Colon Disorders and GI Neoplasms

Tory Davis PA-C

January 2010

Colon Disorders Anorectal Disorders

Fissure Fistula Hemorrhoid

IBS- Irritable Bowel Syndrome Diverticular Disease IBD- Inflammatory Bowel Disease

Crohn’s disease Ulcerative Colitis

GI Neoplasms Esophageal Stomach Colorectal / anorectal Pancreatic Hepatic

Anal Fissure Acute longitudinal tear or chronic ovoid ulcer

in anal epithelium. Located posterior or anterior midline.

Pain, severe with defecation Sometimes bleed Often result from laceration with secondary

infection. Pain internal sphincter spasm

decreased blood supply perpetuating fissure

Anal Fissure Tx Reduce local trauma: stool softener,

fiber Protect: zinc oxide, glycerin

suppository Relieve pain: topical anaesthetic

(benzocaine, lidocaine), warm sitz bath Surgical (last choice) - internal

sphincterotomy

Anorectal Fistula Tube-like tract with one opening in anal tract

and other in perianal skin Usually a chronic condition arising from

acute perirectal abscess Constant to intermittent drainage of purulent

or serosanguinous fluid +/- pain, depends on if infected Exam 1+ openings, +/- palpable cordlike

tract. Probe to see depth, direction Tx: Surgical- deroof or seal with fibrin glue

Hemorrhoids Aka “Piles” Dilated veins of hemorrhoidal plexus in

lower rectum Dentate line divides internal from external

hemorrhoids Locations: L lateral, R anterior, R posterior

zones Often asymptomatic, sometimes itching or

protrusion. External: can thrombose. Ow! Internal: often bleed after BM

Hemorrhoids

Internal- – graded I- IV

I – remain internal II – prolapse with strain, reduce

spontaneously III. Require manual reduction after BM IV. Won’t go back

Thrombosed Hemorrhoid Results in perianal hematoma Acute onset of exquisite pain Firm blue/purple perianal nodule Tx with sitz baths, analgesics If able in 1st 24-48h, excision gives

immediate relief

Tx Non-thrombosed hemorrhoids

Symptomatic Sitz baths Witch hazel compress phenylephrine 0.25% (Preparation H) Anesthetic oint Surgical: photocoag, rubber band

ligation, hemorrhoidectomy

Irritable Bowel Syndrome

Irritable Bowel Syndrome

Poorly understood, but real. Characterized by recurrent upper

and lower GI sx, varying abd pain, constipation and/or diarrhea, abd bloating

IBS Pathophys No consistent motility abnormality Some pts demonstrate abnl gastrocolic

reflex with colonic activity Maybe gastric emptying But even in demonstrated abnormality,

sx don’t correlate Excess mucus production even in

absence of mucosal injury

More pathophys Hypersensitivity to normal amounts of

intraluminal stretch. perception of pain with normal

amounts of intestinal gas Can be exacerbated by hormonal

fluctuations (incr prostaglandins with menses causes more pain)

IBS S & S Abdominal pain related to or relieved

by defecation Change in stool frequency and/or

consistency Mucus in stool Sensation of incomplete evacuation

S & S Onset teens or 20s Irregular, recurrent bouts Sx usually do NOT affect sleep Sx are triggered by stress, also by some

foods Varies per patient

Extra-intestinal sx Fibromyalgia Headache Dyspareunia TMJ syndrome Anxiety Depression

Constipation predominant

Constipation alternates with nl BMs Clear-white mucus Colicky or dull constant pain Often relieved by BM Eating may trigger sx Bloating, flatulence, eructation,

nausea, dyspepsia, heartburn

Diarrhea predominant Diarrhea immediately after eating, especially

after rapid eating Pain, bloating, rectal urgency Incontinence happens

Differential Diagnosis Lactose intolerance Diverticular dz Drug induced Drug abuse Biliary tract dz Bacterial enteritis Parasites

Early IBD Ischemic colitis, esp

if age > 60 Hypothyroid Malabsorption

syndromes

Rome Criteria

Standardized sx-based criteria for dx Three months of the following sx:

– Abdominal pain/discomfort relieved by defecation or assoc with change in freq/consistency of BM

– Disturbed defecation involving at least 2 of these:

Altered stool frequency, form or passage Passage of mucus Bloating or feeling of abdominal distention

Red Flags Onset after age 50 Weight loss Progressive dysphagia S/S bleeding or dehydration Steatorrhea Recurrent vomiting Fever ESR or CRP Anemia, leukocytosis Hypokalemia Strong FHx colon cancer Blood or pus in stool

Physical exam Patient appears healthy Abd +/- tender, esp LLQ

– Possibly palpable tender sigmoid Nl DRE- no occult blood Females: nl pelvic exam (r/o ovarian

tumor/cyst, infection, endometriosis)

IBS testing ONLY if objective abnormalities:

consider abd US or CT, barium enema

Stool cx, O&P - ONLY if supporting travel hx or fever, hematochezia or acute onset of diarrhea

IBS tx Sympathetic understanding, patience,

explain condition and address fears Diet:

– Normal, moderate sized meals eaten slowly. gas-producing food. Consider lactose– Eliminate sorbitol, mannitol in pts with diarrhea– Dietary fiber to bulk up and soften stool, but start

low, go slow or you’ll worsen sx ID stressors, mood d/o, or anxiety and

address them

IBS Drugs Anticholinergics to reduce spasm

Serotonin receptor modulators

IBS Drugs Loperamide (Immodium) for diarrhea TCAs for bloating, constipation, abd pain

– Down-regulates spinal cord and cortical afferent pathways from intestine

Peppermint- relaxes smooth muscle spasm. Significant improvement in clinical studies.

Ginger- digestive aid Aloe vera for constipation Fennel – reduces bloating.

Inflammatory Bowel Disease

Crohn’s Disease

Ulcerative Colitis

IBD 2 distinct disease entities

– Only about 10% are “indeterminate colitis” Usually fairly easy to differentiate

Both – Cause bloody diarrhea– Are characterized by chronic, relapsing and

remitting inflammation of various sites of the GI tract

– Have inflammation from cell-mediated immune response in GI mucosa

IBD Epi Gender equal, all ages, but peak incidence

ages 14-24– UC has 2nd peak 50-70

Most common in people of N. European or Anglo-Saxon origin.

1st degree relatives 4-20x increased risk Smoking increases Crohn’s risk, but

decreases risk of ulcerative colitis

IBD Extra-Intestinal Manifestations

Common to BOTH Crohn’s and UC 1. Disorders which parallel IBD flares

– Peripheral arthritis, episcleritis, aphthous stomatitis, erythema nodosum

2. Disorders probably resulting from IBD but appear independent of flares– Ankylosing spondylitis, sacroiliitis, uveitis,

primary sclerosing cholangitis. Can appear years before IBD sx, and should prompt

eval for IBD!

IBD Extra-Intestinal Manifestations

3. Consequences of disrupted bowel physiology (primarily seen in severe Crohn’s of small bowel)– Malabsorption (causing B12 and mineral

deficiencies), anemia, clotting disorders, bone demineralization, kidney stones, hydroureter & hydronephrosis (from ureteral compression by inflammatory process)

Factors in all 3 categories can increase risk of thromboembolic disease

Crohn’s Disease

Crohn’s Disease Chronic transmural inflammatory dz,

usually effects distal ileum and RIGHT colon, but can occur anywhere along GI tract

Segmental rather than continuous (UC) Not symmetric Can have significant perirectal lesions,

but rare rectal bleeding

Crohn’s pathophys Inflammation of crypts small abscesses &

aphthoid ulcers which deep longitudinal and transverse ulcers with mucosal edema

Transmural spread of inflam lymphedema, bowel wall thickening

Severe inflam muscle hypertrophy, fibrosis, strictures (can cause obstruction)

Crohn’s pathophys

Abscesses common, and resulting fistulas can penetrate nearby structures– Bowel loops, bladder (can pee poop), psoas

muscle (peritonitis sx), enterocutaneous Granulomas- Pathognomonic. Found in

liver, lymph nodes, all layers of bowel wall

Crohn’s pathophys Discontinuous affected segments of bowel

sharply demarcated from normal areas (“skip areas”)

Where is it?– 35% ileum alone

– 45% ileum + colon

– <20% colon alone, usually spares rectum

– Uncommon in esoph, stomach, duodenum (but can be there)

Crohn’s S&S Chronic diarrhea w/ abd pain, fever,

anorexia, wt loss Tender abdomen with mass or fullness Gross rectal bleeding RARE One third with significant perianal

disease: fissures, fistulas, abscesses

Crohn’s S&S Can present w/ acute abd- looks like

appendicitis or obstruction Recurrent disease sx vary- Pain common

with simple recurrence and with abscess Severe flare: pt is SICK: marked

tenderness, guarding, rebound– Segmental stenosis can bowel obstruction with

colicky pain, abd distention, vomiting– Perforation not uncommon. Enterovesicular perf

causes pneumaturia. Draining cutaneous fistulas

Crohn’s Dx To diagnose, you must first suspect! Suspect in

– pt w/ inflam or obstructive sx – pts w/ perianal fistulas– pts w/ unexplained arthritis, fever,

anemia, erythema nodosum, – kiddos with growth retardation

Work-up and Dx Pt presents w/ acute abd:

– flat & upright plain films, abd CT to find obstruction, abscess, fistula, and to r/o other cause (ie appendicitis)

– Consider pelvis U/S for female with predom lower abd/pelvic sx

Work-up and Dx Less acute pres:

– GI series with small bowel follow-thru and spot films of terminal ileum

– Considered diagnostic if shows stricture, fistulas or separation of bowel loops

Work-up and Dx If symptoms predominantly colonic (ie

diarrhea) Order barium enema which may show:

– Barium reflux into terminal ileum– Irregularity and nodularity of bowel wall– Wall stiffness and thickening– Narrowed lumen

Or colonoscopy with bx, sampling for enteric pathogens and visualization of terminal lumen

Labs CBC to monitor for anemia,

leukocytosis CMP to monitor liver function, check

for hypoalbuminemia, electrolyte abnormalities

ESR, CRP- nonspecific, but useful serially to monitor disease status

Crohn’s Prognosis Rare cure Intermittent exac/remit Severe dz can be debilitating, severe

pain and dysfunction Dz related mortality low, with most

caused by GI cancers (small bowel, colon)

Ulcerative Colitis

Ulcerative Colitis Chronic, inflammatory, ulcerative disease

arising in colonic mucosa, most often characterized by bloody diarrhea

Only in the colon. Continuous, not segmental Symmetric Not perirectal. No abscesses. No fistulas.

UC Pathophysiology Begins in rectum

– Can remain localized (ulcerative proctitis), or extend to involve entire colon

Inflammation affects mucosa and submucosa only, with sharp border between healthy/diseased tissue

More UC patho Fulminant colitis: transmural extension

of ulceration (NB this is the only time UC is transmural)ileus & peritonitis

Colon loses muscular tone and dilatesTOXIC MEGACOLON

UC- S&S Bloody diarrhea of varied intensity &

duration. Asymptomatic periods Insidious onset of attack

urge to defecate– Mild low abd cramps– Blood/mucus in stools– Can start s/p infection (ie amebiasis)

UC S&S When ulceration confined to

rectosigmoid:– Stool generally normal to hard– Rectal discharges of mucus loaded with

RBCs and WBCs accompany or occur between bowel movements.

– Systemic sx mild or absent

UC S&S When ulceration extends proximally:

– Stools looser, more frequent (>10/day)– Severe cramps, rectal tenesmus– No night respite (diff from IBS or psychogenic

diarrhea)– Stools watery, or all blood and pus– Severe:

Systemic sx include malaise, fever, anemia, anorexia, and wt loss

Can cause hemorrhage requiring transfusion

UC Diagnosis Typical sx by hx, particular attn to

extra-intestinal S&S or hx prev similar attacks

Need to distinguish from Crohn’s, other causes of acute colitis (infection, ischemia)

UC Testing Labs: same as Crohn’s Stool cx Microscopy of fresh poop for

Entamoeba histolitica Recent hosp or abx? Check C. diff

toxin stool assay Sigmoidoscopy- permits visualization,

but can’t distinguish between Crohn’s and UC

W/U fulminant sx Flat and upright abd xray: look for toxic

megacolon NO SCOPES (perf risk!) CBC, ESR, lytes, PT/PTT, type and cross Watch closely for progressive peritonitis Serial abdominal films to follow course

UC Prognosis Usually chronic with remit/relapse

– 10% recover completely from initial event

– 10% have initial presentation with fulminant colitis; can die

Risk of colon cancer– Proportional to duration of sx and amt of colon

affected, but NOT to disease activity

Colon Cancer in UC Begins to appear about 7 yr from illness

onset in pt w/ extensive disease Cumulative likelihood :

– 3% at 15 yrs, 5% at 20 yrs, 9% at 25 yrs Regular colonoscopies after 8-10 yrs of

disease– ANY grade of dysplasia is high risk to progress

to cancer, and colectomy is advised

IBD Treatment

Both Crohn’s and UC

5-aminosalicylic acid(5-ASA)

Blocks production of leukotrienes and prostaglandins

Only active intraluminally Sulfasalazine Start low, go slow. Add folate supplement. Check CBC, LFTs serially

Corticosteroids For acute flares- not ideal for maint

Until sx remit (7-28 days) then taper

Immunomodulating agents- Azathioprine

Inhibit T cell function Good & effective long term- may steroid

needs. Takes 1-3 months to reach efficacy Monitor for bone marrow suppression 3-5% develop high fever or pancreatitis – do

NOT retry Rare hepatotoxicity, check LFTs q 6 mo

Immunomodulating agents

Methotrexate –– For severe dz not responsive to steroids, failed

azathioprine.

Cyclosporine- blocks lymphocyte activation

– For severe UC unresponsive to steroids, pts who may o/w need colectomy

– In Crohn’s, used for refractory fistulas or pyoderma

– Reserve use, and don’t use >6 mo. Renal toxicity, seizures, opportunistic infection

Anticytokine drugs Infliximab, CDP571, CDP870,

adalimumab Antibodies against TNF

ALSO Antibiotics

– Useful in Crohn’s, not UC– Help heal fistulas– Metronidazole or Cipro

Probiotics Supportive Care

Crohn’s Tx General: cramps/diarrhea

loperamide (except in acute/severe) Mild: 5-ASA, abx Moderate: steroids, transition to maint

– Obstruction: add NG suction, IV fluids, parenteral nutrition

– Usually resolves in few days

Crohn’s Tx Fulminant/abscess: toxic appearance,

fever, persistent vomiting, rebound– IV fluids, abx, surgical or percutaneous

drainage– No steroids till infection controlled

Fistulas: abx, if no response in 3-4 weeks, add immunomodulator

Crohn’s Surgery 70% ultimately will have surgery- but

reserve for recurrent obstruction, intractable fistula/abscess

Resection ameliorates, does NOT cure– Further surgery required in 50% of cases– Recurrence is likely, even if all disease is

removed

UC Tx General

– Limit raw fruits and veggies– Try milk-free– Loperamide prn

Mild Left Sided disease– 5 ASA enema/suppository (kind of topical

tx)– Steroid enema– Maybe oral 5-ASA

UC Tx Moderate-Extensive Disease

– Inflammation proximal to splenic flexure– Oral and enema 5-ASA– +/- steroids

Severe- >10 bloody stools daily, tachycardic, febrile, severe abd pain– High dose IV steroids– IV fluids– +/- blood transfusion– Monitor for toxic megacolon

UC Tx Fulminant colitis

– Discontinue all anti-diarrheals– NPO with NG suction– Aggressive IV fluids and lytes– High dose IV steroid– Abx- cipro and metronidazole– If no improvement in 24-48h, surgery to

avoid perfsepsisdeath

UC Surgery 1/3 of pts with extensive UC ultimately

get colectomy Total proctocolectomy = Cure

– No recurrence, and all colon cancer risk is removed

Diverticular Disease

What are they? Diverticuli are saclike mucosal

outpouchings protruding from a tubular structure (the colon, in this case.)

True diverticulum- contains all layers of parent structure (including muscle)

False diverticulum- Mucosal projection thru muscular layer. – aka pseudodiverticulum

Diverticulosis Presence of multiple pseudodiverticuli in the

colon. Likely result of lifelong low fiber diet Usually asymptomatic, but sometimes

inflame or bleed Usually in sigmoid, but can be anywhere in

large colon Uncommon under age 40. every 90 yo has

them.

Why? Increased intraluminal pressure

causes mucosal extrusion thru weak points in muscular layer of bowel. Usually next to intramural vasculature– Why? – area of weakness, there is

already a hole there

S & S Diverticulosis 70% asymptomatic. Usually incidental

finding 15-25% become inflamed and painful

(diverticulitis) 10-15% painless bleeding. Likely

caused by erosion of adjacent vasculature by local trauma (hard stool)

Diverticulosis Tx Reduce segmental spasm. High fiber

diet, supplement with psyllium seed or bran

Tx of diverticular bleed:– 75% stop spontaneously but many will

bleed enough to require transfusion. Tx of bleeding is surgical. Colonoscopic epi, heat or laser.

Diverticulitis Inflammation of a diverticulum Usually in sigmoid Micro or macro perforation releases

intestinal bacteria Localized inflammation in 75% Remaining 25% can lead to abscess, free

intraperitoneal perforation, bowel obstruction, fistulas to bladder, small bowel,etc

Diverticulitis S & S Abdominal pain LLQ tenderness Fever +/- peritoneal signs If obstructed, n/v, abdominal distention Bleeding is rare Fistula can present as pneumaturia, feculent

vaginal discharge, cutaneous or myofascial infection

Dx High suspicion in known diverticulosis ABD CT with oral and IV contrast

– Need to r/o other causes, like appendicitis, colon CA, ovarian CA

– Labs: CBC shows leukocytosis

Diverticulitis TX Mild- Rest, liquid diet, oral abx, go home.

– cipro 500 mg BID or – amox/clavulanate 500 mg TID PLUS

metronidazole 500 mg QID Sx subside quickly. Proceed to low fiber

diet for 1 month Barium enema in 2-4 weeks to eval colon Then back to high fiber diet

Tx- severe diverticulitis Severe pain, fever, leukocytosis, or if

taking prednisone (can cause risk of perf)

Bed rest, NPO, IV fluids, IV abx– Ceftazidime 1 g q 8h PLUS– Metronidazole 500mg q 6-8h

May do CT guided percutaneous drainage of abscess

Surgery Free perforation General peritonitis No improvement or increase in fever or

pain/tenderness on above measures after 48h

Resect involved segment of colon

Surgery- Who else? 2+ previous diverticulitis attacks Persistent tenderness Endoscopic or imaging signs of cancer Dysuria with diverticulitis in male or in

female with hysterectomy (no barrier between/may have fistula)

GI Neoplasms

Cancer in the GI Tract Cancer: unregulated cell growth (neoplasm)

plus the ability to invade distant tissues (malignancy)

Cancer arises usually from rapidly dividing or damaged tissue

Entire GI tract susceptible:

Esophageal Cancer 13,500 cases and 12,500 deaths

overall annually Squamous cell- Most common type Adenocarcinoma- 2nd most common Other esophageal tumors: spindle

cell, verrucous, pseudosarcoma, sarcoma, malignant melanoma– 3% are metastases

Squamous cell 8k cases annually In US

– 4-5x more common in blacks– 2-3x more common in males

Risk factors: alcohol ingestion, tobacco use (any form), achalasia, HPV infection, ingestion of caustic or hot liquids, irradiation, esophageal webs

Esophageal Adenocarcinoma

Usually in distal esoph 4x more common in whites

– >50% of esoph CA in whites Smoking!

– But not alcohol Most cases develop from Barrett’s

esophagus

Esoph CA S&S Earliest stages- no sx Dysphagia when lumen <14 mm

– Progressive from solids, semisolids, liquids, saliva.

– Wt loss- universal, even with good appetite

Esoph CA S&S Compression of nerves by mass effect

– Recurrent laryngealhoarseness– SympatheticHorner’s sign (ptosis,

miosis, anhidrosis, enophthalmosis, anisocoria) - usually unilateral

– Elsewhere spinal pain, hiccups, paralysis of diaphragm

Dyspnea from malignant pleural effusion or pulmonary metastases

Esoph CA Dx

If suspicious, endoscopy with bx If confirmed

– CT chest/abd to assess spread– Endoscopic U/S to assess depth of tumor

and regional node involvement – CBC, lytes, LFTs

Prognosis Average- 5 year survival <5%

– If restricted to mucosa, 80% survival– If in submucosa, 50%– With extension into muscularis, 20%– Extension to adjacent structure, 7%– Distant metastasis, 3%

Treatment

Stage 0, I, some II- surgical resection only, no benefit to chemo or radiation

Stage II, III- Preoperative radiation/chemo to size, then surgery– Surg: en bloc resection of whole tumor with

clean margins, all potentially malignant lymph nodes, part of prox stomach to get draining lymphatics, then gastric pull-up with esophogastric anastomsis.

– If no surg, both chemo & rad Stage IV- palliation, no surgery

Palliation & Support Relieve obstruction to allow oral intake

– Stent, dilation, radiation, laser coag Nutritional support. Enteral or parenteral

supplementation. Consider early surgical/endoscopic placement of feeding tubes to allow feeding when esoph blocked

End-of-life decisions made early

Gastric Cancer 21k cases, 12k deaths 95% gastric adenocarcinoma 2nd MC cancer worldwide Multifactorial etiology; H. Pylori

causative in most cases

Types of Gastric Adenocarcinoma

Classified by gross appearance 1. Protruding- polypoid. Better prog

b/c detected sooner 2. Penetrating- ulcerated tumor 3. Superficial spreading- spreads

along mucosa or infiltrates superficially within stomach wall

Gastric CA S&S Initially nonspecific dyspepsia Later:

– Early satiety (gets full really easy) If tumor obstructs peptic outlet or if stomach non-

distensible

– Dyspepsia If tumor obstructs esoph outlet

– Weight loss– Hematemesis, melena with secondary anemia– Sometimes primary sx are from mets (jaundice,

bone fracture, ascites)

Physical Exam May be normal, or you may find

– Heme positive stool– Epigastric mass– Adenopathy – umbilical, L

supraclavicular, L axillary– Hepatomegaly

Gastric CA Dx Endoscopy with multiple bx and brush

cytology CT chest/abd for spread- if CT neg,

endoscopic U/S CBC, lytes, LFTs- to assess hydration,

anemia, liver mets

Prognosis Overall 5 year survival 5-15% In mucosa only 80% In local nodes 20-40% More widespread, fatal within 1 year

Treatment Depends on spread and pt preference Surgery- If ca limited to stomach and

local nodes only, gastrectomy with local node removal results in 10 month survival (vs 3-4 without)

Extensive node involvement or metspalliation

Colorectal Neoplasms

Polyps Mass of tissue arising from bowel wall,

protruding into lumen Pedunculated or sessile Occur in rectum, sigmoid, with decreasing

frequency toward cecum Usually no symptoms Concern: malignant transformation in

previously benign adenomatous polyp

Polyp S&S and Dx Usually no sx If any, rectal bleeding Most found incidentally on colonoscopy Tx: snare or electrosurgical bx during

colonoscopy– If incomplete removal, laparotomy– If deep invasion into muscularis, eval for colon

cancer– Monitor with serial scopes

Colorectal Cancer 130k cases, 57 k deaths Incidence rises after 40, peaks 60-75 70% in rectum/sigmoid 95% adenocarcinoma, usually

transformation within adenomatous polyp. 80% sporadic, 20% heritable

Colorectal Ca risk factors Ulcerative colitis Diet

– Low fiber -fiber speeds colonic transit, reduces exposure to carcinogens

– High in animal protein – High fat

Theory: Fats increase anaerobes in colon which convert bile to

– High in refined carbs Smoking Genetic factors

Genetic risk factors: hereditary polyp syndromes

(Look-ups)

– Polyposis coli (Familial Adenosis Polyposis - FAP)

– Hereditary Non-Polyposis Colon CA (HNPCC)

– Peutz-Jeghers Syndrome– Familial Juvenile Polyposis Coli– Found during family medical history– Generally warrant more frequent

screening

S&S-depend on location R colon- bleeding (occult or melena)

anemia fatigue/weakness– Large lumen, liquid contents, so rare obstruction

L colon- Constipation alt with diarrhea or stool freq. Partial or complete obstruction with abd pain can be initial presentation– Smaller lumen, semisolid contents. CA can

encircle bowel. Sigmoid or rectal- tenesmus, ribbon stools

Screening For Colorectal Cancer

Very large part of primary care practices Screening method and frequency based on

risk assessment, average or high– Average Risk:

No 1st order relatives with colon CA No prior Hx colon CA or polyps No Hx IBD

– High Risk: Yes to any of the above

Colon CA Screening Modalities:

– Fecal Occult Blood Testing (FOBT)– Sigmoidoscopy– Colonoscopy

FOBT FOBT alone reduces mortality from colon

CA by 33%– Sensitivity single FOBT is 30%– Annual FOBT screen 92% sensitive– 2% of positive FOBT have CA

Problems with FOBT: – Misses non-bleeding polyps– Reduces mortality only 30%– Many false positives

Sigmoidoscopy Sigmoidoscopy reaches 60 cm to

splenic flexure – Misses about ½ of colon– Reduces mortality by 60%– Screen every 5 years– If polyps or lesions found must do

colonoscopy

Colonoscopy Colonoscopy most sensitive screen

– Finds most polyps– Can remove by bx simultaneously– Requires conscious sedation– Risk of perforation, other hazards– Not usually an office procedure– Prep

DCBE Double Contrast Barium Enema

– Screens entire colon– No sedation required– Some cramping– Prep required– Must do colonoscopy if lesions found

Virtual colonoscopy Virtual colonoscopy using computer-

enhanced spiral CT scan– Initial studies in screening populations

showed high sensitivity similar to colonoscopy

– If lesions found, need colonoscopy anyway

– Still must do prep– No bx possible

Capsule Colonoscopy Pill or Capsule Colonoscopy easier on

patient– Prep, then swallow pill– Recording sensors attached to abdomen– Results downloaded and reviewed after 6-8

hours– No manipulation of camera possible– Colonoscopy for biopsy of lesions– Limited data to date, not recommended, yet

Average risk Average Risk: screen all pts >50 y.o.

Choices:– Offer FOBT or FIT yearly. If positive,

then colonoscopy– Offer sigmoidoscopy every 5 years. If

positive, then colonoscopy– Offer colonoscopy every 10 years – Offer DCBE every 5 years

High-Risk Patient Screening

For High Risk pts begin to screen age 40 1st order relative screen every 3-5 years Genetic syndromes- more frequent

screening. Likely will be followed by specialist

Screening For Colorectal Cancer

Overall screening efforts very poor– And liability very high…

65% of all cases found when symptomatic, not at screening

Prognosis 10 year survival

– CA limited to mucosa 90%– Extension thru bowel wall 70-80%– With positive nodes 30-50%– With metastases <20%

Colorectal Cancer Tx Surgical- wide resection of tumor, plus

regional lymph drainage with reanastomosis

Adjuvant chemo survival by 10-30% If no surgical cure option, consider

palliative surgery, or tumor debulking measures (lessen obstructive sx)

Follow-up Colonoscopy q year x 5 yrs, then q 3

yrs

H&P, CBC, LFTs q 3 months x 3 yrs, then q 6 months x 2 yr

Small Intestine Tumors Less than 5% all GI cancers Many benign tumors: adenomas,

leiomyomas, lipomas, angiomas Increased risk malignancy with Crohn’s Dz,

celiac disease– Adenocarcinoma, lymphoma

Presentation: recurrent cramping abd pain, periodic small bowel obstruction (SBO), intussusception, chronic bleeds

Small Intestine Tumors Diagnose with CT and DCBE

– Usually out of reach of colonoscope or EGD

Exploratory laparotomy for biopsy Stage as colon cancer Treat with surgical resection, +/-

radiation or chemo for debulking

Anorectal cancer Usually adenocarcinoma Mets to lymphatics of rectum and

inguinal nodes Risk factors: HPV, chronic fistulas,

irradiation, receptive anal intercourse, Screening with Pap/HPV testing Tx: wide local excision, chemo and

rad

Pancreatic Cancer 30,500 cases, 29,000 deaths Most are exocrine tumors, primarily ductal

adenocarcinoma 80% found in head of pancreas Mean age 55, 2x more common in males Risk: smoking, chronic pancreatitis,

longstanding DM, some heredity

Pancreatic Cancer Usually no symptoms until lesion too

advanced to resect Symptoms non-specific, with large DDx

– Weight loss, pain, anorexia, fatigue, dyspepsia, reflux, jaundice

– Severe upper abd pain, radiates to back, relieved by forward lean or fetal position

– Obstructive jaundice and resulting pruritis in 80-90%

S&S Palpable mass, ascites in 20% Left supraclavicular lymphadenopathy

(Virchow's node)

90% have locally advanced dz w/ retroperitoneal structure involvement, regional lymph spread, or mets at time of pres

Diagnosing Pancreatic Cancer

U/S initially to show ducts, stones, masses CT better defines tumor, and vascular

involvement MRI great for vasculature Biopsy: transcutaneous, ERCP, guided fine-

needle aspiration

Prognosis/tx Overall, <2% survival 80-90% unresectable (mets or invasion of

major blood vessels) If resectable- Whipple procedure

(pancreaticoduodenectomy) with adjuvant chemo+ rad 40% 2 yr and 25% 5 yr survival if node negative

Treatment Appropriate end-of-life care:

managing death, hospice care, etc Sx Control! PAIN- opioids (without concern for

addiction as barrier to effective pain control)

Hepatic cancer Liver is common place for metastasis for

many primary cancers, esp from GI tract, breast, lung, pancreas.– Mets more common than primary hepatocellular

carcinoma Primary cancer14k deaths annually in US Primary liver cancer more common in pts

with cirrhosis, common in areas with prevalent Hep B & C infections– Risk 100 fold in chronic hep B carriers

Liver Ca S&S

Initially nonspecific: abd pain, fever PE may show RUQ mass, or BIG,

hard, tender liver Hepatic bruits with pleuritic pain Late: jaundice, hepatic

encephalopathy

Primary Liver Cancer Dx with

– imaging: U/S, MRI or abd CT w/ contrast– Labs: AFP– Liver bx for definitive dx

Overall 2 year survival <5%– IF tumor is <2cm and localized to one

lobe, can try resection or transplant. Chemo/rad NO help.

Hepatic Ca Prevention Hep B vaccination Prevent cirrhosis Screen pts with cirrhosis for CA

– AFP and liver U/S q 6-12 mo