General Surgery - Toronto Notes Abridged for the PDA To be used only in conjunction with the printed Toronto

Notes

y of the Abdominal Wall

Shady Ashamalla, Connie Chiu and Stacy Woods, chapter editors Cagla Eskicioglu and Nadra Ginting, associate editors Dr. Andrew J. Smith and Dr. Frances Wright, staff editors Acute Abdominal Pain Hernia Bowel Obstruction Small Bowel Obstruction Large Bowel Obstruction Appendicitis Ostomies Diverticular Disease Angiodysplasia Volvulus Colorectal Polyps Colorectal Carcinoma Hemorrhoids Anal Fissures Anorectal Abscess Fistula-in-ano Cholelithiasis Biliary Colic Acute Cholecystitis Acalculous Cholecystitis Choledocholithiasis Acute Cholangitis Breast Cancer Post-operative Fever

Acute Abdominal Pain

Table 1. Differential Diagnosis of Acute Abdominal Pain
GASTROINTESTINAL gastritis penetrating/perforated peptic ulcer acute cholecystitis biliary colic pancreatitis appendicitis diverticulitis/Meckels bowel obstruction/perforation intestinal ischemia inflammatory bowel disease (IBD) severe gastroenteritis mesenteric adenitis (more in children) abscess flatus

History
pain associated symptoms systemic: fever, chills, night sweats, weight loss, jaundice, pruritus gastrointestinal: anorexia, nausea, vomiting, diarrhea, constipation, tenesmus, obstipation, melena, hematochezia, hematemesis, pale stools, steatorrhea urinary: dysuria, hematuria, urinary frequency, dark urine gynecological: menstrual irregularities, vaginal discharge, previous sexually transmitted disease (STD), intrauterine device (IUD) use, sexual history extra-intestinal features: eyes, skin, joints other: food intolerances, time since last meal, travel history, contact history, usual bowel habits, LMP, drug history (NSAIDs, EtOH, laxatives, steroids, ulcer medications), family history (IBD, stones, cancers)

Physical Examination
general observation: patient position (i.e. lying still vs. writhing), facial expression vitals: postural changes, fever status of hydration: vital signs, mucous membranes, skin turgor, urinary output, jugular venous pressure (JVP), mental status cardiovascular/respiratory examination abdominal examination inspection: guarding, distention, bulging flanks, scars, visible peristalsis, stigmata of liver disease auscultation: absent, decreased, normal, increased, tinkling bowel sounds, bruits percussion: hypertympanic sounds (bowel obstruction), hepatosplenomegaly, ascites, percussion tenderness (peritonitis) palpation: tenderness, abdominal masses (including pulsatile AAA), hepatosplenomegaly, ascites costovertebral angle (CVA) tenderness, cough and shake tenderness (peritonitis) specific signs Castells Sign: dullness to percussion over Traubes space on inspiration (indicates splenomegaly) Courvoisiers sign: palpable, non-tender gall bladder with jaundice (pancreatic or biliary malignancy) Cullens sign: blue discoloration around umbilicus (peritoneal hemorrhage) Grey Turners sign: flank discoloration (retroperitoneal hemorrhage) Murphys sign: inspiratory arrest on deep palpation of RUQ (cholecystitis) hernias (femoral, direct and indirect inguinal), male genitalia rectal/pelvic exam

Investigations
laboratory CBC and differential (G&S/C&T, if necessary)

electrolytes, BUN, creatinine amylase, lipase levels liver enzymes, liver function tests urinalysis (plus C&S, R&M if necessary) stool for occult blood others ECG, -hCG, ABG, septic workup, lactate (ischemic bowel) radiology AXR: 3 views (supine abdomen, upright abdomen, upright diaphragmatic) Look for free air, air-fluid levels, bowel dilatation/thickening Left lateral decubitus view also for free air, air-fluid levels CXR others U/S, CT, endoscopy, intravenous pyelogram (IVP)

Indications for Urgent Operation (i.e. surgical abdomen)

diffuse peritonitis (localized peritonitis is not always an indication) severe or increasing localized tenderness progressive distension tender mass with fever or hypotension (abscess) septicemia and abdominal findings bleeding and abdominal findings suspected bowel ischemia (acidosis, fever, tachycardia) deterioration on conservative treatment radiologic free air massive bowel distention (colon > 12 cm (> 4.72 in)) space occupying lesion with fever endoscopic : perforation, uncontrollable bleeding paracentesis : blood, pus, bile, feces, urine

Hernia
Epidemiology
male:female = 9:1 lifetime risk of developing hernia: males 5%, females 1% most common surgical disease of males

Clinical Features
mass of variable size tenderness worse at end of day, relieved with supine position or with reduction abdominal fullness, vomiting, constipation transmits palpable impulse with coughing or straining

Investigations
ultrasound

Classification
complete hernia sac and contents protrude through defect incomplete incomplete protrusion through the defect internal hernia sac is within abdominal cavity external hernia sac protrudes completely through abdominal wall strangulated hernia vascular supply of protruded viscus is compromised (ischemia) incarcerated hernia irreducible hernia, not necessarily strangulated Richters hernia contents of the sac consist of only one side of intestinal wall, usually antimesenteric danger is self-reducing gangrenous bowel sliding hernia part of wall of hernia formed by protruding viscus (usually cecum, sigmoid colon, bladder) Anatomical Types groin (see Table 4) indirect and direct inguinal, femoral (see Figure 8) pantaloon: combined direct and indirect hernias, peritoneum draped over inferior epigastric vessels epigastric: defect in linea alba above umbilicus incisional: ventral hernia at site of wound closure, may be secondary to wound infection Littres: hernia involving Meckels diverticulum lumbar: defect in posterior abdominal wall (superior = Grynfeltts, inferior = Petits) obturator: through obturator foramen Spigelian: ventral hernia through defect in linea semilunaris umbilical: passes through umbilical ring congenital, ascites, pregnancy, obesity

Risk Factors
activities which increase intra-abdominal pressure obesity, chronic cough, pregnancy, constipation, straining on urination, ascites congenital abnormality patent processus vaginalis previous hernia repair

Complications
incarceration strangulation small, new hernias more likely to strangulate intense pain followed by tenderness

intestinal obstruction, gangrenous bowel, sepsis surgical emergency do not attempt to manually reduce hernia if sepsis or if contents of hernial sac gangrenous

Treatment
surgical to prevent strangulation, eviscerations and for cosmesis repair may be done open or laparascopic and may use mesh for tension-free closure most repairs are now done with a plug in the hernial defect and a patch over it

Postoperative Complications
1. Scrotal hematoma deep bleeding may enter retroperitoneal space and not be initially apparent difficulty voiding painful scrotal swelling from compromised venous return of testes

2. Nerve entrapment ilioinguinal genital branch of genitofemoral 3. Stenosis/occlusion of femoral vein acute leg swelling Table 4. Groin Hernias
Direct Inguinal Epidemiology Indirect Inguinal most common hernia in men and women Femoral

1 % of all men

affects mostly females

Etiology

Anatomy

acquired weakness of transversalis fascia wear and tear increased intra-abdominal pressure, e.g. straining to urinate or defecate, coughing, heavy lifting through Hesselbachs triangle medial to inferior epigastric artery

males > females congenital persistence of processus vaginalis in 20% of adults pregnancy weakness of pelvic floor musculature increased intra-abdominal pressure,

originates in deep inguinal ring lateral to inferior epigastric artery

e.g. straining to urinate or defecate, coughing, heavy lifting

Complications Treatment Prognosis

usually does not descend into scrotal sac

into femoral canal, below inguinal ligament but may override it

often descends into scrotal sac (or labia majora) narrow neck causes incarceration (1/3) and strangulation

medial to femoral vein within femoral canal

plug and patch repair 3-4% risk of recurrence

plug and patch repair < 1% risk of recurrence

plug and patch repair

Bowel Obstruction

Bowel Obstuction (SBO)

Differential Diagnosis
small bowel obstruction (SBO), large bowel obstruction (LBO), pseudo-obstruction

Pathogenesis
disruption of the normal flow of intestinal contents proximal dilation + distal decompression may take 12-24 hrs to decompress and therefore, passage of feces and flatus may occur after the onset of obstruction bowel ischemia may occur if blood supply is strangulated or bowel wall inflammation leads to venous congestion bowel wall edema and disruption of normal bowel absorptive function increased intraluminal fluid transudative fluid loss into peritoneal cavity, electrolyte disturbances

Clinical Features
must differentiate between obstruction and ileus, and characterize obstruction as acute vs. chronic, partial vs. complete (constipation vs. obstipation), small vs. large bowel, and strangulating vs. non-strangulating

Table 5. Bowel Obstruction vs. Paralytic Ileus

Nausea, vomiting Abdominal pain Abdominal distension Constipation/obstipation Other Bowel sounds SBO early, maybe bilious colicky + (prox) ++ (distal) + visible peristalsis normal, increased, absent if secondary ileus air-fluid levels ladder pattern (plicae circularis) proximal distension (>2cm) + no colonic gas LBO late, maybe feculent colicky ++ + visible peristalsis normal, increased, (borborygmi) absent if secondary ileus air-fluid levels picture frame appearance proximal distension + distal decompression no small bowel air if competent ileocecal valve Paralytic ileus present minimal or absent + + decreased, absent

AXR findings

air throughout small bowel and colon

Complications
strangulating obstruction (10% of bowel obstructions) surgical emergency fever, leukocytosis, tachycardia cramping pain turns to continuous ache, hematemesis, BRBPR, melena (if infarction) peritoneal signs, early shock see also Intestinal ischemia, GS19 other perforation: secondary to ischemia and luminal distension septicemia hypovolemia

Investigations
radiological upright CXR or left lateral decubitus (LLD) to rule out free air AXR (3 views) to determine SBO vs. LBO vs. ileus (Table 5) if ischemic bowel look for: free air, pneumatosis, thickened bowel wall, air in portal vein other: CT provides information on level of obstruction, severity, cause

upper GI series/small bowel series for SBO (if no cause apparent, i.e. no hernias, no previous surgeries) hypaque enema for LBO (oral contrast in LBO may inspissate and convert partial to complete LBO) may consider ultrasound in pregnant patients laboratory may be normal early in disease course BUN, creatinine, hematocrit (hemoconcentration) to assess degree of dehydration fluid, electrolyte abnormalities amylase elevated metabolic alkalosis due to frequent emesis if strangulation: leukocytosis with left shift, lactic acidosis, elevated LDH (late signs)

Small Bowel Obstuction (SBO)

Etiology
extrinsic: adhesions (60%) if previous abdo surgery > hernia (20%) > volvulus, neoplasm, annular pancreas intraluminal: gallstone, feces, meconium, foreign body, intussusception intrinsic: neoplasm (15%) > strictures (Crohns, radiation) > congenital malformations, cystic fibrosis, superior mesenteric artery syndrome

Treatment
consider whether complete or partial obstruction, ongoing or impending strangulation, and cause 1. stabilize vitals, fluid and electrolyte resuscitation (with normal saline/Ringers first, then with added potassium after fluid deficits are corrected) 2. NG tube to relieve vomiting, prevent aspiration and decompress small bowel 3. Foley catheter to monitor in/outs 4. partial SBO ^ conservative management (likely to resolve) surgery if no resolution in 24-48h 5. complete SBO, strangulation ^ urgent surgery after stabilizing patient 6. trial of medical management may be indicated in crohns, recurrent SBO, carcinomatosis location

Prognosis
mortality: non-strangulating < 1%, strangulating 8% (25% if > 36 hours), ischemic = up to 50%

Large Bowel Obstruction (LBO)

Etiology
colorectal carcinoma (65%) diverticulosis (20%) strictures from repeated attacks volvulus (5%) - sigmoid > cecum other causes: IBD, benign tumours, fecal impaction, foreign body, adhesions, hernia (especially sliding type), intussusception (children), endometriosis, extrinsic mass

Clinical Features (unique to LBO)

open loop (10-20%) (safe): incompetent ileocecal valve allows relief of colonic pressure as contents reflux into ileum, therefore clinical presentation similar to SBO

 closed loop (80-90%) (dangerous): competent ileocecal valve, allowing build up of colonic pressures to dangerous level massive colonic distention ^ high risk of perforation, ischemia cecum at greatest risk of perforation due to Laplaces Law (pressure = wall tension/radius) suspect impending perforation in the presence of tenderness over the cecum

Treatment
initial management: correct fluid and electrolyte imbalance, NG suction, continuous observation surgical correction of obstruction (usually requires resection + temporary diverting colostomy) volvulus ^ sigmoidoscopic decompression or barium enema followed by operative reduction if unsuccessful

Prognosis
mortality: overall: 10% cecal perforation + fecal peritonitis: 20%

Appendicitis
Epidemiology
6% of population, M > F 80% between 5-35 years of age

Pathogenesis
luminal obstruction ^ bacterial overgrowth ^ inflammation/swelling ^ increased pressure ^ localized ischemia ^ gangrene/perforation ^ localized abscess (walled off by omentum) or peritonitis etiology children or young adult: hyperplasia of lymphoid follicles, initiated by infection adult: fibrosis/stricture, fecolith, obstructing neoplasm other causes: parasites, foreign body

Clinical Features
most reliable feature is progression of signs and symptoms low grade fever (38C), rises if perforation abdominal pain; then anorexia, nausea and vomiting classic pattern: pain initially periumbilical, constant, dull, poorly localized ^ then, well localized pain over McBurneys point due to progression of disease from visceral irritation (causing referred pain from structures of the embryonic midgut, including the appendix) to irritation of parietal structures McBurneys sign: tenderness at 1/3 from anterior superior iliac spine (ASIS) to umbilicus signs: inferior appendix: McBurneys sign (see above), Rovsings sign (palpation pressure to left abdomen causes McBurneys point tenderness) retrocecal appendix: psoas sign (pain on flexion of hip against resistance or passive hyperextension of hip) pelvic appendix: obturator sign (flexion then external or internal rotation about right hip causes pain) complications: perforation (especially if > 24h duration) abscess, phlegmon

Investigations
labs mild leukocytosis with left shift (may have normal WBC counts) higher leukocyte count with perforation -hCG to rule out ectopic pregnancy, urinalysis imaging should only be used with equivocal presentation of appendicitis upright CXR, AXR: usually nonspecific - free air if perforated, calcified fecolith, loss of psoas shadow ultrasound: may visualize appendix, but also helps rule out gynecological causes overall accuracy 90-94% CT scan: thick wall, appendicolith, inflammatory changes overall accuracy 94-100%, optimal investigation

Treatment
hydrate, correct electrolyte abnormalities surgery + antibiotic coverage if localized abscess, consider radiologic drainage + antibiotics x 14d + interval appendectomy in 6 weeks

 need to be aggressive young females risk of tubal damage and infertility due to perforation children - incomplete growth of omentum appendectomy: laparascopic or open complications: spillage of bowel contents, pelvic abscess, enterocutaneous fistula perioperative antibiotics: ampicillin + gentamicin + metronidazole (antibiotics x 24h only if non-perforated) other choices: 2nd/3rd generation cephalosporin for aerobic gut organisms

Prognosis
morbidity/mortality 0.6% if uncomplicated, 5% if perforated

Ostomies
Definition
iatrogenic connection of the GI tract to abdominal wall skin Types: colostomy vs. ileostomy, temporal vs. permanent, continent vs. incontinent, end vs. loop ileostomies: Brooke (incontinent, continuous drainage), Koch (continent ileostomy, manual drainage) complications (10%) obstruction: herniation, stenosis (skin and abdominal wall) peri-ileostomy abscess and fistula skin irritation prolapse or retraction

Diverticular Disease
Definitions
diverticulum abnormal sac or pouch protruding from the wall of a hollow organ diverticulosis presence of multiple false diverticula diverticulitis inflammation of diverticula right sided (true) diverticula = contains all layers (congenital) (see Figure 9) left sided (false) diverticula = contain only mucosal and submucosal layers (acquired)

DIVERTICULOSIS Epidemiology
35-50% of general population (M=F) increased incidence in 5th to 8th decades of life 95% involve sigmoid colon (site of highest pressure) higher incidence in Western countries, related to low fibre diet

Pathogenesis
risk factors: low-fibre diet (increases gut transit time and intraluminal pressure) muscle wall weakness from aging and illness possible genetic component high intraluminal pressures cause outpouching to occur at area of greatest weakness: most commonly at the site of penetrating vessels at antimesenteric tenia, therefore increased risk of hemorrhage

Clinical Presentation
uncomplicated diverticulosis: asymptomatic (70-80%) episodic LLQ abdominal pain, bloating, flatulence, constipation, diarrhea absence of fever/leukocytosis no physical exam findings or poorly localized LLQ tenderness complications: diverticulitis (15-20%) bleeding (5-15%): PAINLESS rectal bleeding, 2/3 of massive LGI bleeds

Treatment
uncomplicated diverticulosis: high fibre, education diverticular bleed: initially work up and treat as any lower GI bleed (see Gastroenterology, G31) if hemorrhage does not stop, resect involved region

DIVERTICULITIS (left sided appendicitis) Pathogenesis

erosion of the wall by increased intraluminal pressure or inspissated food particles ^ inflammation and focal necrosis ^ microperforation/macroperforation usually mild inflammation with perforation walled off by pericolic fat sigmoid colon most often involved

Clinical Features
depends on severity of inflammation and presence of complications LLQ pain/tenderness, present for several days before admission alternating constipation and diarrhea, urinary symptoms (dysuria if inflammation adjacent to bladder) palpable mass if phlegmon or abscess, nausea, vomiting low-grade fever, mild leukocytosis

 occult or gross blood in stool less common generalized tenderness suggests perforation and peritonitis complications abscess on physical exam palpable abdominal mass fistula colovesical (most common), coloenteric, colovaginal, colocutaneous obstruction due to scarring from repeated inflammation perforation ^ peritonitis (feculent vs. purulent) recurrent attacks RARELY lead to peritonitis

Investigations
to confirm the diagnosis and rule out other pathology AXR, upright CXR: localized diverticulitis (ileus, thickened wall, SBO, partial colonic obstruction) free air may be seen in 30% with perforation and generalized peritonitis CT scan (optimal method of investigation) 97% sensitive, very useful for assessment of severity and prognostication very helpful in localizing an abscess Hypaque (water soluble) enema SAFE (under low pressure) saw-tooth pattern (colonic spasm) may show site of perforation, abscess cavities or sinus tracts, fistulas barium enema: contraindicated during an acute attack risk of chemical peritonitis (if perforation) sigmoidoscopy/colonoscopy not during an acute attack, only done on an elective basis rule out other lesions, polyps, cancer, take biopsies

Treatment
admit, NPO, fluid resuscitation, NG + suction, IV antibiotics covering B. fragilis (e.g. ciprofloxacin, metronidazole) indications for surgery: Hinchey stage 3, 4 (see Table 6) after 1 attack if: (a) < 50 y.o., (b) immunosuppressed, (c) abscess needing percutaneous drainage after 2 attacks for others complications: hemorrhage, fistula, obstruction, generalized peritonitis, rule out colon cancer, or failure of medical management

Procedures
Hartmann procedure: resection + colostomy and rectal stump colostomy reversal in 3-6 months (see Figure 10) resection + primary reanastomosis ( pre-op bowel prep or on-table lavage): controversial

Prognosis
30% recurrence after 1st attack (higher if 2nd attack, or if patient < 50 y.o.)

Angiodysplasia
vascular anomaly: focal submucosal venous dilatation and tortuosity

Clinical Features
most frequently in right colon of patients > 60 years old bleeding typically intermittent (melena, anemia, guaiac positive stools) and in the elderly

Investigations
endoscopy (cherry red spots, branching pattern from central vessel) angiography (slow filling/early emptying mesenteric vein, vascular tuft) RBC technetium scan barium enema is contraindicated (obscures other x-rays, i.e. angiogram)

Treatment
none if asymptomatic cautery, right hemicolectomy, embolization, vasopressin infusion, sclerotherapy, band ligation, laser, octreotide

Volvulus
Definition
rotation of segment of bowel about its mesenteric axis

Risk Factors
age (50% of patients > 70 yrs: stretching/elongation of bowel with age is a predisposing factor) high fibre diet, elongated colon, chronic constipation, laxative abuse, pregnancy, elderly, bedridden, institutionalized (less frequent evacuation of bowels) congenitally hypermobile cecum

Clinical Features
symptoms due to bowel obstruction or bowel ischemia sigmoid (70%), cecum (30%)

Investigations
AXR: omega, bent inner-tube, coffee-bean signs barium/gastrografin enema: ace of spades appearance due to funnel-like luminal tapering of lower segment sigmoidoscopy or colonoscopy as appropriate

Treatment
initial supportive management with fluid, electrolyte resuscitation cecum: 1) may attempt colonscopic detorsion and decompression 2) laparotomy cecopexy or right colectomy + ileotransverse colonic anastomosis sigmoid: nonsurgical: decompression by flexible sigmoidoscopy and insertion of rectal tube past obstruction subsequent elective surgery recommended (50-70% recurrence) surgical: Hartmann procedure (if urgent) indications: strangulation, perforation or unsuccessful endoscopic decompression

Colorectal Polyps
Definition
polyp: small mucosal outgrowth into the lumen of the colon or rectum sessile (flat) or pedunculated (on a stalk) see Figure 11

Epidemiology
30% of population have polyps by age 50, 40% by age 60, 50% by age 70

Clinical Features
50% in the rectosigmoid region, 50% are multiple usually asymptomatic, but may have rectal bleeding, change in bowel habits usually detected during routine endoscopy or family screening

Pathology
hyperplastic most common pseudopolyps inflammatory, associated with IBD, no malignant potential hamartomas: juvenile polyps, Peutz-Jegher syndrome often in small bowel low malignant potential ^ most spontaneously regress or autoamputate adenomas premalignant, often carcinoma in situ some may contain invasive carcinoma (malignant polyp 2.6-9.4%): invasion into muscularis tubular, villous, tubulovillous (see Table 7)

Investigations
60% within reach of flexible sigmoidoscope, if any polyps detected, proceed to colonoscopy for examination of entire bowel biopsy

Treatment
indications: symptoms, malignancy, or risk of malignancy (i.e. adenomatous polyps) endoscopic removal of entire growth surgical resection for those invading into muscularis (high risk of malignancy) and those too large to remove endoscopically follow-up endoscopy 1 year later, then every 3-5 years

Colorectal Carcinoma (CRC)

Epidemiology
third most common carcinoma (after lung, prostate/breast), 2nd most common cancer death

Risk Factors
most patients have no specific risk factors FAP, HNPCC, family history of CRC adenomatous polyps (especially if > 1 cm, villous, multiple): age > 50 (dominant risk factor in sporadic cases): mean age = 70y IBD (especially UC: risk is 1-2%/yr if UC > 10 yrs) previous colorectal cancer (also gonadal or breast) diet (increased fat, decreased fiber, red meat) and smoking diabetes mellitus (insulin is a growth factor for colonic mucosal cells) and acromegaly

Pathogenesis
adenoma-carcinoma sequence; rarely arise de novo

Clinical Features (see Table 8)

hematochezia/melena, abdominal pain, change in bowel habits others: weakness, anemia, weight loss, palpable mass, obstruction 3-5% have synchronous lesions spread direct extension, lymphatic, hematogenous (liver most common, lung, rarely bone and brain) peritoneal seeding: ovary, Blumers shelf (pelvic cul-de-sac) intraluminal

Investigations
initial: DRE + fecal occult blood, anoscopy + flexible sigmoidoscopy, barium enema colonoscopy ^ detects synchronous lesions, biopsy, polypectomy air contrast barium enema + sigmoidoscopy not as good as colonoscopy alone metastatic workup: CXR, abdominal CT/ultrasound bone scan, CT head only if lesions suspected labs: CBC, urinalysis, liver function tests, CEA staging (see Table 9)

Treatment
surgery (indicated in all stages) curative: wide resection of lesion (5 cm margins) with nodes and mesentery palliative: if distant spread, then local control for hemorrhage or obstruction 80% of recurrences occur within 2 years of resection improved survival if metastasis consists of solitary hepatic mass that is resected colectomy: most patients get primary anastomosis (e.g. hemicolectomy, low anterior resection) if cancer is below levators in rectum, patient requires an abdominal perineal resection (APR) with a permanent end colostomy complications: anastomotic leak or stricture, recurrent disease, pelvic abscess, enterocutaneous fistula radiotherapy and chemotherapy chemotherapy (5FU + levamisole): for patients with node-positive disease radiation: for patients with node-positive disease or transmural rectal cancer (pre or post-op)

Screening Tools
digital rectal exam (DRE): most common exam, but poor sensitivity fecal occult blood test (FOBT): proper test requires 3 samples of stool low sensitivity and positive predictive value (17-46%), high false positives still recommended annually by the World Health Organization (WHO) results in 16-33% reduction in mortality in RCTs Minnesota Colon Cancer Study : RCT of 46445 people between the ages if 50 and 80 without a prior diagnosis of colorectal cancer, randomized to annual fecal occult blood testing (FOBT), biennial FOBT and control showed a reduction in mortality from colorectal cancer by one third. sigmoidoscopy: can identify 50-70% of lesions sigmoidoscopy + FOBT misses 24% of colonic neoplasms colonoscopy: can remove or biopsy lesions during procedure can identify proximal lesions missed by sigmoidoscopy used as follow-up to other tests if lesions found disadvantages: expensive, not always available, poor compliance, requires sedation, risk of perforation (0.2%) virtual colonoscopy: 91% sensitive, 17% false positive rate double contrast barium enema: 50% sensitive for large (> 1cm) adenomas, 39% for polyps CEA: not good for screening but appropriate to monitor for recurrence

Case finding for colorectal cancer (symptomatic or history of UC, polyps, or CRC)
surveillance (when polyps are found): colonoscopy at least 3 years after initial finding patients with past CRC: colonoscopy every 3-5 years IBD: some recommend colonoscopy every 1-2 years after 8 years of disease (especially UC)

Hemorrhoids
Etiology
vascular and connective tissue complexes from a plexus of dilated veins (cushion) internal: superior hemorrhoidal veins, above dentate line, portal circulation external: inferior hemorrhoidal veins, below dentate line, systemic circulation

Risk Factors
increased intra-abdominal pressure: chronic constipation, pregnancy, obesity, portal hypertension, heavy lifting

Clinical Features and Treatment

Internal Hemorrhoids (see Figure 12) engorged vascular cushions usually at 3, 7, 11 oclock positions (patient in lithotomy position) painless rectal bleeding, anemia, prolapse, mucus discharge, pruritus, burning pain, rectal fullness 1st degree: bleed but do not prolapse through the anus treatment: high fibre/bulk diet, sitz baths, steroid cream, rubber band ligation, sclerotherapy, photocoagulation 2nd degree: prolapse with straining, spontaneous reduction treatment: rubber band ligation, photocoagulation 3rd degree: prolapse requiring manual reduction treatment: same as 2nd degree, may require closed hemorrhoidectomy 4th degree: permanently prolapsed, cannot be manually reduced treatment: closed hemorrhoidectomy External Hemorrhoids (see Figure 12) dilated venules usually mildly symptomatic pain after bowel movement medical treatment: dietary fiber, stool softeners, avoid prolonged straining thrombosed hemorrhoids are very painful resolve within 2 weeks, may leave excess skin = perianal skin tag treatment: hemorrhoidectomy within first 48 hours of thrombosis, otherwise medical treatment

Anal Fissures
tear of anal canal below dentate line (very sensitive squamous epithelium) 90% posterior midline, 10% anterior midline if off midline: IBD, STDs, TB, leukemia or anal carcinoma repetitive injury cycle after first tear spasm occurs preventing edges from healing and leads to further tearing ischemia may ensue and contribute to chronicity

Etiology
large, hard stools and irritant diarrheal stools tightening of anal canal secondary to nervousness/pain others: habitual use of cathartics, childbirth

Clinical Features
Acute Fissure very painful bright red bleeding especially after bowel movement treatment is conservative: stool softeners, sitz baths Chronic Fissure triad: fissure, sentinel skin tags, hypertrophied papillae treatment topical nitroglycerine increases local blood flow, promoting healing and relieves sphincter spasm surgery, most effective objective is to relieve sphincter spasm ^ increases blood flow and promotes healing alternative treatments botulinum toxin inhibits release of acetylcholine (ACh), stopping sphincter spasm

Anorectal Abscess
infection in one (or more) of the anal spaces (see Figure 13) usually bacterial infection of blocked anal gland at the dentate line E. coli, Proteus, Streptococci, Staphylococci, Bacteroides, anaerobes

Clinical Features
throbbing pain that may worsen with straining and ambulation abscess can spread vertically downward (perianal), vertically upward (supralevator) or horizontally (ischiorectal) tender perianal/rectal mass on exam Figure 13. Schematic of Different Types of Perianal Abscesses

Treatment
incision and drainage curative in 50% of cases 50% develop anorectal fistulas may also require antibiotics

Fistula-In-Ano
a connection between two epithelial lined surfaces, one must be the rectum or anus an inflammatory tract with internal os at dentate line, external os on skin

Etiology
see GS19 same perirectal process as anal abscess therefore usually associated with abscess other causes: post-op, trauma, anal fissure, malignancy, radiation proctitis

Clinical Features
intermittent or constant purulent discharge from para-anal opening pain palpable cord-like tract

Treatment
identification internal opening Salmon Goodsalls rule (see Figure 14) , - a fistula with an external opening anterior to the transverse anal line will have its internal opening at relatively the same position (e.g. external opening at 2 oclock = internal opening at 2 oclock) whereas all external openings posterior to the line will tend to have their internal openings in the midline fistulous tract probing or fistulography under anesthesia surgery Fistulotomy: unroof tract from external to internal opening, allow drainage low lying fistula (does not involve external sphincter) ^ primary fistulotomy high lying fistula (involves external sphincter) ^ staged fistulotomy with seton suture placed through tract promotes drainage promotes fibrosis and decreases incidence of incontinence delineates anatomy usually for high or complicated fistula to spare muscle cutting

Post-operative

 sitz baths, irrigation and packing to ensure healing proceeds from inside to outside

Complications
recurrence, fecal incontinence

Cholelithiasis
Pathogenesis
imbalance of cholesterol and its solubilizing agents (bile salts and lecithin) excessive hepatic cholesterol secretion ^ bile salts and lecithin are overloaded ^ supersaturated cholesterol can precipitate and form gallstones North America: cholesterol stones (80%), pigment stones (20%)

Risk Factors
cholesterol stones obesity, age < 50, estrogens North American First Nations peoples have highest incidence terminal ileal resection or disease (e.g. Crohns disease) impaired gallbladder emptying: starvation, rapid weight loss, TPN, DM type I pigment stones black pigment stones: cirrhosis, chronic hemolytic states calcium bilirubinate stones: bile stasis (strictures, dilatation, biliary infection)

Clinical Features
asymptomatic (80%) most do NOT require treatment consider operating if calcified porcelain gallbladder, sickle cell disease, DM biliary colic (10-25%) cholecystitis choledocholithiasis (8-15%) cholangitis gallstone pancreatitis (see Acute pancreatitis, GS41) gallstone ileus

Investigations
ultrasound diagnostic procedure of choice image for signs of inflammation, obstruction, localization of stones not accurate for visualizing stones in CBD ERCP (endoscopic retrograde cholangiopancreatography) visualization of upper GI tract, ampullary region, biliary and pancreatic ducts preferred method for diagnosis and treatment of CBD stones in periampullary region complications: traumatic pancreatitis (1-2%), pancreatic or biliary sepsis PTC (percutaneous transhepatic cholangiography) injection of contrast via needle passed through hepatic parenchyma useful for proximal bile duct lesions or when ERCP fails or not available require prophylactic antibiotics contraindications: coagulopathy, ascites, peri/intrahepatic sepsis, disease of right lower lung or pleura complications: bile peritonitis, chylothorax, pneumothorax, sepsis, hemobilia MRCP (magnetic resonance cholangio-pancreatography) same information gained as ERCP but non-invasive cannot be used for therapeutic purposes HIDA scan radioisotope technetium excreted in high concentrations in bile does not visualize stones, diagnosis by seeing occluded cystic duct or CBD

Biliary Colic
Pathogenesis
gallstone transiently impacted in cystic duct, no infection

Clinical Features
steady pain in epigastrium or RUQ for minutes to hours, crescendo-decrescendo pattern frequently occurs at night or after fatty meal can radiate to right shoulder or scapula associated nausea/vomiting, belching, flatus, heartburn no peritoneal findings, no systemic/constitutional signs

Investigations
normal blood work: CBC, lytes, LFTs, bilirubin, amylase ultrasound shows cholelithiasis, may show stone in cystic duct

Treatment
analgesia, rehydration elective cholecystectomy (95% success) anatomic landmarks: triangle of Calot (borders: cystic duct, common hepatic duct, inferior border of liver), cystic artery complications: CBD injury (0.3-0.5%), hollow viscus injury, bile peritonitis, vessel injury

Acute Cholecystitis
Pathogenesis
inflammation of gallbladder resulting from sustained gallstone impaction in cystic duct or Hartmanns pouch no cholelithiasis in 5-10% (acalculous cholecystitis see GS38)

Clinical Features
often have history of biliary colic severe constant epigastric or RUQ pain, anorexia, nausea, vomiting, low grade fever (<38.5C/101.3F) focal peritoneal findings (eg. Murphys sign); palpable, tender gallbladder in one third of patients complications hydrops mucus accumulation in gallbladder; may lead to necrosis gangrene, perforation may cause abscess or peritonitis empyema of gallbladder (suppurative cholangitis) cholecystoenteric fistula, gallstone ileus (see GS40) from repeated attacks of cholecystitis emphysematous cholecystitis (risk if patient is diabetic) bacterial gas present in gallbladder lumen and tissues

Investigation
elevated WBC + left shift LFTs: mildly elevated bilirubin, ALP, AST and ALT - may increase if inflammation affects liver ultrasound: 1) distended, edematous gallbladder, 2) pericholecystic fluid, 3) stone in gallbladder neck, 4) sonographic Murphys sign (maximum tenderness when probe at site of gallbladder) ultrasound is 98% sensitive, may consider HIDA scan if ultrasound is negative

Treatment
admit, hydrate, NPO, NG tube (if persistent vomiting from associated ileus), analgesics once diagnosis is made antibiotics E. coli, Klebsiella, Enterococcus and Clostridium ac25ount for > 80% of infections ampicillin + gentamicin/ciprofloxacin + metronidazole cholecsytectomy early (within 72h) vs. delayed (after 6 weeks) equal morbidity and mortality early cholecystectomy preferred: shorter hospitalization and recovery time emergent OR indicated if high risk, e.g. emphysematous laparoscopic vs. open laparoscopic: reduced risk of wound infections, shorter hospital stay, reduced post-op pain, increased risk of bile duct injury (intra-operative cholangiography) indications: clarify bile duct anatomy, obstructive jaundice, history of biliary pancreatitis, small stones in gall bladder with a wide cystic duct (>15 mm), single faceted stone in gallbladder, bilirubin > 137 mol/L (8 mg/dL) percutaneous cholecystostomy tube if general anaesthetic contraindicated

IOC

Acalculous Cholecystitis
Clinical Features
acute or chronic cholecystitis in the absence of stones; typically due to gallbladder stasis localized peritonitis (i.e. Murphys sign), palapable gallbladder may lead to gallbladder necrosis

Risk Factors
DM, immunosuppression, ICU stay

Investigations
U/S: shows sludge in gallbladder CT or HIDA scan

Etiology
decreased bowel mobilization: starvation, dehydration, surgery, TPN, anaesthesia, narcotics infection: Salmonella, sepsis, Kawasakis disease decreased cystic artery blood flow: CHF, collagen vascular disease, thrombosis, DM, shock cystic duct obstruction: extrinsic compression, sphincter spasm

Treatment
cholecystectomy cholecystostomy often patients who get acalculous cholecystitis are too sick to undergo general anesthetic

Choledocholithiasis
Definition
stones in common bile duct (CBD)

Clinical Features
50% asymptomatic often have history of biliary colic tenderness in RUQ or epigastrium acholic stool, dark urine, fluctuating jaundice primary vs. secondary stones primary: formed in bile duct, indicates bile duct pathology (e.g. benign biliary stricture, sclerosing cholangitis, choledochal cyst) secondary: formed in gallbladder (85% of cases in U.S.) complications: cholangitis, pancreatitis, biliary stricture and biliary cirrhosis

Investigations
CBC: usually normal; leukocytosis suggests cholangitis LFTs: increased bilirubin > 171 mol/L (10 mg/dL), ALP, 5-NTD amylase/lipase: to rule out gallstone pancreatitis ultrasound: intra/extra-hepatic duct dilatation ERCP PTC MRCP (90% sensitive, almost 100% specific, not therapeutic)

Treatment
if no evidence of cholangitis: treat with pre-op ERCP for CBD stone extraction followed by elective cholecystectomy

Acute Cholangitis
Pathogenesis
obstruction of CBD leading to biliary stasis, bacterial overgrowth, suppuration, and biliary sepsis

Etiology
gallstones (60%), stricture, pancreatic or biliary neoplasms organisms: E. coli, Klebsiella, Pseudomonas, Enterococcus, B. fragilis, Proteus

Clinical Features
Charcots triad (50-70% of cases), Raynauds pentad may have nausea, vomiting, abdominal distension, ileus, acholic stools, tea-coloured urine

Investigations
CBC: elevated WBC + left shift LFTs: obstructive picture (elevated ALP and conjugated bilirubin, mild increase in AST, ALT) ultrasound: intra/extra-hepatic duct dilatation

Treatment
initial: NPO, fluid and electrolyte resuscitation, NG tube antibiotics (eg. ampicillin + ciprofloxacin/gentamicin + metronidazole) most patients with only Charcots triad respond to conservative treatment if no response or Raynauds pentad (which usually denotes acute suppurative cholangitis), then urgent decompression needed - ERCP + sphincterotomy (diagnostic and therapeutic), PTC (if ERCP not available), open decompression all patients should also have a cholecystectomy

Prognosis
suppurative cholangitis mortality rate: 50%

Breast Cancer
Epidemiology
2nd leading cause of cancer mortality in women (1st is lung cancer) most common cancer diagnosis in Canadian women excluding non-melanoma skin cancer 1/9 women in Canada will be diagnosed with breast cancer in their lifetime 1/27 women in Canada will die from breast cancer

Risk Factors
sex (99% female) age (80% > age 40) prior history of breast cancer, prior breast biopsy (regardless of pathology) 1st degree relative with breast cancer (greater risk if relative was premenopausal) increased risk with nulliparity, first pregnancy at > age 30, menarche < age 12, menopause > age 55 decreased risk with lactation, early menopause, early childbirth radiation exposure possibly OCP, > 5 years HRT obesity

BREAST MASS: HISTORY

mass when and how first noticed, tenderness, change in size with time and menstruation mastalgia correlation with menstrual cycle constitutional features anorexia, weight loss, poor energy advanced disease bony pain, shortness of breath, appetite, weakness, headache, chest nipple discharge increased concern if unilateral, spontaneous or bloody (4-12% malignant) < 2% of carcinomas associated with discharge differential: papilloma, papillomatosis, fibrocystic change, carcinoma, abscess, Pagets disease, mammary duct ectasia if milky discharge (galactorrhea): pregnancy, lactation, pituitary adenoma, acromegaly, hypothyroidism, stress, drugs (OCP, antihypertensives, certain psychotropic drugs) assess risk factors: gynecologic history (OCP, HRT, menarche/menopause, breast feeding), past medical history (benign breast disease, breast cancer, radiation exposure/therapy to breast or axilla, ovarian cancer, last mammogram and results), past surgical history (lumpectomy, mastectomy, hysterectomy, oophorectomy), family history (first-degree relatives, members with ovarian cancer) estimation of performance status, daily living e.g. ECOG performance status: ability to carry out work activities, ambulation, self-care

pain

BREAST MASS: PHYSICAL EXAM

examine sitting and supine inspection skin changes: edema, bulging, dimpling, retraction, redness, ulceration, peau dorange nipple: bloody discharge, crusting, ulceration, inversion, retraction palpation carcinoma usually firm, nontender, poorly circumscribed, immobile palpable axillary, supraclavicular or infraclavicular lymph nodes, arm edema, skin warmth, prominent veins best time to palpate breast usually 1 week before menses

Investigations

 Mammography indications screening (see Table 11) every 1-2 years for women age 50-69 positive FHx in 1st degree relative: every 1-2 years starting 10 years before the youngest age of presentation women age 40-49 with average risk- no evidence to include or exclude a screening exam (level C evidence) diagnostic investigation of patient complaints (discharge, pain, lump) metastatic adenocarcinoma of unknown primary follow-up post-lumpectomy findings indicative of malignancy poorly defined, spiculated border microcalcifications architectural distortion increased vascularity interval mammographic changes normal mammogram does not rule out suspicion of cancer based on clinical findings compression views to clarify results if intermediate suspicion Other Radiographic Studies U/S: differentiate between cystic and solid MRI: high sensitivity, low specificity galactogram (for nipple discharge): identifies lesions in ducts as indicated: bone scan, liver enzymes, head CT

Diagnostic Procedures
needle aspiration for palpable cystic lesions; send fluid for cytology if serosanguinous or bloody fine needle aspiration (FNA) for palpable solid masses, obtains cellular material; hematoma most common complication U/S guided core needle biopsy larger sample than FNA, allow evaluation of invasive vs. in situ excisional biopsy definitive method for tissue diagnosis

Genetic Screening
consider testing for BRCA1/2 if: patient diagnosed with breast AND ovarian cancer strong family history of breast/ovarian cancer (e.g. among Ashkenazi Jewish) family history of male breast cancer risk consultation may include: pedigree documentation, pathological review of affected family members, review of basic concepts of cancer, genetics, risk factors, limitations of testing, cost and implications of positive, negative or inconclusive testing

Staging (see Table 12)

clinical tumour size by palpation, mammogram nodal involvement by palpation metastasis by physical exam, CXR, liver enzymes, bone scan pathological tumour size grade: modified Bloom and Richardson score (I to III) - histologic, nuclear and mitotic grade number of axillary nodes positive for malignancy out of total nodes resected, extranodal extension, sentinel node positive/negative estrogen/progesterone receptor testing

Her2Neu receptor testing margins: negative, < 1 mm, positive lymphovascular space invasion (LVI) extensive in situ component (EIC): DCIS in surrounding tissue involvement of dermal lymphatics (automatically Stage IIIb)

Etiology and Presentation

Non-invasive ductal carcinoma in situ (DCIS) proliferation of malignant ductal epithelial cells completely contained within breast ducts 80% non-palpable - detected by screening mammogram risk of infiltrating ductal carcinoma in same breast up to 35% in 10 years histology comedo vs. non-comedo: comedo tumours more frequently show tumour necrosis, high nuclear grade, association with invasive ductal carcinoma often multifocal (multiple tumour foci in same quadrant of breast) treatment lumpectomy with wide excision margins radiation more common today (5-10% risk invasive cancer) - indicated if low grade, small lesion, single focus mastectomy if large area of disease (risk of invasive cancer reduced to 1%) tamoxifen as an adjuvant treatment under investigation 99% 5-year survival 50% of recurrences are invasive cancer lobular carcinoma in situ (LCIS) neoplastic cells completely contained within breast lobule no palpable mass, no mammographic findings, usually incidental finding on breast biopsy risk of developing infiltrating ductal carcinoma in either breast is 20-30% at 20 years, tamoxifen prophylaxis may be beneficial managed non-operatively with life-long surveillance Invasive infiltrating ductal carcinoma (most common 80%) originates from ductal epithelium and infiltrates supporting stroma characteristics hard, scirrhous, infiltrating tentacles, gritty on cross-section invasive lobular carcinoma (8-15%) originates from lobular epithelium 20% bilateral (i.e. more often than infiltrating ductal carcinoma) better prognosis than infiltrating ductal, often receptor positive does not form microcalcifications, harder to detect mammographically peritoneal, retroperitoneal, uterine, gastric, meningeal metastasis can occur Pagets disease (1-3%) ductal carcinoma that invades nipple with scaling, eczematoid lesion inflammatory carcinoma (1-4%) ductal carcinoma that invades dermal lymphatics most aggressive form of breast cancer clinical features erythema, skin edema, warm, swollen and tender breast lump peau dorange indicates advanced disease (IIIb-IV) male breast cancer (<1%) most commonly infiltrating ductal carcinoma

often diagnosed at later stages stage-for-stage similar prognosis to breast cancer in females other papillary, medullary, mucinous, tubular cancers generally better prognosis Sarcomas rare, most commonly cystosarcoma phyllodes, a variant of fibroadenoma (1 in 10 malignant) Lymphoma rare

Treatment Primary: Surgical

breast-conserving surgery (BCS) - lumpectomy with wide local excision for treatment of stage I and II disease must be combined with radiation for equivalent outcome as mastectomy axillary lymph node dissection (ALND) or sentinel node biopsy often added for staging of nodes and reduced recurrence in axilla complications of ALND: arm lymphedema (5%), arm numbness, shoulder pain sentinel node biopsy (not standard of care): sentinel node: the first node(s) receiving direct lymphatic drainage from a tumour site technetium +/- blue dye injected at tumour site to identify sentinel node(s) send for frozen section, H&E and cytokeratin staining ALND if any nodes positive for micrometastasis false-negative rate 0-10% uncertain if sentinel node biopsy yields comparable long-term survival to ALND BCS not appropriate if: factors present that increase risk of local recurrence: extensive malignant-type calcifications on mammogram, multifocal primary tumours or failure to obtain tumour-free margins after re-excision contraindications to radiation therapy lesion difficult to evaluate mammographically (e.g. fibrosis, lesion not apparent on mammogram) large tumour size relative to breast patient prefers mastectomy mastectomy modified radical mastectomy (MRM) removes all breast tissue, nipple-areolar complex, skin, pectoralis minor and axillary nodes simple mastectomy similar to MRM but axillary nodes not removed total mastectomy removes all breast tissue, nipple-areolar complex, skin (axillary nodes and pectoralis minor spared) offer breast reconstruction if mastectomy chosen

Adjuvant/Neoadjuvant
Radiation breast radiation almost always used after BCS axillary nodal radiation may be added if nodal involvement for high-risk of local recurrence, inoperable locally advanced cancer, metastases stage I/II disease: decreases local recurrence, increases disease-free survival; effect on overall survival controversial Hormonal indications

ER positive (pre-/post-menopausal) plus node-positive or high-risk node-negative palliation for metastases tamoxifen is current standard, continue for 5 years alternatives to tamoxifen: aromatase inhibitors (eg. anastrozole), ovarian ablation (eg. goserelin/GnRH agonist, oophorectomy), progestins (eg. megestrol acetate), androgens (eg. fluoxymesterone) Chemotherapy indications almost all patients with stage III disease have micro/macro distant metastasis ER negative plus node-positive/high-risk node-negative ER positive and young age Stage I disease at high risk of recurrence (High grade, LVI) palliation for metastatic disease classically CMF (cyclophosphamide, methotrexate, 5-flurouracil) x 6 months Prophylactic chemoprevention tamoxifen secondary prevention screening for early detection (see above) mastectomy - high-risk women (e.g. BRCA1/2), occasionally contralateral in women with personal history of breast cancer

Post-Treatment Follow-up
visits q 3-6 months x 2 years and annually thereafter (frequency is controversial) annual mammography psychosocial support and counselling signs of recurrence: metastasis vs. new primary CXR, CT abdomen, liver enzymes, bone scan, CT brain, MRI spine, solitary lesion biopsy as indicated

Local/Regional Recurrence
recurrence in treated breast or ipsilateral axilla 10% develop contralateral malignancy 50% have metastatic disease - most frequently in first 3-5 years, although can be as many as 20 years treatment usually palliative (complete surgical excision and/or radiation)

Metastasis
bone > lungs > pleura > liver > brain treatment is palliative - hormone therapy, chemotherapy, radiation

Prognosis (see Table 12)

nodal status most important prognostic feature, grade also important also tumour size, LVI, receptor status, cell proliferative indices, Her2Neu

Surgical Endocrinology

Post-Operative Fever
fever does not necessarily imply infection timing of fever may help identify cause POD #0-2 usually atelectasis (most common cause of fever on POD#1) early wound infection (especially Clostridium, Group A Streptococcus) leakage of bowel anastomosis (tachycardia, hypotension, oliguria, abdominal pain) aspiration pneumonia other: Addisonian crisis, thyroid storm, transfusion reaction POD #3 after day 3 infections more likely UTI, wound infection, IV site infection, septic thrombophlebitis POD #5+ intra-abdominal abscess (usually POD 5-10) DVT/PE (POD 7-10) drug fever (POD 6-10) other : cholecystitis, peri-rectal abscess, URTI, factitious fever, infected seroma/biloma/hematoma

Treatment
treat primary cause antipyrexia (e.g. acetaminophen)

References