Hi All,

The #ProjectSmackdown team understands how difficult things are now with #Coronavirus.  We've been working from home for weeks and it's just not easy.

To help out and thank you all for your support, the team has decided to release our Colorectal review section along with an audio version so that you can get some review done while you're out, working, or on the road.

Take a look at the audio version, video lecture, and written section beneath.  If you like the review, the whole course (with review book included) is available here on our site.

Thanks for everything you're doing, and remember:

#AbsiteSmackdown!

The Project Smackdown Team

 

 

 

Absite Smackdown! Colorectal Absite Review from Steven President on Vimeo.

 

 

Colorectal

 

Development begins during the fourth gestational week

Except for the distal anal canal from ectoderm, colon is endoderm.  Dentate line is dividing line between this ectoderm and endoderm

R colon and proximal transverse colon (2/3) are SMA supplied and come from midgut

Distal 1/3 transverse colon, L colon, sigmoid colon, and rectum (proximal) are IMA supplied and come from hindgut

Marginal artery of Drummond:  runs along colon at margin and is a collateral between IMA and SMA

Arc of Riolan:  direct, short connection between IMA and SMA 

 

Watershed areas where hypotension may cause ischemia

• Griffith’s point:  at splenic flexure.  SMA and IMA junction
• Sudeck’s point:  at rectum/rectosigmoid area.  Superior rectal and middle rectal area.

 

Urogenital sinus divided from rectum during development.  Occurs by urorectal septum formation.

While sigmoid and transverse colon are intraperitoneal, R and L colon are retroperitoneal.

Colonocytes use butyrate (fuel of the colonocyte).  Main nutrient of colonocytes is short chain fatty acids.

Colon absorbs H20 (up to 5L per day) but again small bowel absorbs more H20.  Does so via passive absorption.

Colon secretes K+ and reabsorbs Na+ and water.

Four histologic layers superficial to deep:  serosa, muscularis propria (circular muscle layer), submucosa, mucosa (columnar epithelium).

Plicae semilunares:  form haustra.  These are transverse bands along colon.

Actively absorbs sodium, choride, and potassium.

Bacteria in colon produce ammonia and fatty acids.

 

Gross anatomic layers (superficial to deep)

• Serosa
• stops at level of peritoneal reflection (low / mid rectum)
• Outer longitudinal muscle
• In rectum, the longitudinal muscle is entire circumference of bowel
• Elsewhere, longitudinal muscle comprises the tenia coli which coalesce at base of appendix and more distally splay out toward distal sigmoid.
• Tenia coli are 3 muscle bands that run longitudinally along colon.  At junction of rectum and sigmoid, these broaden and encompass circumference of bowel.
• Inner circular muscle
• Forms internal anal at level of anal canal.  Internal sphincter is involuntary.
• Submucosa
• Mucosa
• Includes epithelium, lamina propria, and muscularis mucosa

 

External anal sphincter is voluntary, comprised of striated muscle, and contiguous with levator ani muscle.

 

Fascial layers near colon with unique names

• Waldeyer’s fascia
• Attaches to presacral fascia
• Attaches to fascia propria of mesorectum anteriorly
• Denonvillier’s fascia
• In males separates rectum from seminal vesicles and prostate
• In females separates rectum from vagina
• Presacral fascia
• Covers venous plexus in presacral area

 

Colon vs. small bowel

• Colon has haustra which, unlike plicae circulares, are not circumfrential.
• Colon has appendices epiploicae
• Colon has tenia coli (outer longitudinal muscle)
• Colon has intestinal glands (such as Crypts of Lieberkuhn) which are deeper than those of the small bowel.
• Colon lacks villi, small bowl has those.

 

Vascular supply

• SMA and IMA supply midgut and hindgut regions listed above
• Also middle hemorrhoidal artery from iliacs supplies portion of rectum
• Also inferior hemorrhoidal artery from pudendal supplies portion of rectum
• Watershed area at splenic flexure is vulnerable to ischemia
• In contrast, superior, middle, and inferior rectal arteries supply rectum making ischemia less likely
• Marginal artery of Drummond connects branches that supply colon

 

Internal anal sphincter is innervated by sympathetic and parasympathetics, while external anal sphincter is innervated via branch of pudendal (inferior rectal nerve).  So external sphincter is under conscious control.

Rectoanal reflex occurs when feces reach rectum.  Internal anal sphincter and pelvic floor relax.  External anal sphincter contracts.  Feces approach anus and anoderm.

 

Acute Appendicitis

• More common in men

• Typically seen in 2^nd to 4^th decades
• Affects approximately 7% of the population
• Due to occlusion of appendiceal lumen, most commonly due to lymphoid hyperplasia in adults.  Other causes include fecalith and tumor.
• In older patients, incidence of tumor significantly increases (However still less common than lymphoid hyperplasia.) This is why appendicitis in older people should increase clinical suspicion of underlying appendiceal tumor.
• Elderly patients, pregnant patients, and children under 5 years of age present late with acute appendicitis owing to their atypical symptoms.
• High grade fever, symptom onset > 24 hours previously, or generalized peritonitis should increase clinical suspicion for perforation.  Notice that elderly patients (who present late) are typically more commonly perforated.
• Classic history (often not seen in elderly)
• Early on, non-specific abdominal discomfort, nausea, fever, anorexia.
• Later, peri-umbilical pain is present and shifts to the RLQ at McBurney’s point.
• Sometimes pain may be demonstrated in RLQ by palpation of LLQ.  This is called Rovsing’s sign.  Or with hip flexion (psoas sign).  Or with internally rotating the R leg (obturator sign).
• Lab tests may demonstrate a mild leukocytosis with or without left shift.
• CT scans are often used in addition to exam owing to approximately 95% sensitivity.  Classic findings include:
• Enlarged appendix with enhancement (> 6mm)
• Fecalith
• Wall thickening
• Fat stranding
• Ultrasound is especially useful in children and pregnant women given radiation exposure considerations, although it is less sensitive compared to CT
• MRI is especially useful in pregnant women to assist in diagnosing appendicitis in order to minimize radiation effects.
• Treatment is appendectomy
• Use tenia coli to locate base of appendix.  They will come together over base of appendix.
• If phlegmon or abscess, delay resection, give antibiotics, and perform interval appendectomy.
• 15% negative appendectomy rate despite current advances in imaging and adjunct tests

 

Carcinoid

• Most common malignancy of appendix
• 90% or more of cases are at appendix or distal ileum
• From enterochromaffin cells
• Usually found incidentally with appendectomy
• May be found with obstruction too or pain
• If you happen to suspect it, confirm with serum and urine serotonin (usually elevated) or chromogranin A.  Octreotide scan may localize.  Path shows stains positive for chromogranin A as well.  However, as mentioned, usually found incidentally.
• Only about 10% of cases or less are associated with carcinoid syndrome (see earlier section on carcinoid syndrome)
• Most are < 2 cm at near appendiceal tip; however, again:
• If base involved, needs right hemicolectomy no matter what size.
• If > 2 cm, needs right hemicolectomy
• If there are mets to liver, no matter what size and whether involves base, needs R hemicolectomy
• Resect hepatic mets (debulk) if present
• Octreotide is used to treat symptoms if mets
• Streptozocin, doxorubicin are used as chemotherapy for palliation if unresectable mets.

 

Typhlitis

• May masquerade as appendicitis
• Neutropenic enterocolitis that affects the terminal ileum, cecum, & right colon.
• When patient has leukemia or is immunosuppressed (eg AIDS, chemo, transplant) consider this diagnosis
• Presents as diahrrea, fever, emesis, RLQ pain, etc.
• Useful to calculate absolute neutrophil count (ANC)
• Treatment is medical and includes NGT, NPO, IV fluid, and antibiotics.  May treat ANC with neupogen as well.

 

 

 

Large bowel obstruction

• Whether patient has had previous surgery or has NOT had previous surgery:  most common cause of large bowel obstruction is cancer
• Trostle’s rule:  don’t let a patient with any question of large bowel obstruction leave the hospital without an operation unless it’s due to Ogilvie’s.  Don’t see them in the ER and discharge them with a partial colon obstruction, etc.
• 15% of intestinal obstruction cases
• other causes include diverticulitis, volvulus, impaction, post op adhesions, hernia, pseudo-obstruction.
• Emesis is more commonly a later finding owing to presence of ileocecal valve
• Lab tests are often non-specific
• Dilated colon without rectal air suggests mechanical obstruction while presence of air suggests pseudo-obstruction
• CT imaging very useful to make diagnosis.
• Fluid resuscitate, place NGT, correct electrolytes
• Unlike small bowel obstruction where NGT and wait is often first-line treatment, surgical intervention is first line treatment for large bowel obstruction.
• Unless it’s due to Ogilvie’s (pseudo-obstruction) large bowel obstruction requires operation.  (Not necessarily emergent but generally on same hospital stay.  See Trostle’s rule.)
• For pseudo-obstruction (Ogilvie’s syndrome), decompression and neostigmine may be utilized.
• Mortality rate for patients with large bowel obstruction is approximately 20%

 

Volvulus

• Cause of about 5% of large bowel obstructions
• Closed loop which is obstruction due to twist of bowel more than 180 degrees on its mesentery.  Results in obstruction at two locations that are included where bowel twists.
• Risk factors include being bedridden, chronic constipation, megacolon, pregnancy, redundant segment.
• Typically seen in patients > 70 years old.
• Cecal bascule is folding of cecum anteromedially on itself.
• Cecal volvulus occurs when cecum rotates around ileocolic vessels and is owing to twisting of mesentery.
• Volvulus may and often does result in ischemia.  Abdominal pain and hemodynamic instability may be seen.
• Classic sign of sigmoid volvulus on xray is “bent inner tube” narrowing into “bird’s beak”.
• “Coffee bean” appearance may be seen on xray in patients with cecal volvulus.
• If nonstrangulated sigmoid volvulus, may perform endoscopic decompression with placement of rectal tube.  Surgery is typically indicated even with successful reduction to avoid recurrence.  Urgent surgical intervention should be performed for sigmoid volvulus if there is a question of strangulation.
• Cecal volvulus requires emergent surgery which may include cecopexy or right hemicolectomy.  Cecostomy is an option but carries a high risk of recurrence and so is performed in select patients only.

 

Diverticulae

• Most common disease of the colon
• Greater than 90% of the time affects the sigmoid colon of geriatric patients
• Obesity, low fiber diet, tobacco use, constipation, and sedentary lifestyle are all risk factures
• Herniation of mucosa at weak areas in muscularis externa.  Areas where blood vessels enter and leave are some of these weak areas.
• Diverticulosis is presence of these non-inflamed lesions
• Diverticulitis is when inflammation is present at these diverticuli, often due to a microperforation.  Complications include frank perforation, stricture (long term), obstruction, or gross perforation.
• Diverticulosis may bleed and present as bright red blood per rectum
• Remember:  “-osis bleeds, -itis perfs”.
• Diverticulitis typically causes lower quadrant pain with associated leukocytosis and fever.
• WBC is non-specific.  CT scan is useful to demonstrate whether diverticulitis, diverticulosis, and / or a related complication is present.
• Diverticulosis
• High fiber diet
• Bleeds usually resolve spontaneously but requires surgery if persists or recurs
• Diverticulitis
• Typically treated with bowel rest and oral antibiotics
• Drain if abscess present
• Operate emergently if perforation and significant free air.  Hartmann’s procedure is resection of diseased portion of colon, abdominal lavage, and end colostomy.  Note that proximal extent of colonic resection is to the level of induration and NOT all of the colon that demonstrates diverticulae.
• Perforation with abscess often amenable to percutaneous drainage.
• If there is an episode of complicated diverticulitis, eg abscess, elective resection at a later date is indicated.  Other indications to operate include young patient (because will likely have many more episodes and issues throughout life), immunosuppressed patients, or after multiple (typically two) attacks.

 

Lower GI bleed

• When you see blood per rectum, remember that UPPER GI bleed is most common cause
• Lower GI bleed (LGIB) More common in men
• Average age at diagnosis is 63 to late 70s
• Lower GI bleeding is defined as bleeding distal to the ligament of Treitz (LOT)
• Angiodyplasia, diverticulosis, Meckel’s, ischemia, inflammatory bowel disease, infection (eg E. Coli or C. Diff), cancer, or hemorrhoids are all potential causes.
• Lower GI bleed usually stops spontaneously
• Transfusion of more than 6U PRBCs within first 24 hours of stay predicts need for operative intervention
• Remember, an NGT is one of the first steps to localize a GI bleed to UGI or LGI bleed.
• An NGT negative for UGI is one that demonstrates no blood but DOES demonstrate bile.  Just because an NGT does NOT demonstrate blood does NOT mean an UGI bleed is ruled out.
• And even when an NGT is truly negative (shows bile and NO blood) it is NOT a perfect test to rule out UGI bleeding.
• If NGT is positive for UGI bleed, perform EGD, establish source, and treat as appropriate.
• If NGT does not demonstrate UGI bleed, perform colonoscopy.
• If source visualized, injection / thermal therapy.
• If GI source not visualized, and if “fast bleed” (more than 1 mL / min), perform angiography with angioembolization if possible.  (Localizes and treats.)
• If GI source not visualized, and if not a “fast bleed” performed tagged red blood cell scan to localize.
• If severe bleeding present, and this prevents visualization during colonoscopy…
• if “fast bleed” (more than 1 mL / min), perform angiography with angioembolization if possible.  (Localizes and treats.)
• If not a “fast bleed” performed tagged red blood cell scan to localize.
• Yes, this is similar to nonvisualization portion above.
• If bleeding is uncontrolled after angioembolization attempted, patient requires surgical intervention.
• If bleeding is controlled, but no colonic source is identified, evaluate small bowel with capsule endoscopy or other technique.

 

Inflammatory bowel disease

• Crohn’s and Ulcerative Colitis (UC)
• Underlying causes for each are not clear
• Extra-intestinal manifestations of both
• Primary sclerosing cholangitis (more especially with UC)
• Erythema nodosum
• Pyoderma gangrenosum
• Sacro-ileitis
• Arthritis
• Uveitis & scleritis
• Pericarditis
• Ankylosing spondylitis
• Patients with inflammatory bowel disease require annual colonscopies starting after disease has been present for 8-10 years owing to risk of colorectal cancer.

Specifics of ulcerative colitis

• Typically affects patients in 3^rd or 7^th decade
• 10 / 100,000 is incidence
• Ashkenazi Jewish descent is risk factor
• Interestingly, tobacco DECREASES risk
• Typically seen in left colon and rectum
• Diarrhea, blood per rectum, abdominal pain, fever are typical symptoms
• Colonoscopy with biopsy makes diagnosis
• Depth of involvement includes mucosa and submucosa
• Path features friable mucosa, crypt abscesses, pseudopolyps, and continuous involvement of bowel (NO skip lesions)
• Bleeding, toxic megacolon, fulminant UC, colorectal cancer and extra-intestinal manifestations may be seen
• Extra-intestinal manifestations include aphthous ulcer, iritis, uveitis, episcleritis, seronegative arthritis, ankylosing spondylitis, sacroilitis, erythema nodosum, pyoderma gangrenosum, DVT & PE, autoimmune hemolytic anemia, clubbing, primary sclerosing cholangitis
  • Some manifestations get better with colectomy eg anemia, arthritis, ocular issues.
  • Some manifestations do NOT get better with colectomy: primary sclerosing cholangitis, ankylosing spondylitis
  • Half of pyoderma gangrenosum patients get better with colectomy.
• Treatment for an acute attack may include steroids, 5-ASA, Infliximab (severe disease), cyclosporine (for steroid refractory disease)
• Maintenance treatment may include sulfasalazine or 5-ASA. May include 6-mercaptopurine / azathioprine
• Subtotal colectomy / proctocolectomy with end ileostomy is performed if emergency surgery is required
• Total proctocolectomy with ileal pouch and anal anastomosis is most common procedure if patient is candidate for elective procedure. However, total proctocolectomy and permanenet ileostomy may also be performed in this context.

Specifics of Crohn’s disease         

• 2^nd and 6^th decade is peak incidence
• affects around 3/100,000 people
• Ashkenazi Jewish descent is risk factor
• Tobacco increases risk
• Unlike UC that is seen in the colon, Crohn’s is more commonly seen anywhere along the GI tract. Most common in the terminal ileum.
• Obstruction, abdominal pain, weight loss, diarrhea, bleeding, and fever may be seen
• Colonscopy and biopsy may give diagnosis. If present in small bowel (and not colon) CT scan with oral contrast may be useful
• Involvement of bowel wall is transmural
• Skip lesions seen. Non-caseating granulomas, fistulae (sometimes perianal), cobblestoning, and strictures are seen
• Toxic megacolon, small bowel cancers, colorectal cancer, and extra-intestinal manifestations, are all seen
• Perianal disease is treated with flagyl.
• Treatment for maintenance and acute attacks is similar to ulcerative colitis.
• Elective surgical intervention involves resection of diseased portions of bowel.
• Stricturoplasty is used when possible to minimize the risk of short bowel syndrome.

 

Carcinoid of the colon and rectum

• Approximately 15% of carcinoid tumors
• Low rectal carcinoids
• Greater than 2 cm:  wide excision with negative margins
• Less than 2 cm or any size with invasion of muscularis propria:  perform APR
• Colonic or high rectal carcinoids
• Greater than 1 cm:  resection
• Less than 1 cm:  polypectomy may be performed

 

Colorectal syndromes associated with hamartomatous polyps

• Peutz-Jegher

• Polyps typically in ileum or jejunum. May also be in rectum.
• Autosomal dominant
• Polyps are hamrtomatous
• Buccal mucosa is hyperpigmented
• Increased risk of adenomatous degeneration and increase risk of extra-intestinal cancers
• Breast, testis/ovary, pancreas, biliary

• Cowden’s syndrome
• PTEN mutation
• Autosomal dominant
• GI polyps
• Leiomyomas of uterus
• Breast and thyroid cancers
• Mucocutaneous lesions
• Juvenile polyposis
• Autosomal dominant
• Polyps throughout GI tract
• Colorectal cancer risk is increased
• Cronkite-Canada syndrome
• Sporadic
• Dystrophic nails
• Hyperpigmentation
• Alopecia

 

Colorectal cancer

• Equal incidence in men and women
• Second leading cause of cancer death in US
• Age > 50 is risk factor
• History of colonic adenoma is a risk factor
• Inflammatory bowel disease is a risk factor
• Family history of colon cancer is a risk factor
• APC, DCC, p53 and k-ras are main gene mutations
• Adenomas are premalignant.  Tubular adenomas are most common, villous adenomas have increased risk of cancer compared to tubulovillous and tubular.
• Change in stool caliber, rectal bleeding, and obstruction are some of many signs
• Increased carcinoembryonic antigen (CEA) is sometimes seen
• Digital rectal exam (DRE) and fecal occult blood testing (FOBT) are useful
• CT colonoscopy, colonoscopy, and barium enema are useful to make diagnosis.
• Tools for staging include endoscopic ultrasound (EUS), MRI pelvis, and CT.
• Resections for colon cancer should include at least 12 lymph nodes to allow for correct staging
• Treatment for rectal cancer is DIFFERENT than colon cancer and includes radiation and chemotherapy.  Colon cancer receives chemo ONLY.
• Need colonoscopy as part of staging to be sure there’s no synchronous lesion.
• T portion of TNM staging is based on invasiveness not tumor size:
• Tis = lesion does NOT invade submucosa
• T1 = invades submucosa
• T2 = invades muscularis propria
• T3 = invades into subserosa / non-peritonealized pericolic or perirectal tissue
• T4 = invades adjacent organ
• N portion of TNM staging is generally related to the number of nodes involved
• N0 = no nodes involved
• N1 = 1-3 nodes involved
• N2 = 4 or more nodes involved
• N3 = lymph node adjacent to major vessel is positive
• M portion
• M0 metastatic disease absent
• M1 positive mets
• Stage 1 is TisN0M0
• Stage 2 is T1 or T2 N0M0
• Stage 3 is any tumor with positive nodes but no metastasis
• Best for T and N status is TRUS (trans-retal ultrasound) if lesion is accessible
• Stage 4 is any tumor with or without nodes but positive metastasis
• Most common site for mets is liver.  If resectable and isolated 5 year survival is 35%
• Lung mets (isolated and resectable) with 25% 5 year survival rate
• Isolated liver or lung mets should receive resection
• Rectal cancer may metastasize to spine directly via Batson’s plexus
• Alternative staging for colon cancer is Duke’s classification
• Stage A:  submucosal invasion
• Stage B:  invasion into muscularis propria with negative nodes
• Stage C:  positive nodes
• Stage D:  presence of metastasis or invasion into adjacent structures
• Less commonly used that TNM classification
• Each TNM stage aligns with a Duke’s classification
• Five year survival by stage:
• Stage 1(Duke’s A) = 95%
• Stage 2 (Duke’s B) = 85%
• Stage 3 (Duke’s C) = 30-60%
• Stage 4 (Duke’s D) = 5%

 

Amsterdam criteria are used to determine whether patient has hereditary non-polyposis colon cancer (HNPCC)

• Also known as 3, 2, 1 rule
• Confirmation that tumor is NOT familial adenomatous polyposis (FAP) related by biopsy / testing
• 3 or more relatives, including at least one first degree relative, with a known HNPCC
• 2 or more generations affected in family
• 1 or more affected patient who is less than 50 years old

 

Colon cancer syndromes

• 20% of patients with colon cancer have a family history of colon cancer
• HNPCC (Lynch Syndrome)
• Due to mutations in DNA mismatch repair genes, eg hMLH1, hMSH2
• Lifetime risk of colon cancer is 85%
• Lynch 1 leads to onset of colorectal cancer at a young age
• Lynch 2 give increased risk of GI malignancy such as stomach, small bowel, pancreas, biliary, endometrial, and genitourinary tumors
• Annual colonoscopy starting at 20-25 years or 10 years earlier than age at which youngest family member diagnosed with colorectal cancer.  For females with Lynch syndrome, screening recommendations include transvaginal ultrasound annually at 25-35 years or annual endometrial biopsy.
• Turcot’s syndrome
• Due APC gene mutation (on chromosome 5q)
• Increased risk of colorectal cancer and brain tumors.  Colonic adenomas seen.
• Screening recommendations are same as for familial adenomatous polyposis (FAP) as beneath.
• Gardner’s syndrome
• Due to APC gene mutation on chromosome 5q as with Turcot’s
• Increased risk of colorectal cancer with desmoid tumors, osteoid tumors, and skin cysts.  Colonic adenomas seen.
• Screening as with FAP as beneath.
• FAP
• APC mutation (chromosome 5q)
• Colon ademonas seen and lifetime risk of colorectal cancer is 100%.
• Increased risk of multiple other tumors as well including periampullary tumors, thyroid tumors, and adrenocortical tumors.
• Flexible sigmoidoscopy annually at 10 -15 years old.
• Upper endoscopy each 1-3 years after age 25
• Diagnosis of FAP requires surgery
• Procedure chosen depends on whether rectum is involved, whether cancer is already present, and also patient age
• Outcomes for resection in FAP patients are similar to colorectal cancer cases that are NOT related to a hereditary syndrome if resection is prophylactic in nature when performed.
• If cancer present, subtotal colectomy or segmental colectomy is performed.  And total abdominal hysterectomy with bilateral salpingo-oopherectomy is often added in women with Lynch 2 owing to risk of eventual cancer in reproductive organs.
• Otherwise, total proctocoletomy with ileostomy, total abdominal colectomy with ileorectal anastomosis, or total proctocolectomy with J pouch (aka Ileal Pouch Anal Anastamosis [IPAA] is chosen.

 

Most common causes of acute pain at anus are external hemorrhoid thrombosis, perianal abscess, and anal fissure.

 

Condyloma acuminata

• Due to human papilloma virus (HPV)
• Fulgaration is treatment (laser or alternative)

 

Anal fissure

• Ulcer or tear which is distal to dentate line in the anoderm
• Typically posterior and in midline
• May be related to insufficient fiber in diet
• Pain and bleeding with defecation
• Caused by hypertonic internal anal sphincter
• At times, may see sentinel pile distal to the ulcer / tear in anoderm
• May see hypertrophy of anal papillae proximally
• Exam makes diagnosis, and internal anal sphincter spasm is also seen
• Should perform endoscopy / anoscopy to rule out more serious underlying condition
• Treatment includes stool softeners, nifedipine ointment, Sitz baths.  When medical treatment fails, requires lateral internal anal sphincterotomy or injection of botox into sphincter
• Note that lateral internal sphincterotomy may give incontinence

 

Hemorrhoids

 

• Risk factors include things that increase intra-abdominal pressure, eg:  obesity, pregnancy, needing to strain with defecation
• Common positions are left lateral, right anterolateral, and right posterolateral
• Due to engorged anal submucosa cushions and NOT varicose veins
• Types include internal and external
• Internal are Insensate.  Also are superior to dentate line.  (Therefore columnar or transitional epithelium.) Staged by degree of prolapse.
• First degree:  no prolapse
• Second degree:  spontaneously reducing prolapse
• Third degree:  prolapse that requires reduction
• Fourth degree:  prolapse that can not be reduced
• External hemorrhoids are beneath the dentate line (therefore squamous epithelial tissue) in the innervated anoderm.  These hurt.
• May present as red blood per rectum.  May cause bothersome swelling and difficulties with hygiene in area.
• Digital rectal exam, anoscopy, and sigmoidoscopy help make diagnosis.
• Screen for colon cancer with endoscopy if patient is less than 40 years old, unusual symptoms are noted, or there is a family history of colon CA.
• Treatments include Sitz baths, stool softeners, increasing water and fiber intake, creams, ointments.
• Many options for treatment exist if medical management fails, including rubber band ligation, sclerotherapy, and hemorrhoidectomy.
• If large hemorrhoids and/or significant external component, perform surgical hemorrhoidectomy.
• Office excision may be performed for isolated, thrombosed external hemorrhoid that presents less than 4-5 days from onset.  Fiber and Sitz baths may be used for patients with later presentation.

 

Pilonidal cyst

• Infected hair containing sinus.  Usually seen in gluteal cleft but may also be seen on hands of hairstylists.
• Usually seen in men
• Diagnosed on exam.
• Treated with incision and resection of cyst lining with marsupialization or closure

 

Proctitis

• HPV, CMV, UC, Crohn’s, radiation, C diff, STDs…all can cause inflammation of the anorectum.
• Treatment is based on the underlying cause.

 

Anal fistula

• Occurs between anal canal and peri-anal skin
• Inter, trans, supra, or extra-sphincteric are classifications.
• Starts as abscess in a crypt gland of dentate line which becomes an interphincteric abscess and then peri-anal abscess
• Although most are idiopathic, Crohn’s may be a cause
• Most are anterior or posterior
• Lateral fistula are more often due to less common causes such as HIV or TB
• Presents as drainage from an external opening, often in a location where there was a perianal abscess that “never healed”.
• Goodsall’s rule (sometimes called the “dog rule”):  more anterior openings tract directly into anal canal, and posterior openings take a curved tract into the anal canal.  Dogs’ noses are straight and their tails are curved, so Goodsall’s rule is sometimes nicknamed the dog rule.
• Treatment is fistulotomy, and remember that incontinence is a potential complication if sphincter is divided.  So fistulae that may involve external sphincter often receive a staged fistulotomy with a non-cutting seton.
• Remember that Crohn’s and malignancy may cause fistulae.  These should be considered before treating anorectal complaints.

 

Rectal prolapse

• Usually seen in women > 60 years old
• Rectal wall protrudes through anus and presents as incontinence, vaginal / uterine prolapse, cystocele, enterocele, or constipation.
• Often associated with weak pelvic floor
• True prolapse (full thickness) demonstrates circumferential mucosal folds
• False prolapse (mucosa only) demonstrates radial folds
• The rectum may become ischemic which causes tenderness.  This is rare.
• Colonscopy or contrast enema should be performed to rule out underlying lesion
• For good operative candidates, laparotomy and rectopexy (with or without sigmoid resection) is performed
• For others, rectosigmoidectomy via perineal approach (Altemeier procedure) is performed or Delorme’s procedure (perineal approach with resection of mucosa and submucosa of prolapsed segment only)

 

Anal cancer

• Usually squamous cell cancer from HPV infection
• Adenocarcinoma is 10% of cases only and prognosis is worse
• Most common in young male patients who engage in receptive anal intercourse
• HIV, Crohn’s, Hodgkin’s, HSV2, and STDs are other risk factors.
• May be asymptomatic or demonstrate pain, puritis, rectal bleeding, or anal fullness.
• Exam may reveal anal mass with or without lymphadenopathy
• Colonscopy with biopsy reveals diagnosis.  Staging performed with CT abdomen and pelvis.
• Nigro protocol (5FU and mitomycin with radiation) is used for larger lesions or anal canal lesions.  Small lesions or those on perianal skin receive wide local excision.
• Abdomino-perineal resection (APR) is used for recurrent or persistent disease after these treatments.
• 5 year survival is 60-70%
• rarely basal cell CA
• treatment is wide local excision.  Only 3mm margin needed.  APR rarely necessary…typically only if sphincter is involved.

 

Miscellaneous facts from colorectal

External anal sphincter is puborectalis muscle and is under conscious control.  Internal pudendal nerve is innervation (inferior rectal branch).  This sphincter is actually a continuation of levator ani muscle which is striated.

Internal anal sphincter is innervated by pelvic splanchnic nerves and its normal state is to be contracted.  It is a continuation of muscularis propria from colon.

Colonic inertia is significant slow transit time.  Patients may need subtotal colectomy.

Stump pouchitis (aka diversion or disuse pouchitis) is treated with short chain fatty acid enemas

Infectious pouchitis is treated with flagyl

False positive guiac (fecal occult blood screen) with cimetidine, beef, vitamin C, or iron.

 

Polypectomy performed by colonoscopy and pathology shows T1 cancer

• If 2mm clear margin, poly is well differentiated, there is no vascular / lymph invasion…nothing else to do.  Continue surveillance
• If ANY of those criteria are violated, needs colon resection

 

Overall screening recommendations for colorectal cancer:  colonscopy starting at 50YOA for normal risk patients, 40 YOA (or ten years before youngest case) if family history colon cancer.  Exceptions as noted in hereditary colon cancer syndromes as above.

 

Low rectal villous adenoma with atypia:  transanal resection of as much as possible.  APR only if cancer is present.

• Pathology shows T1 lesion after transanal for villous polyp:  no need for further resection if 2mm margins are clear AND no vascular / lymph invasion.  If there is either or both of those findings, APR / LAR.
• Pathology shows T2 lesion after transanal for villous polyp:  APR or LAR.

 

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