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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 Indirect Inguinal Femoral


Epidemiology 1 % of all men most common hernia in men affects mostly females
and women
males > females
Etiology acquired weakness of congenital persistence of pregnancy weakness of pelvic
transversalis fascia processus vaginalis in 20% of floor musculature
wear and tear adults increased intra-abdominal
increased intra-abdominal pressure,
pressure, e.g. straining to urinate e.g. straining to urinate or
or defecate, coughing, heavy defecate, coughing, heavy lifting
lifting
Anatomy through Hesselbachs triangle originates in deep inguinal ring into femoral canal, below
medial to inferior epigastric lateral to inferior epigastric inguinal
artery artery ligament but may override it
usually does not descend into often descends into scrotal sac medial to femoral vein within
scrotal sac (or labia majora) femoral canal
Complications narrow neck causes incarceration
(1/3) and strangulation
Treatment plug and patch repair plug and patch repair plug and patch repair
Prognosis 3-4% risk of recurrence < 1% risk of recurrence

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


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

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, location
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

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 IOC
(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
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 pain
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

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

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