Disorders of the colon Flashcards
diverticular disease of the colon
-Colonic diverticulosis increases with age in Western societies:
-<20% in those under age 40
-60% by age 60
-More than 70% over age 80
-Very uncommon in developing countries
-asymptomatic
-vary in size- few mm to several cm
-vary in number
-almost all pts have involvement in sigmoid colon -> smaller diameter -> intraluminal pressures
-common in pts with not enough fiber, processed foods
-areas of inherit weakness
anti-mesenteric
-lateral colon
-most common for diverticulosis
-The prevalence of diverticular disease affecting the left colon is higher in Western countries compared to Asia
diverticulosis pathogenesis
-Years of diet deficient in fiber
-Undistended contracted segments of colon have higher intraluminal pressures: -> More common in sigmoid-> increase intraluminal pressures
-Abnormal motility and hereditary factors may contribute
-left sided more common in US
-Connective tissue ds:
Ehlers- Danlos syndrome, Marfan’s syndrome, scleroderma
diverticulosis complications
-Bleeding and diverticulitis
-Approx 4% develop diverticulitis
-5-15% have diverticular bleed -> 50% of acute lower GI bleeding is attributable to diverticulosis
-diverticular bleeds are bad
diverticulitis
-Perforation of a colonic diverticulum:
-Microperforation (most common) with localized paracolic inflammation
-Macroperforation with abscess or generalized peritonitis -> catastrophe
-Erosion of the diverticular wall by increased intraluminal pressure or inspissated food particles
-Inflammation and focal necrosis ensue -> resulting in perforation
-S&S- mild to moderate LLQ pain, constipation, nausea and vomiting **
diverticulitis PE and labs
-Low-grade fever
-Left lower quadrant tenderness, +/-palpable mass (rare)
-Stool occult blood- common, hematochezia (rare)
-Leukocytosis
-Free/Macroperforation:
Dramatic picture of generalized abdominal pain and peritoneal signs
-imaging- plain abdominal films (usually only with macroperforation)
-CT of abdomen and pelvis***
-colonoscopy and barium enema -> contraindicated bc of perforation
diverticulitis differential dx
-Perforated colonic carcinoma** -> 6-8 weeks after do colonoscopy bc it can be a perforated colonic carcinoma
-IBD
-Appendicitis
-Ischemic colitis
-C difficile–associated colitis
-Gynecologic disorders (ectopic pregnancy, ovarian cyst or torsion)
diverticulitis complications
-Abscess or phlegmon (early abscess)
-Bleeding
-Fistula
-Stricturing of colon
outpatients tx diverticulitis***
-uncomplicated disease:
-Pain medication
-Liquid then low residue diet
- +/- Antibiotics- reassess every three days
-Reassess in 3 days, then follow closely
-complicated disease:
-Metronidazole* 500 mg three times daily plus Ciprofloxacin* 500 mg twice daily x 10 days or augmentin*
-Liquid then low residue diet (low fiber at first) -> then high fiber
-Antibiotic treatment can be used selectively rather than routinely in immunocompetent patients with mild acute uncomplicated diverticulitis -> Antibiotic treatment is strongly advised in immunocompromised pts
-fu with clinical exam NOT imaging
diverticulitis hospitalize and tx
-Increasing pain, fever, or inability to tolerate oral fluids
-Elderly or immunosuppressed
-Serious comorbid ds
-Treatment:
-NPO with intravenous fluids
-If ileus -> nasogastric tube for decompression
-IV antibiotics to cover anaerobic and gram-negative bacteria
surgical management: diverticulitis
-20–30%
-Elective vs. Emergent
-Surgical consultation*:
-Complicated/Severe disease
-Fail to improve after 72 hours of medical management
-Recurrent disease- not # episodes
-Fistulas, colonic obstruction, abscess
-Emergent* surgical management- Free perforation/peritonitis and large abscesses
diverticulitis prognosis
-16 to 42 % risk of developing recurrent diverticulitis
-Obesity, sedentary lifestyle, smoking, NSAIDs, genetics
-Number of prior attacks is no longer used as a criterion for elective surgery
-Future care:
-Colonoscopy 6-8 weeks after to make sure perf wasnt from colon cancer
-High fiber diet
why is colorectal cancer screening important
-Facts about colorectal cancer:
-Colorectal cancer is # 2 cause of cancer death in the US and affects both men and women.
-Preventable
-More preventable than breast or prostate cancer
-Screen for colorectal cancer in all adults aged 45-75 years
-Adults aged 76-85 years: determine whether is appropriate in individual cases
-pts and clinicians should consider the patient’s overall health, prior screening history, and preferences
colorectal cancers start in polyps
-A polyp is a warty growth on the inner lining of the colon (mucosa)
-Polyps are usually benign
-Polyps that can turn into cancer are called adenomas; not all polyps are adenomas
-Polyps can be removed during colonoscopy
-Removal of polyps prevents the development of colorectal cancer
screening for colon cancer
-screen for colorectal cancer in all adults aged 45-75 years
-adults aged 76-85 -> determine whether appropriate in individual cases
-pts and clinicians should consider the pts overall health, prior screening history and preferences
polyps of colon and small intestine
-Discrete mass lesions that protrude into lumen
-3 major pathologic groups:
-Mucosal neoplastic: adenomatous polyps***
-Mucosal nonneoplastic polyps: hyperplastic, juvenile polyps, hamartomas, inflammatory polyps (mostly not cancer)
-Submucosal lesions: lipomas, lymphoid aggregates, carcinoids (non cancerous except carcinoids)
nonfamilial adenomatous polyps
-Tubular, tubulovillous, villous or serrated
-Sessile (flat) or pedunculated (on stalk) - always
-pedunculated - stalk is non cancerous but the tip is adenomatous
-Present in 25% of adults over 50 years of age
->95% of cases of colon adenocarcinoma are believed to arise from adenomatous polyps
-Small (< 1 cm) have low risk of becoming malignant- less than 5% of these enlarge with time
-“Advanced” adenomas:
- ≥ 1 cm
-Villous features
-Dysplasia
-Higher risk of harboring or progressing to malignancy
-5 years for a medium-sized polyp to develop from normal-appearing mucosa
-7-10 years for a gross cancer to arise
symptoms of adenomatous polyps
-Most pts completely asymptomatic
-people dont know until they start bleeding -> melena or rectal bleeding -> Iron deficiency anemia
-Intermittent hematochezia
malignant polyp tx
-Histologic assessment found to contain cancer that has penetrated through muscularis mucosae into submucosa
-Malignant polyps considered adequately treated by polypectomy alone if:
-(1) polyp is completely excised and submitted for pathologic examination
-(2) well differentiated
-(3) margin is not involved (clear margins)
-(4) no tumor budding vascular invasion
-excision site of “favorable” malignant polyps should be checked in 3 months for residual tissue
colonoscopy recheck (chart)
-10 years- normal colonoscopy / < 20 HP < 10mm
-7-10 years- 1-2 adenomas <10 mm
-5-10 years- 1-2 SSPs < 10mm
-3-5 years- 3-4 adenomas < 10 mm, 3-4 SSPs <10 mm, HP > 10 mm
-3 years- 5-10 adenomas, 5-10 SSPs, adenomas or SSP > 10 mm, adenoma with villous or tubulovillous histology and/or high grade dysplasia, SSP with dysplasia, traditional serrated adenoma
-1 year- > 10 adenomas
colonoscopy
-goes to the cecum (unless you have IBD it goes to ileum?)
screening frequency
-45-75 years- average risk - every ten years
-stool based tests
-direct visualization- colonoscopy, CT colonography every 5
-personal hx or polyps, IBD, polyposis syndrome -> more frequent
-family history, genetic syndromes - more frequent
-colonoscopy - most specific and detects the smallest
hereditary colorectal cancer and polyposis syndromes
-3-4% of all colorectal cancers are caused by genetic mutations* that impose a high lifetime risk of developing colorectal cancer
-rare
-Consider these disorders in patients with:
-family history of colorectal cancer that has affected >1 family member (first degree)
-personal or family history of colorectal cancer < 50yo
-personal or family history of multiple polyps (> 20)
-personal or family history of multiple extracolonic malignancies
familial adenomatous polyposis (FAP)
-Affects 1:10,000 people
-0.5% of colorectal cancer- rare
-Hundreds to thousands of colonic adenomatous polyps and a variety of extracolonic manifestations
-Autosomal dominant inherited mutations in the adenomatous polyposis coli (APC) gene on chromosome 5q21
-Attenuated variant produces less polyps
-Colorectal polyps develop by a mean age of 15 years and cancer at 40 years.
-Colorectal cancer is inevitable by age 50 years
-colon removal
-genetic counseling and testing- first degree family members of pts with the disease
monitoring FAP
-Annual colonoscopy till colectomy deemed appropriate
-Complete proctocolectomy with ileoanal anastomosis or colectomy with ileorectal anastomosis is recommended, usually before age 20 years -> If retain rectum flex sig q 6-12 mos
-EGD every 1–3 yrs to look for adenomas or carcinoma
hamartomatous polyposis syndromes
-Rare, < 0.1% of colorectal cancers
-Peutz-Jeghers syndrome
-Familial juvenile polyposis
-PTEN multiple hamartoma syndrome (Cowden disease)
peutz-jeghers syndrome
-Autosomal dominant condition on gene 19p13.3
-Hamartomatous polyps throughout the GI tract
-Mucocutaneous pigmented macules on the lips, buccal mucosa, and skin*
-dark spots
-Hamartomas may become large -> bleeding, intussusception (telescoping), or obstruction
-Not malignant but adenomatous change can occur within the hamartomas-> lifetime risk is 39% for CRC
-Extracolonic malignancies: GI malignancies 40%, breast cancer 50%, testicular, pancreatic cancer
-Screening every 2-3 yrs with EGD, Colon, MRE
-Genetic testing for family
familial juvenile polyposis
-Rare, 1/3 familial
-Autosomal dominant germline mutation in SMAD4 gene on chromosone 18q21.1
-Several (>10) juvenile hamartomatous polyps located most commonly in colon
-Increased risk ( 20%) of adenocarcinoma due to synchronous adenomatous polyps/cancer*** or adenomatous change within hamartomatous polyps
-2 types at once
-Genetic testing is available
-Colonoscopy q 1-2yrs starting at 15-18yo
PTEN multiple hamartoma syndrome (Cowden disease)
-Hamartomatous polyps and lipomas throughout the GI tract
-Trichilemmomas*:
-Slow-growing flesh-colored flat-topped facial papules or plaques 1-5 mm in diameter
-Grow, warty appearance
-Cerebellar lesions
-Increased malignancy- Thyroid, breast, and urogenital tract
lynch syndrome
-3% of all colorectal ca
-Autosomal dominant- Defect in one of several genes that are important in the detection and repair of DNA base-pair mismatches: MLH1, MSH2, MSH6, and PMS2
-Increased risk of colorectal ca, endometrial ca** + others
-Few adenomas, but aggressive, larger, sessile, villous features, dysplastic, right sided - Rapid transformation
who to suspect lynch syndrome
-pts with synchronous or metachronous CRC
-CRC or endometrial cancer prior to 50 years of age
-multiple Lynch-associated cancers (eg, CRC and endometrial, ovarian, stomach, small intestine, or renal pelvis/ureter)
-familial clustering of Lynch-associated cancers.
-Thorough family history is essential to identify families - genetic screening
-Screened with colonoscopy every 1–2 years beginning at age 25 (or 2-5 years younger than the age at diagnosis of the youngest affected family member) -> dont need to know age
colorectal cancer
-3rd mc cancer in males and in females- 2nd leading cause of death due to malignancy in the US
-Almost all adenocarcinomas
-Gradual increase in incidence of cancers in cecum and ascending colon.
- >50% of cancers now develop proximal to the splenic flexure
-risk factors:
-age
-family hx
-personal or family hx of polyps
-race
-hereditary polyposis syndromes
-IBD
colorectal cancer S&S and PE
-Right-sided colon cancer- Iron deficiency anemia -> Obstruction uncommon
-no obstruction and liquid goes around on right side -> not symptomatic until bleeding, anemic, SOB
-Left sided colon cancer:
-Often involve bowel circumferentially
-Obstructive symptoms
-Anemia/Heme+ stool
-catch earlier
-Rectal cancers: Tenesmus, urgency, recurrent hematochezia
-PE- usually normal except in advanced disease -> +/- palpable mass, +/- hepatomegaly, digital exam, rectal exam
differential dx colorectal cancer
-Irritable bowel syndrome
-Diverticular disease
-Ischemic colitis
-Inflammatory bowel disease
-Infectious colitis
-Hemorrhoids
colorectal cancer labs
-Complete blood count
-Liver function tests (metastases)
-Carcinoembryonic antigen (CEA)- tumor marker -> monitor
colorectal cancer imaging
-Inspection of the colon:
-CT colonography or colonoscopy
-+ CT warrants colonoscopy for removal
-Colonoscopy: diagnostic procedure of choice
-Imaging: Once establish have cancer*:
-Chest, abdominal and pelvic PET CT for preoperative staging-
-Rectal Ca: Endorectal ultrasonography -> Depth of penetration of cancer through rectal wall and pararectal lymph nodes
-Staging: TNM
follow up after surgery
-Optimal cost-effective strategy is not clear
-Evaluated every 3–6 months for 3–5 years with history, physical, CEA
-Annual CT Scan at least for 3 years
-Colonoscopy:
-1 year after surgical resection
-Surveillance colonoscopy performed every 3–5 years
-Rectal cancer- Sigmoidoscopy every 3–6 months for 3 years
5 year relative survival rates for colon cancer
-localized- 90%
-regional- 72%
-distant- 13%
-all SEER stages combined- 63%
anal cancer
-Relatively rare
-Squamous cancers make up majority
-Increased among people practicing receptive anal intercourse and history of STDs
-In over 80%: HPV detected
-bleeding, pain are MC symptoms
-testing- bx, MR scan and endoluminal rectal US
-tx- depends on tumor stage -> excision +/- chemo and radiation
lower GI bleeding
-Arising below the ligament of Treitz
-Severity ranges from mild anorectal bleeding to massive, large-volume hematochezia
-Spontaneous cessation: >85% of cases
-Hospital mortality < 3%
-to determine the cause -> consider age of pt and severity of bleed
-if under 50 -> infectious colitis, anorectal disease, and IBD
-older pts -> significant hematochezia is most often diverticular -> other causes: vascular ectasias, malignancy, ischemia
diverticular bleed
-Acute hemorrhage occurs in 3–5% of pts with diverticulosis
-MC cause of overt major lower GI bleeding (50%)
-Bleeding more commonly originates on the right side
-**Presents as acute, painless, large-volume maroon or bright red blood in pts over age 50
-Spontaneously resolves in 80%
-May recur in up to 25%
vascular ectasis (angiodysplasias)
-5–10% of cases of lower GI bleeding
-Occur throughout the upper and lower intestinal tracts
-MC in patients >70 years and in those with chronic renal failure
-Mucosal capillaries* in colon dilate and become incompetent -> Most often in cecum and ascending colon
-Painless bleeding ranging from occult to melena to hematochezia
neoplasms and polyps
-Colonic neoplasms may cause up to 10% of acute lower gastrointestinal hemorrhage.
-MC cause of slow occult bleed, chronic ooze.
-Post polypectomy bleed:
-After endoscopic removal of colonic polyp significant overt (heavy) bleeding may occur up to 2 weeks later in 0.3% of patients
inflammatory bowel disease
-Diarrhea with variable amounts of bright red blood
-Abdominal pain, tenesmus, and urgency are often present
anorectal disease
-Small amounts of bright red blood noted on toilet paper, streaking of stool, or dripping into toilet bowl
-Bleeding is slight & seldom results in sig blood loss
-Painless bleeding associated with BM- Hemorrhoids
-Bleeding & pain during BM- Anal fissure
ischemic colitis
-Commonly in older patients, with ASHD
-5% of patients after surgery for ileoaortic or abdominal aortic aneurysm
-In young patients, may develop due to vasculitis, coagulation disorders, estrogen therapy, and long distance running
-Hematochezia or bloody diarrhea with mild cramps
-Typically, bleeding is mild and self-limited
-Other causes: Radiation-induced proctitis and Acute infectious colitis
approach to pt with lower GI bleed (chart)
-pt with acute, severe hematochezia
-initial eval and resucitation
-nasogastric tube aspiration- rule up upper GI bleed
-if aspirate copious bile and no blood -> colonoscopy -> arteriography is severe
-if aspirate blood -> EGD
evaluation and management of significant acute bleed
-Initial stabilization, blood replacement, & triage managed same way as acute UGI bleed
-Exclusion of an Upper Tract Source: NGT (hemodynamically compromised patients)
color of stool helps distinguish upper from lower bleed
-Large volumes bright red blood -> colonic source
-Brown stools mixed/streaked with red blood -> rectosigmoid or anus
-Maroon stools -> right colon or small intestine
-Black stools (melena) ->proximal to ligament of Treitz
small volume bleeding
-Under age 45 with small-volume bleeding -> DDX: anorectal disease, inflammatory bowel disease, or infectious colitis, tumor but less likely
-Over age 45 years with small-volume bleeding or anemia -> DDX: exclude tumor, vascular ectasias, plus above
-All will have a colonoscopy, CBC, additional diagnostic w/u depends on presentation and findings
large volume bleeding that has stopped
-stable vital signs
-colonoscopy within 24 hours of admission
large volume active lower GI bleed tx
-Urgent colonoscopy within 6–12 hours of admission
-Probable site of bleeding ID in 70-85% of patients
-tx- therapeutic colonoscopy- epinephrine injection, cautery (bipolar or heater probe), or metallic endoclips
-intra-arterial vasopressin or embolization:
-Selective mesenteric arterial angiography followed by embolization of bleeding lesion provides definitive control of bleeding in up to 90%
unable to ID site with colonoscopy or too severe
-Nuclear Bleeding Scan:
-Technetium-labeled red blood cell scanning can detect significant active bleeding and localize it to the small intestine, right colon, or left colon.
-Less than half of studies are diagnostic -Accuracy of a positive study is only 78%
-Angiography:
-Angiograms: in patients with positive technetium scans or with hemodynamically significant, ongoing bleeding.
Localization of an actively bleeding vessel in up to 80%
High complication rate
lower GI bleed treatment
-Therapeutic Colonoscopy
Epinephrine injection, cautery (bipolar or heater probe), or metallic endoclips
-Intra-arterial Vasopressin or Embolization
-Selective mesenteric arterial angiography followed by embolization of bleeding lesion provides definitive control of bleeding in up to 90%
bleeding diverticulum or vascular ectasia surgical treatment
-Bleeding diverticulum or vascular ectasia
-Localized resection:
-Preoperative localization of bleeding site by nuclear scan or angiography
-Indicated: ongoing excessive bleeding
-Total abdominal colectomy with ileorectal anastomosis: very rare
-Accurate localization is not possible or emergency surgery is required for massive hemorrhage
-Significantly higher morbidity and mortality
occult lower GI bleed
-Bleeding that is not apparent to the pt
-Chronic gastrointestinal blood loss of less than 100 mL/d may cause no appreciable change in stool appearance
-Identified by a positive FOBT or iron deficiency anemia in the absence of visible blood loss
-In US 2% of men and 5% of women have iron deficiency anemia
-Premenopausal women: MC menstruation and pregnancy
-GI source is present in 10% of premonopausal women
-Men and postmenopausal women:
-Upper gastrointestinal tract in 35–55%
-Colonic source in 15–30%
-Malignancy is present in 10%
MC causes of occult bleed are
-Acid-peptic lesions
-Colon Neoplasms
-Vascular abnormalities
-Infections
-Medications
-Inflammatory bowel disease
-Celiac ds
evaluation and treatment of occult bleed
-Colonoscopy and EGD- For all adults over age 40–45 years with positive FOBTs or iron deficiency anemia
-Remains unexplained in 30–50% of patients
-Unexplained bleeding:
-Capsule endoscopy
-Double balloon enteroscopy- Treatment of vascular ectasias, bleeding ulcers, polyp removal etc
lower GI bleed: massive, moderate, occult
-massive bleeding:
-pt > 65 with multiple medical problems
-hematochezia or bright red blood
-hemodynamically unstable
-hmg level = 6
-mc due to diverticulosis or angiodysplasias
-mortality rate may be as high as 27%
-moderate:
-any age
-hematochezia or melena
-hemodynamically stable
-benign anorectal, congenital inflammatory, and neoplastic diseases may cause moderate amount of acute or chronic bleeding
-occult:
-any age
-pts present with microcytic hypochronic anemia due to chronic blood loss
-congenital, inflammatory, and neoplastic diseases may cause chronic occult bleeding
