. Tumors of the perianal skin (anal margin carcinomas)

2. Tumors of the anal canal. INCIDENCE: Rare (1–2% of all colon cancers).

RISK FACTORS

1. Human papillomavirus (HPV)

2. Human immunodeficiency virus (HIV)

3. Cigarette smoking

4. Multiple sexual partners

5. Anal intercourse

6. Immunosuppressed state

SIGNS AND SYMPTOMS

1. Often asymptomatic

2. Can present with anal bleeding

3. Lump

4. Itching

5. An irregular nodule that is palpable or visible externally (anal margin tumor)

6. Or a hard, ulcerating mass that occupies a portion of the anal canal (anal canal tumor).

DIAGNOSIS Surgical biopsy with histopathologic evaluation. Histology: Anal margin tumors include:

1. Squamous and basal cell carcinomas

2. Paget’s disease

3. Bowen’s disease. Anal canal tumors are usually:

1. Epidermoid (squamous cell carcinoma or transitional cell/ cloacogenic carcinoma)

2. Or malignant melanoma.

DIAGNOSIS

Clinical staging: Involves:1. History 2. Physical exam 3. Proctocolonoscopy 4. Abdominal or pelvic CT or MRI 5. CXR 6. Liver function tests.

TREATMENT

Epidermoid carcinoma of anal canal:

1. Chemoradiation is mainstay— 5-FU, mitomycin C, and 3,000 cGy external beam radiation (Nigro protocol) surgery is reserved for recurrence.

Anal canal tumors:

1. Local excision not an option

2. Combined chemotherapy (5-FU and mitomycin C) with radiation often successful

3. APR only if follow-up biopsy indicates residual tumor.

TREATMENT

Other anal margin tumors:

1. Wide local excision alone

2. Or in combination with radiation and/or chemotherapy is successful in 80% of cases without abdominal-perineal resection (APR) if tumor is small and not deeply invasive.

PROGNOSIS

Anal margin tumors: 80% overall 5-year survival. Anal canal tumors:

1. Epidermoid carcinoma: 50% overall 5-year survival.

2. Malignant melanoma: 10–15% 5-year survival.

Colorectal Polyps

MORPHOLOGY: Can be classified into:

1. Sessile (flat)

2. Pedunculated (on a stalk). HISTOLOGIC TYPES:

1. Inflammatory (pseudopolyp): Seen in UC.

2. Lymphoid: Mucosal bumps containing intramucosal lymphoid tissue; no malignant potential.

Colorectal Polyps

3. Hyperplastic: Overgrowth of normal tissue; no malignant potential.

4. Adenomatous: Premalignant; Are classified (in order of increasing malignant potential) as:

A. Tubular (75%)

B. Tubulovillous (15%)

C. Villous (10%).

5. Hamartomatous: Normal tissue arranged in abnormal configuration; juvenile polyps, Peutz-Jeghers polyps.

Colorectal Polyps

INCIDENCE: 30-40 % of individuals over 60 in the United States. SIGNS AND SYMPTOMS:

1. Asymptomatic (most common)

2. Melena

3. Hematochezia

4. Mucus

5. Change in bowel habits

Colorectal Polyps DIAGNOSIS: Flexible endoscopy (sigmoidoscopy or colonoscopy). TREATMENT:

1. Attempt colonoscopic resection if :

A. Pedunculated

B. Well or moderately well differentiated

C. No venous or lymphatic invasion

D. Invades only into stalk

E. Margins negative.

Colorectal Polyps

2. Otherwise, a segmental colon resection is indicated.

Polyposis Syndromes

INCIDENCE

Second most common cause of cancer deaths overall (behind lung cancer).

130,000 new cases and 55,000 deaths each year. Incidence increases with increasing age starting at age 40 and peaks

at 60–79 years of age. See Table 10-5 for screening recommendations from the U.S.

Preventative Services Task Force.

RISK FACTORS

1. Age > 50.

2. Personal history of resected colon cancer or adenomas.

3. Family history of colon cancer or adenomas.

4. Low-fiber, high-fat diet.

5. Inherited colorectal cancer syndrome (familial adenomatous polyposis [FAP], hereditary nonpolyposis colon cancer [HNPCC]).

6. Long-standing UC or Crohn’s disease.

Adenoma-Carcinoma Sequence

Normal → hyper proliferative → early adenoma → intermediate adenoma → late adenoma → carcinoma (→ metastatic disease).

1. APC gene loss or mutation

2. Loss of DNA methylation

3. Ras (gene) mutation

4. Loss of DCC gene

5. Loss of p53 gene

SIGNS AND SYMPTOMS1. Typically asymptomatic for a long period of time2. Symptoms, if present, depend on location and size.3. Right-sided cancers:A. Occult bleeding with melena B. Anemia C. Weakness 4. Left-sided cancers:A. Rectal bleedingB. Obstructive symptomsC. Change in bowel habits and/or stool caliber.5. Both: Weight loss, anorexia.

DIAGNOSIS

Colon cancer:

1. Flexible sigmoidoscopy or colonoscopy (need to evaluate entire colon and rectum to look for synchronous lesions).

Rectal cancer:

1. Digital rectal exam

2. Proctoscopy/colonoscopy

3. Barium enema

4. Also consider transrectal ultrasound (TRUS), CT, or magnetic resonance imaging (MRI) to assess depth of local tumor invasion and local lymph node status.

STAGING AND PROGNOSIS

Dukes System (old system):

A. Limited to wall

B. Through wall of bowel but not to lymph nodes

C. Metastatic to regional lymph nodes

D. Distant mets

STAGING AND PROGNOSIS TNM System (more current system):• T1: Invasion of submucosa• T2: Invasion of muscularis propria• T3: Invasion of subserosa, or nonperitonealized pericolic or perirectal

tissues• T4: Invasion of visceral peritoneum/direct invasion of other organs• N0: No nodal disease• N1: 1–3 pericolic or perirectal lymph nodes• N2: 4 or more lymph nodes• M0: No evidence of distant mets• M1: Distant mets

TREATMENT

Surgical resection (see Table 10-6 and Figure 10-5): Goal is to remove primary tumor along with lymphatic's draining

involved bowel. In rectal cancer, the circumferential radial margin (CRM) is crucial to

local recurrence. Total mesorectal excision (TME) reduces the rates of local

recurrence. Adjuvant treatment: Stage III: 5-fluorouracil (5-FU)-based chemotherapy.

TREATMENT

Rectal cancer: Preop radiation using 5-FU as a radiosensitizer (this sequence is called “neoadjuvant” therapy because it occurs prior to the definitive surgical treatment.