Clin Med Diverticulosis/litis & Colon Polyps Flashcards
Large Intestine Anatomy
- The Colon and Rectum are considered the Large Intestine
- U-shaped Tube of several layers
- Approximately six (6) feet in length
Cecum
a pouch like passage that connects ileum to the proximal ascending colon.
Where is the ascending colon located?
begins in the right lower quadrant and ascends to the right upper quadrant where it terminates at the hepatic flexure.
Where is transverse colon?
- Transverse colon is situated across the upper abdomen.
- Starts at the hepatic flexure and ends at the splenic flexure.
- Mid transverse colon may sag as low as the umbilicus.
Which part of the colon is retroperitoneal?
Ascending colon
Which part of the colon is peritoneal?
Transverse colon
Where is descending colon? Is it retro or peritoneal?
- left side of abdomen
- retroperitoneal
Sigmoid colon characteristics
- S-shaped
- Last part of the colon.
- Lies in the pelvis about 40 cm long
The gastrointestinal tract ends with…
Rectum – 6” long
Anus = exit
Define diverticulum
Saclike protrusion in the colonic wall that develops as a result of herniation of the mucosa and submucosa through the muscularis propria, through points of weakness in the muscular wall of the colon
Define diverticular disease
- symptomatic and asymptomatic disease with underlying pathology of colonic diverticula
- Diverticulosis is an acquired disease
Population affected by diverticular disease
- In the US, < age 40 uncommon
- Up to 50% of the population by age 60; 70% by age 80
- Mean age at presentation of the disease is 59 years
- More common with Western diet (aka low fiber)
- Dubbed a “disease of Western Civilization”
Diverticular disease incidence/epidemiology
- Prevalence among females and males is similar (males tend to present at a younger age)
- In Western countries: left-sided, in Asia: right-sided
What are the 6 parts of diverticular disease pathophysiology?
- Segmentation
- Protrusion
- Mychosis
- Colonic wall changes
- Chronic inflammation
- Dietary fiber deficiency
Pathogenesis - Segmentation
- Contractions of the circular muscles of the colon produces a closed segment of colon with increased intraluminal pressure.
- Elevated intraluminal pressures may ultimately result in herniation of the mucosa and submucosa at sites of weakness
Pathogenesis - Protrusion
Protrusion occurs in weak areas of the bowel wall where blood vessels (vasa recta) penetrate through the muscularis propria
Pathogenesis - Mychosis
Myochosis (thickening of muscle layer and resultant lumina narrowing) is seen in most patients with sigmoid diverticula.
- -Results from increased deposition of collagen and elastin within the muscle
- -Also decreases the resistance of the colon wall
Pathogenesis - Colonic Wall Changes
- With age, tensile strength of the collagen and muscle fibers of the colonic wall decreases
- -Contribute to the creation of more distensible muscle fibers
- With age, collagen fibers in the left colon become smaller and more tightly packed.
- -Lower colonic compliance in the sigmoid and descending colon
Pathogenesis - Chronic Inflammation
- Chronic low grade inflammation - Segmental colitis.
- Inflammatory process that is localized to the portion of the colon with diverticula, sparing the rectum and right colon.
Pathogenesis - Dietary Fiber Deficiency
- Fiber binds water and salt in the colon, leading to bulkier and more voluminous stools.
- -Therefore, fiber decreases the frequency of contractions and prevents an exaggerated form of segmentation
- Dietary fiber also influences growth and maintenance of colonic cellular function
- -deficient diet increases the chances of intense, more frequent segmentation, thus predisposing to herniation of mucosa by allowing isolated increases of intraluminal pressure
Define diverticulosis
- Diverticulosis refers to presence of one or multiple diverticula and generally implies an absence of symptoms.
- Often incidental finding and no further w/u.
- Approximately 80-85% patients with diverticula are asymptomatic.
Symptomatic diverticular disease is characterized by
attacks of (LLQ) abdominal pain without evidence of inflammatory process
- -Colicky pain, often relieved by passing stool or flatus.
- -Often precipitated by eating
Other symptoms found with symptomatic diverticulosis
- Bloating, nausea, irregular bowel movements (intermittent diarrhea or constipation – MC)
- Bleeding alone can sometimes be the only sign of diverticulosis!
Symptomatic diverticulosis on physical exam
- fullness or tenderness to LLQ with possible voluntary guarding on exam
- No abnormal vital signs, such as tachycardia or fever (which would indicate an inflammatory/infectious process)
Imaging/Diagnosis - Symptomatic Diverticulosis
- Barium enema - will demonstrate the presence, localization, and number of diverticula.
- Colonoscopy is the preferred diagnostic study to r/o other causes that are on DDx, such as IBD, colorectal cancer, and ischemic colitis.
When is colonoscopy contraindicated?
- can be difficult to perform d/t narrowing of the colonic lumen and possible colonic fixation from fibrosis.
- in patients in whom acute diverticulitis is suspected, d/t increased risk of colonic perforation.
Treatment/Management – Diverticulosis
-Therapies used to treat uncomplicated diverticular disease include fiber-rich diets, nonabsorbable antibiotics, mesalazine, probiotics, and prebiotics.
Note: Nothing encourages regression of the diverticuli.
Treatment/Management: Fiber - Diverticulosis
- Shortens gut transit time, reduces intracolonic pressure and helps with constipation.
- Recommended daily fiber intake for adults is 20–35 g/day
- High fiber foods – whole grain breads/cereals, fresh fruits and vegetables, beans
- Fiber supplements available contain either soluble fiber (psyllium, ispaghula, calcium polycarbophil) or insoluble fiber (corn fiber, wheat bran)
Treatment/Management: Non-Absorbable Antibiotics
Rifaximinis a broad-spectrum antibiotic (80 to 90%remains within the gut)
Treatment/Management: Mesalazine
- Anti-inflammatory drug that acts topically on the gut mucosa
- May help symptoms related to chronic mucosal inflammation
Treatment/Management: Probiotics
- Probiotics contain microorganisms with the goal to reestablish the normal bacterial flora (BifidobacteriaandLactobacilliare used most frequently)
- Normal bacterial flora may be altered by slowed colonic transit and stool stasis.
- Theorized that reestablishing normal gut flora may lead to symptomatic improvement.
Treatment/Management: Prebiotics
- substances that promote the growth and metabolic activity of beneficial bacteria, especially BifidobacteriaandLactobacilli.
- Frequently indigestible complex carbohydrates.
- Bacteria ferment these substances, leading to a more acidic luminal environment, which suppresses the growth of harmful bacteria.
- -Substances shown to promote the growth ofBifidobacteriaandLactobacilli- psylliumfiber,lactulose, fructose, oligosaccharides, germinated barley extracts, and inulin
Acute Diverticulitis results from…
Results from the micro- or macroperforation of a diverticulum, resulting in anything from subclinical inflammation to feculent peritonitis
Acute Diverticulitis Characteristics
-Male predominance younger than 45 years; equal distribution between 45 and 54; female predominance after the age of 54.
Pathogenesis – Acute Diverticulitis: Elevated Colonic Pressure
- Erosion of the diverticular wall d/t increased intraluminal pressure or thickened/congealed food particles.
- Leads to inflammation and focal necrosis, with resultant perforation of the thin-walled diverticulum.
Pathogenesis – Acute Diverticulitis: Changes in Bacterial Flora
- Altered microbial composition within the gut may impair the mucosal barrier, resulting in chronic low-grade inflammation.
- Growth ofBifidobacteriais promoted by soluble fiber, the fermentation of which leads to the generation of short-chain fatty acids, the preferred energy source for colonocytes.
- -The increased production of short-chain fatty acids may aid in maintaining the colonic barrier.
Which drug class is associated with acute diverticulitis and perforation? Mechanism?
- NSAIDs
- Postulated to be d/t decreased prostaglandin synthesis and direct topical mucosal damage and irritation.
What role do prostaglandins play in the colon?
Prostaglandins aid in maintaining colonic mucosal barrier by stimulating mucin and bicarbonate secretion and increasing mucosal blood flow. (NSAIDs decrease these)
Other role of NSAIDs in acute diverticulitis
NSAIDs are weak acids that may denude epithelial cells, resulting in increased mucosal permeability, ulceration, and the translocation of bacteria and toxins
Pathogenesis - Diet (Acute Diverticulitis)
- Diet low in fiber may not only predispose to formation of diverticula, but may also predispose to the development of diverticulitis.
- By increasing stool weight and water content, fiber helps reduce colonic segmentation pressures, which may protect against perforation.
What role does red meat play in acute diverticulitis?
Heterocyclic amines, products of cooking meat, have been associated with apoptosis of colonic epithelial cells - may predispose to perforation.
Pathogenesis - Perforations (Acute Diverticulitis)
- After micro-perforation, infection contained by pericolonic fat, mesentery and/or adjacent organs.
- -Localized area of infection/inflammation occurs.
- Macro-perforation – infection less restricted.
- -Peritonitis or pericolic abscess can occur.
- If septic process erodes into adjacent structures, results in fistula formation.
Clinical Findings – Acute Diverticulitis
- LLQ pain (MC complaint) - gradual onset. It is constant, with intermittent exacerbations
- Fever
- Leukocytosis
- Nausea and vomiting (20–62%)
- Constipation (50%)
- Diarrhea (25–35%)
- Urinary symptoms (10–15%)
Acute Diverticulitis on Physical Exam
- Tenderness in the LLQ, with a tender mass being present in 20% (possible guarding and rebound tenderness)
- Tenderness in the RLQ - from either a large sigmoid loop or from right-sided diverticulitis.
- Fever
- Diffuse tenderness suggests free perforation and peritonitis.
- Abdominal distention and hypoactive bowel sounds may be present if an ileus has developed.
- In free perforation, hemodynamic instability may develop, along with a rigid, distended abdomen
Lab Findings – Acute Diverticulitis
- Leukocytosis most common.
- -Marked leukocytosis suggestive of peritonitis or abscess. - Liver function tests are usually normal.
- Serum amylase - normal or mildly elevated.
- -If amylase elevated, suggestive of possible peritonitis or perforation.
Imaging Studies – Acute Diverticulitis
- Plain radiograph normal except with ileus, bowel obstruction or larger perforation
- CT - radiographic test of choice for diagnosing diverticulitis.
Which forms of imaging are no longer recommended for acute diverticulitis?
- Barium enema – no longer recommended d/t risk of extravasation of contrast material if perforation.
- Rigid proctoscopy, flexible sigmoidoscopy, and colonoscopy are relatively contraindicated (required air insufflation can unseal or worsen a perforation!)
Outpatient Treatment – Acute Diverticulitis
If patient has uncomplicated case & is stable:
1. Bowel reset and antibiotics
(to cover gram-negative rods and anaerobes - Metronidazole + Quinolone; Metronidazole + Trim-Sulfa; Augmentin)
2. Clear liquid diet, with slow advancement of the diet.
Inpatient Treatment – Acute Diverticulitis
considered for patients with more severe presentations, older pts, inability to tolerate oral intake, or comorbid illnesses:
Bowel rest, IV fluids, and IV antibiotics
Antibiotics for inpatient acute diverticulitis
- Metronidazole OR Clindamycin PLUS Aminoglycoside (Gentamicin or Tobramycin or Aztreonam) or Third-generation Cephalosporin (Ceftriaxone, Ceftazidime, Cefotaxime)
- Alternatively – IV Second generation Cephalosporin (Cefoxitin, Cefotetan)
- Alternatively – IV Ampicillin-Sulbactam, Ticarcillin-Clavulanate
Complicated Diverticular Disease - Abscess
when pericolic tissues fail to control spread of inflammatory process.
- High fever, leukocytosis or both despite adequate trial of appropriate antibx.
- Localized peritonitis and possible tender mass on exam
Complicated Diverticular Disease - Fistula
abscesses can progress to this between colon and surrounding structures.
- Bladder (most common esp men), cutaneous, vaginal.
- Passage of stool through the skin or vagina or the presence of stool or air in the urinary stream (pneumaturia).
- -Colovaginal fistulas more common in women s/p hysterectomy
Complicated Diverticular Disease - Intestinal Obstruction
caused by adhesions, luminal narrowing from inflammation or compression by abscess.
- Severe abdominal distention with nausea and vomiting.
- Generally self-limited with conservative tx, but persistent may require endoscopic or surgical techniques.
Complicated Diverticular Disease - Perforation with peritonitis
increases mortality rate as high as 35% and needs urgent surgical intervention.
- -Diffuse peritonitis - generalized tenderness, involuntary guarding, or decreased or absent bowel sounds.
- -Linked with NSAID, and maybe glucocorticoid steroid use.
Uncomplicated vs. Complicated Diverticular Disease
Uncomplicated:
- abdominal pain
- fever
- leukocytosis
- anorexia/obstipation
Complicated:
- abscess
- perforation
- stricture
- fistula
Diverticular Hemorrhage
Most common cause of major lower GI bleed, yet only 15-20% of patients with diverticulosis will have gastrointestinal bleeding.
*At times first (and only) sign of diverticular disease!
Risk of Diverticular Hemorrhage
Increased risk if hypertensive, have h/o atherosclerosis, and regularly use aspirin and NSAIDs.
Diverticular Hemorrhage – Imaging
Colonoscopy and angiography (diagnostic and therapeutic – can cauterize, vasoconstrict, etc.), and nuclear bleeding scans (diagnostic only).
- 75–90% of patients, bleeding stops spontaneously.
- Surgery required when medical management not successful!
Colon Polyps
Considered a cancer precursor - majority of colorectal cancers are believed to arise within benign adenomatous polyps
Colon polyps characteristics
-They can be symptomatic or asymptomatic, pedunculated or sessile, and range in size from millimeters to many centimeters in diameter
+/- 10 yrs time interval to transition to invasive cancer
-Removal of these precursor adenomatous polyps decreases the risk for lethal colorectal cancer significantly!
National polyp study predictors for development of future advanced adenomas or cancers as High-Risk Adenomas (HRAs):
(1) three or more adenomas,
(2) adenoma size greater than 1 cm, and
(3) adenoma with villous features or high-grade dysplasia
Management of colon polyps
Current recommendation is surveillance colonoscopy in 3 years!
Familial Adenomatous Polyposis
- Hundreds to thousands of adenomatous polyps in the colon.
- Nearly 100% risk of developing CRC by middle age if affected colon is not surgically removed.
- Autosomal-dominant inheritance, but 30% of cases emerge as de novo gene mutation.
When is familial adenomatous polyposis discovered?
Second or third decade of life- usually discovered during endoscopic evaluation for bleeding or diarrhea, or during routine screening in individuals with a known family history.
What other malignancies are associated with familial adenomatous polyposis?
Extracolonic malignancies associated with papillary thyroid cancer, adrenal carcinomas, and central nervous system tumors.
When should you begin screening for familial adenomatous polyposis?
Age 11.
