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GS22 General and Thoracic Surgery Toronto Notes 2023
Treatment
• if early stage (non-transmural and without evidence of nodal disease)
• endoscopic mucosal resection can be considered for early mucosal cancer or high-grade dysplasia
• esophagectomy (transthoracic or trans-hiatal approach) and lymphadenectomy
anastomosis in chest or neck
stomach is used for reconstruction; colon is rarely used
• if locally advanced (locally invasive disease or nodal disease on CT or HUS)
• multimodal therapy
concurrent external beam radiation and chemotherapy (cisplatin and fluorouracil)
possibility of curative esophagectomy after chemoradiation if disease responds well
« if unable to tolerate multimodal therapy or if highly advanced disease, consider palliative
resection, brachytherapy, or endoscopic dilatation/stenting/laser ablation for palliation
• if present with distant metastatic disease, treat with systemic therapy and treat symptoms (esophageal
stent or radiation)
Camelon'sCriteria (or Conservative
Management of Esophageal Perforation
. Perforation contained in mediastinum
• Contrast drains back into esophagus
• No signs of sepsis
• Minimal symptoms
Prognosis
• TNM status - usually poor because presentation is usually at advanced stage
OTHER DISORDERS
• esophageal motor disorders (see Gastroenterology. ( ,S)
• esophageal varices(see tiastroenteroloitv. G9)
• Mallory-Weiss tear (see Gastroenterology, G30) A.Median sternotomy
B.Transverse thoracotomy (clam shell)
C.Anterolateral thoracotomy
0.Lateral thoracotomy
E.Thoracoabdominal thoracotomy
VF.Posterolateral thoracotomy
Esophageal Perforation
Etiology
• iatrogenic (most common)
endoscopic, dilatation, biopsy, intubation, operative, and NG tube placement (rare)
barogenic
• trauma
repeated, forceful vomiting (Boerhaave’
ssyndrome)
• other: convulsions, defecation, or labour (rare)
• ingestion injury
• foreign body or corrosive substance
• carcinoma
• penetrating trauma
Figure 7.Typical thoracic surgery
incisions
Boerhaave
m 'ssyndrome:transmural
esophageal perforation
Mallory-Weiss tear: non-transmural
esophageal tear (partial thickness tear)
Both arc associated with forceful emesis
Clinical Features
• neck or chest pain
• fever,tachycardia, hypotension, dyspnea, and respiratory compromise
• subcutaneous emphysema, pneumothorax, pleural effusion, voice changes, and hematemesis
Investigations
• CXR:subcutaneous emphysema, pneumothorax, pneumomediastinum, pleural effusion,
subdiaphragmatic air, and widened mediastinum
• CT chest with oral and IV contrast: pneumomediastinum, pleural effusion, pneumothorax, contrast in
the chest, and subcutaneous emphysema
• contrast esophagram
Gastrografin* (water-soluble contrast) upper G1 study is the first choice
• if negative, followed by dilute barium upper G1 study: contrast extravasation
Standard of Care in 2019
1. Pre- and postoperative
FLOTchemotherapy for gastric and GE
junction adenocarcinoma (docetaxel,
oxaliplatin. and fluorouracil/
leucovorin)
2. Neoadjuvant CROSS
chemoradiotherapy for esophageal
cancer with squamous histology
or mid-body adenocarcinoma
(carboplatin and paditaxel plus
radiotherapy)
Treatment
• supportive if rupture is contained (see sidebar Cameron'
s Criteria)
• NPO. antibiotics, IV fluids,
percutaneous drainage of mediasti
enteral /parenteral feed, and repeat imaging
• surgical (preferred treatment in progressively deteriorating or toxic patient)
• <24 h from perforation
• primary closure of a healthy esophagus with buttressed intercostal muscle flap or resection of
diseased esophagus
>24 h from perforation, non-viable esophagus, or morbidly toxic patient
diversion and exclusion followed by delayed reconstruction (i.e. esophagostomy proximally,
close esophagus distally, and gastrostomy/jejunostomy for decompression/feeding)
nal collections/abscess if needed.
6
%
Ss of SCC
Smok ing
Spirits(alcohol)
Seeds (betel nut)
Scalding (hot liquid)
Strictures
Sack (diverticula)
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Complications
• sepsis, abscess, fistula, empyema, mediastinitis, and death
• postoperative esophageal leak
• mortality 10-50% depending on timing of diagnosis, or etiology of the perforation, and underlying
health and age of the patient +
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GS23 General and Thoracic Surgery Toronto Notes 2023
Hiatus Hernia
Esophagus
Esophagus
Diaphragm GE junction
Stomach
GE junction
Stomach
Diaphragm
Normal Anatomy TypeI:Sliding Hiatus Hernia
-Esophagus
-Stomach
- GE junction
Esophagus
Stomach
Diaphragm
Diaphragm 1
\
GE junction
4
Typo II: Paraosophagoal Hiatus Hernia Type III:Mixed Hiatus Hernia
Figure 8. Types of hiatus hernia:TypeI:Sliding (GE junction above the level of the diaphragm) Type II:
Paraesophageal (GE junction below the diaphragm,fundus rolls past it) Type III: Mixed and Type IV:Massive (not
shown) (containing another intra-abdominal organ:bowel/spleen/etc.)
SLIDING HIATUS HERNIA (TYPE I)
•reducible and/or limited herniation of both the stomach and the gastroesophageal (GE) junction into
thorax
•90% of esophageal hernias
Risk Factors
•age
•increased intra-abdominal pressure (e.g.obesity, pregnancy,coughing, and heavy lifting)
•smoking
Clinical Features
•majority are asymptomatic
•symptoms in decreasing frequency are heartburn, regurgitation, eructation,sour taste, and cough
Complications
•complications are due to acid rellux when clinically significant and include these three categories:
• esophagitis (dysphagia and heartburn)
• consequences of esophagitis (peptic stricture, Barrett'
s esophagus, and esophageal carcinoma)
• extra-esophageal complications (aspiration pneumonitis/pneumonia, bronchospasm, cough, and
laryngitis)
Investigations
•barium study
•CXR or CT scan
•24 h esophageal pH monitoring to quantify reflux and esophageal manometry (technique for
measuring LES pressure)
•endoscopy with biopsy to document type and extent of tissue damage and rule out esophagitis,
Barrett’
s esophagus, and cancer
Treatment
•lifestyle modification
smoking cessation, weight loss, elevate head of bed, no meals <3 h prior to sleeping,smaller and
more frequent meals, avoid alcohol, coffee,mint, chocolate, and fatty foods
•medical
PP1, antacid, H2-antagonist,prokinetic agent
•surgical (<15% of cases)
consider if: volume regurgitation, patient unwilling or unable to stay on PPI indefinitely,
suboptimal medical therapy, complications of GERD such as pharyngitis, esophageal stricture,
recurrent nocturnal aspiration, Barrett'
s esophagus, patient preference
• laparoscopic hiatus hernia repair and fundoplication
• fundus of stomach is wrapped around the gastroesophageal junction and sutured in place
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GS2-1General and Thoracic Surgery Toronto Notes 2023
operative principles are reduction of hernia, removal of hernia sac, fundoplicatlon, and
partial closure of hiatus
360 degree wrap: Nissen Eundoplication (most commonly performed). Dor, and T
'
oupet are
partialfundoplications
expect transient postoperative clinical changes:dysphagia, bloating, excessive gas
long-term complications may include post-prandial diarrhea and hernia recurrence in
minority of patients
dysphagia and gas bloat may be less with partial fundoplications (Toupet/Dor), however
accompanied with higher risk of mild reflux symptoms
90% success rate for alleviating GERD
PARAESOPHAGEAL HIATUS HERNIA (TYPE II)
• least common esophageal hernia (<10%)
• herniation of all or part of the stomach through the esophageal hiatus into the thorax with an
undisplaced GE junction
Clinical Features
• usually asymptomatic due to normal GE junction
• dysphagia (most common), chest pain, and pressure sensation in lower chest
$
WebSurg
https://websurg.com/en/
WebSurg is an excellent resource which
allows traineesto leam many different
surgical techniques via videos and
lectures. This resource primarily focuses
on laparoscopic surgeries
Elective laparoscopic proceduresfor
paraesophageal hiatal hernia repair are
associated with relatively low mortality.
However, this value increases greatly
with emergency repairs(7.5% vs.0.5%)
Complications
• hemorrhage, incarceration,strangulation (gastric volvulus), obstruction, gastric stasis ulcer
(Cameron'
s lesion - causes 1 e-deliciency anemia )
MIXED HIATUS HERNIA (TYPE III)
• most common indication forsurgical repair
• second most common type of hernia - combination of typesI and 11
• includes giant hernias or intrathoracic stomach
• rare incidence of gastric volvulus (Borschadt'
s Triad: chest pain, retching, inability to pass NG tube)
• may present with long-standing Ee-deficiency anemia of unknown etiology
Clinical Features
• symptoms may include reflux or heartburn
• most common symptoms: abnormal postprandial fullness after normal-sized meal, chest pain or
retrosternal discomfort (gastric angina), and bloating
• can present with gastric outlet obstruction or gastric necrosissecondary to strangulation in the
setting of gastric volvulus
Treatment
• surgery to address symptoms or treat/prevent complications
• reduce hernia and excise hernia sac, repair defect at hiatus, and anti
-reflux procedure (e.g. Nissen
fundoplication)
• may considersuturing stomach to anterior abdominal wall (gastropexy) to reduce the risk of gastric
reherniation
• in very elderly patients at high surgical risk consider reduction of hernia and PEG (percutaneous
endoscopic gastrostomy) insertion to anchor the stomach in the abdomen
TYPE IV HERNIA
• herniation ofstomach and other abdominal organsinto thorax:colon,spleen, pancreas, and small
bowel
• similar presentation as type 111 hernia and may include intermittent large bowel symptoms(pain,
hematochezia, constipation, etc.) if it is herniated
Achalasia
•esophageal smooth muscle motility disorder which occurs because the lower esophageal sphincter
fails to relax
•esophagus does not have peristalsis
•in 50% of patients,the lower esophageal tone is hypertensive resulting in obstruction at the GE
junction
Risk Factors
•spinal cord injury
Clinical Features
•dysphagia, initially solid than to liquids though a majority of patients will initially present with
dysphagia to both solids and liquids
•regurgitation
•late symptoms include chest pain, nocturnal cough, and weight loss from difficulty eating
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GS25 General and Thoracic Surgery Toronto Notes 2023
Investigations
• barium esophagram with a classic finding ofsmooth tapering of the lower esophagus to a “
bird’
s
beak" appearance
• upper endoscopy
• esophageal manometry will show incomplete lower esophageal sphincter relaxation in response to
swallowing and sometimes a lack of peristalsis in the lower esophagus
Treatment
• non-surgical treatment:
pharmacologic: nitrates, calcium channel blockers, and phosphodiesterase-5 inhibitors to reduce
LES pressure
endoscopic botulinum toxin injection
pneumatic dilation
• surgical treatment options:
» laparoscopic Heller myotomy
• peroral endoscopic myotomy
Complications
• esophageal perforation
• GEKD
• bloating
Stomach and Duodenum
Peptic Ulcer Disease
GASTRIC ULCERS
• see Gastroenterology,Gil
Indications for Surgery
• treat complications: bleeding (common indication for emergency management), perforation,
obstruction (3x greater risk compared to duodenal ulcers)
• refractory to medical management time period is unclear but generally after 8- 12 wk of medical
therapy
• suspicion of malignancy (even if biopsy benign) especially if ulcer fails to heal after 12 wk of medical
therapy
• surgery’ increasingly rare due to H. pylori eradication, medical treatment, and endoscopic treatments
(injection therapy with adrenaline, polidocanol, or fibrin glue) or coagulation therapy (heater probe or
argon plasma)
Procedures
• ligation ofbleeding vessels
• distal gastrectomy with ulcer excision: Billroth 11, Roux-en-Y gastrojejunostomy, or Billroth I (rarely)
reconstruction
• vagotomy and pyloroplasty only if acid hypersecretion (very rare)
• wedge resection if possible
• biopsy for suspicion of malignancy, followed by gastroscopy to minimize further bleeding and aid
with healing
DUODENAL ULCERS
• see Gastroenterology, Peptic Ulcer Disease, (
’
ll
• most within 2 cm of pylorus (duodenal bulb)
Indications for Surgery
• hemorrhage, rebleed in hospital, perforation, gastric outlet obstruction
• refractory to medical and endoscopic management
Procedures
• omental (Graham ) patch: plication of perforated ulcer supported by overlying omental patch
• oversewing of bleeding ulcer ± pyloroplasty
• treat with H . pylori eradication protocol postoperatively
Complications of Gastric Surgery
• retained antrum
• fistula (gastrocolic/gastrojejunal)
• dumping syndrome, postvagotomy diarrhea, afferent loop syndrome
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GS26 General and Thoracic Surgery Toronto Notes 2023
Table 12. Complications of Duodenal Ulceration
Complication Clinical Features Management
Perforated Ulcer
(typically on anterior
surface)
Sudden onset of pain (possibly in RIO due lo track down Investigation
tight paiacolic gutter)
Acute abdomen:rigid,diffuse guarding
CXR lice air under diaphragm PO'L of patients)
Treatment
Oversew ulcer (plication) and omental (Graham) patch most
common treatment
Elevated amylase/lipase if penetration into pancreas Management should follow theintensive measures for
Elevated hepatic transaminases if penetration into liver refractory ulcers
(rare,but serious)
Constant mid epigastric pain burrowingInto back,
unrelated to meals
Ileus
Initial chemical peritonitis followed by bacterial
peritonitis (1=1 limb) — distal
gastrectomy +
gastroduodenostomy
Penetration to Nearby
Organs
Hemorrhage (typically
on posterior surface)
Gaslroduodenal artery involvement Resuscitation initially with crystalloids:blood transfusion
if necessary
Diagnostic andfor therapeutic endoscopy (laser,cautery,or
injection);if recurs,may have second scope
Consider interventional radiology:angiography with
embolirationfcoiling
Surgery if severe or recurrent bleeding,hemodynamically
unstable,or failure olendoscopy and IR:oversewing of
ulcer,pyloroplasty
NG tube decompression and correction of hypochloremic,
hypokalemic metabolic alkalosis
Medical management initially:high-dose PPI therapy
Surgical resection if obstruction does not resolve:either
BillrothI.pyloroplasty,or gastrojejunostomy
Billroth II
(II-2limbs) — distal
gastrectomy +
gastrojejunostomy
Gastric Outlet
Obstruction
Ulcer can lead to edema,librosis olpyloric channel,
and neoplasm
N/V (undigested food,non-bilious).dilated stomach,
and crampy abdominal pain
Succussion splash (splashing noise heard with
stethoscope over the stomach when patient is shaken)
Auscultate gas and fluid movement in obstructed organ LigamentofTreitr
Roux-on-Y Gastric Carcinoma
Epidemiology
• 5th most common cancer in the world
• M:F=3:2
• most common age group = 50-59 yr
• incidence has decreased by 2/3 in past 50 yr
• incidence highest in Asian, Latin American, and Caribbean countries
Risk Factors
• compensatory epithelial cell proliferation via gastric atrophy from:
H.pylori, causing chronic atrophic gastritis
pernicious anemia associated with achlorhydria and chronic atrophic gastritis
• previous partial gastrectomy (>10 yr post
-gastrectomy)
• lifestyle and environmental factors:
salt and salt-preserved food (e.g.salted fish, cured meat, and salted vegetables)
obesity
• cigarette smoking
LBV infection
abdominal radiation therapy
• host-related factors
• blood type A - also associated with pernicious anemia
• hereditary nonpolyposis colorectal cancer (HNPCC), hereditary diffuse gastric carcinoma
(HDGC)
gastric adenomatous polyps
• hypertrophic gastropathy
genetic syndromes: hereditary diffuse gastric cancer e.g. E-cadherin (CDH1) gene
Clinical Features
• clinical suspicion
• ulcer fails to heal
• lesion on greater curvature of stomach or cardia
• asymptomatic, insidious, or late onset of symptoms
• postprandial abdominal fullness, pseudoachalasia (in older patients), vague epigastric pain
• anorexia or weight loss
eructation, N/V,dyspepsia, and dysphagia
hepatomegaly, epigastric mass(25%)
hematemesis, fecal occult blood, melena, and iron-deficiency anemia
• metastasis
• peritoneum, ovarian, liver, lung, and brain
Investigations
• OGD and biopsy;consider EUS to assess preoperative T -stage and N-stage
• Cl'
chest/abdomen/pelvis
Ligament of Treitz
£
Jefusha Ellis after Sonya Amin 2012
Figure 9. BillrothI and Billroth II
with Roux-en-Y reconstruction
(gastrojejunostomy)
Kissing Ulcer:combination of
perforation and bleeding
Signs of Metastatic Gastric Carcinoma
Virchow’s Node:left supraclavicular
node
Blumer’s Shelf:mass in pouch of
Douglas
Krukenberg Tumour:metastases to
ovary
Sister Mary Joseph Node:umbilical
metastases
Irish's Node: left axillary nodes
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GS27 General and Thoracic Surgery Toronto Notes 2023
$
Table 13. TNM Classification System for Staging of Gastric Carcinoma (AJCC/IUCC 2017, 8th
edition)
Staging and 5 Yr Survival Rates for
Gastric Cancer
Primary Tumour (T) Regional Lymph Nodes (N) Distant Metastasis (M)
TX NX Cannot be assessed MO
No regional node metastasis
Metastasis in 1-2 regional nodes
Metastasis in 3-6 regional nodes
Primary tumour cannot be assessed
No evidence of primary tumour
Carcinoma insitu
Invasion into lamina propria or muscularis N2
mucosae
Invasion into submucosa
Invasion into muscularis propria
Pcnelration of subserosal connective tissue
without tissue invasion of visceral peritoneum
or adjacentstructures
Invasion intoserosa
Invasion into adjacent structures
No distant metastasis
Distant metastasis Stage TNM 5 Yr Survival TO NO MT
TTNOMO
T2N0M0
1A 7t% Tis NT
IB 57%
TYa
T1NTM0
T3N0M0
T2N1M0
Metastasis in 715 regional nodes IIA 45%
Metastasis in -16 regional nodes
T1b N3a
T2 N 3b
T1T2M0
T4aN0M 0
T3NIM0
T2N2M0
T3
MB 33%
T4a
T4b
T1N3M0
T4aN1M0
T312MO
I2N3M0
T 4PN 0M0
T4PN1M0
T4aN2M0
Treatment IIIA 20%
• adenocarcinoma
• proximal lesions
total gastrectomy and Roux-en-Y esophagojejunostomy
• distal lesions IIIB 14%
subtotal gastrectomy:wide margins, en bloc removal of omentum and lymph nodes (D2
lymphadenectomy) with Roux-en-Y or Billroth II reconstruction
• adjuvant therapies
perioperative chemotherapy or postoperative chemoradiotherapy in addition to surgery is
standard of care in curative intent strategy
T3N3M0
T4UM 2 M0
T 4PN 3M0
me 9%
• palliation
limited gastric resection or endoscopic stenting to decrease bleeding and relieve obstruction,
enables the patient to eat
radiation therapy
studies are showing larger role for adjuvant/neoadjuvant and palliative chemotherapy
T4dN3M0
IV TiNiMT 4%
• lymphoma
H. pylori eradication, chemotherapy ± radiation, and surgery in limited cases (perforation,
bleeding, and obstruction)
Gastrointestinal Stromal Tumour
Epidemiology
most common mesenchymal neoplasm of Cil tract
derived from interstitial cells of Gajal (cells associated with Auerbach'
s plexus that have autonomous
pacemaker function which coordinate peristalsis throughout the Gl tract)
75-80% associated with tyrosine kinase (c-KIT) mutations
most common in stomach (50%) and proximal small intestine (25%), but can occur anywhere along Gl
tract
often discovered incidentally on CT,laparotomy, or endoscopy
Heoadjuvant Chemotherapy in Advanced Caslric
and fsophagO’Caitric Cancer. Meta-Analysis of
Randomitcd Trials
Ini JSurg 2018:51:120 127
Study: Meta anaiysrseveluatingthe effects of
neoadjuvant chemotherapy on advanced gastric
cancer.
ResiiltsfConclusious:Neoadjuvant chemotherapy
and resection reduces overall mortality at 3 and
5yr in advanced gastric cancer (RR-0.74; 0.82
respectively). Morbidity and perioperative mortality
rale ore not influenced by NACI. tecovrence rate is
reduced by NAG -surgery in EGC IRM.80).
Risk Factors
Carney triad:gastric GISTs, extra-adrenal paraganglioma, and pulmonary chondroma
type I neurofibromatosis
Carney-Stratakissyndrome
Clinical Features
most commonly in stomach (40-60%) and jejunum (25-30%)
typically present with vague abdominal mass, feeling of abdominal fullness, or svith secondary
symptoms of bleeding and anemia
sometimes asymptomatic (13-18%)
nonspecific symptoms (8-17%): bloating, early satiety, abdominal pain/discomfort
overt or occult Gl bleeding (50% of gastric GISTs)
Investigations
• contrast-enhanced CT is preferred imaging for screening and staging;MRI if IV contrast not feasible
• preoperative biopsy (endoscopic ultrasound): useful for indeterminate lesions (not recommended if
high index of suspicion for GIST)
• given that lesion is submucosal, biopsy issometimes not helpful
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GS28 General and thoracic Surgery Toronto Notes 2023
Treatment
• surgical resection if >2 cm;follow with serial endoscopy if <2 cm and resect if growing or
symptomatic
• localized GIST
surgical resection with preservation ofintact pseudocapsule
• lymphadenectomy NOT required,as GISTs rarely metastasize to lymph nodes
consider adjuvant treatment with imatinib (Gleevec*) if high-risk of relapse (large, >4 cm with
significant mitoticactivity)
• advanced disease (Le. metastases to liver and/or peritoneal cavity)
palliative intent chemotherapy with imatinib
metastasectomv may be considered for liver limited disease
bleat of Lyapk lodeDissection for
Adenocarcinoma of ikeSiwack
Cochrane DBSjsi ter 20K:D:C00019M
Study:Systematic rare
*
and seS-aalyssoiike
eiridence iiat ersied itjerdmg tke epact of ike
threeman types of prcgressmeljso~eeiiended
lynpk node d ssection (Hats.Dl D2and D 3
lyapbedenedoay) on tke ctazloitcoce of patieots
itk primary resedatile caciwma of tkestiaadL
Besnlts Conclusions:DaS sqyested no sqnrkan*
ikfference in oieralsnrriial betmeen D2and D3
type Assertion.Theremas no sgnffost tfeence
in overall sirrural betmeen Dl and 02type node
dissection.In contrast D2 lyapkadenectomy mas
associated mitk asignicasCy better diseasespecie
snrmal compared to Dl tympkadenectomy Dot
wasalso associated mtt a kicker postoperathe
mortality raa.
Prognosis
• risk of metastatic potential depends on
tumour size (worse if >10 cm)
mitotic activity (worse if >5 mitotic figures/50 HPF)
degree of nuclear pleomorphism
location: with identical sizes, extra-gastric location has a higher risk of progression than GISTs in
the stomach
• frequently metastasize to the liver and omentum: nodal and lung metastases rare
Bariatric Surgery
•weight reduction surgery- for morbid obesity
•indications: BMI >40 without illness or BM1 >35 with 1+ serious comorbidity (e.g. DM, CAD, sleep
apnea,GtR D, or severe joint disease)
Asian patients:growing evidence to lower BMI criteria by 2.5, BM1> 37.5 or BM1>35.5 (higher
prevalence oftruncal obesity)
•consult with a multidisciplinary bariatric team: nutrition, psychological deterrents, life modifications,
lifelong surveillance, reliable bariatric program (details realistic outcomes) to optimize success postoperation
Surgery forHeigkt lossin Adults
Cochrane D3Systiei2014:3
*
3 C 03W1
Study:Update of a 2003 Cock-eceremassessog
tire^
ectsof bariatric surgery andcontrol of
coararkdkties.
Conclusions:S.'
cey resided a deceasedSHI
one totmo years postnperatnre.3KIsfondtka*
laparoscopic Bom-es-T gastric kypess ectered
signriicentiy greater msgtt lossandMlredoctioo
opto 5 yr after surgery comparedmrtk laparoscopic
ad., stable gastric Patdng(meandeference -52kg'
35% Cl-4.4to-4.01Harepatentsaqeraicel
remission of tatietesrnitk lap t-et-T.komeier.
different de&nrtmasmere ssed.Disks of ssrgery
indndeleaks,kenrias.Infection,prioonary
emtiolism.ckaiecystitis.and posioperaSit mortality.
Surgical Options
•combination malabsorptive and restrictive
laparoscopic Roux-en-Y gastricbypass (most common, most effective;higher complication rates)
small gastric pouch (restrictive), from distal stomach, anastomosed with Roux limb ofsmall
bowel (malabsorptive); connect to biliopancreatic limb to maintain digestive enzymes and
bile
• complications:gastric remnant distention,stomal stenosis, marginal ulcers, cholelithiasis,
ventral incisional hernia,short bowel syndrome,dumping syndrome, metabolic
perturbations,gastrogastric fistula
restrictive laparoscopic sleeve gastrectomy
• creation of tubular stomach via removal of majority of greater curvature
• complications:bleeding from gastric or short gastric vessels from dissection of greater curve,
stenosis at the gastroesophageal junction, gastric leaks
•malabsorptive
• biliopancreatic diversion with duodenal switch (performed as a rescue operation after traditional
Roux-en-y)
• anastomosis of stomach todistal ileum, anastomosis of biliopancreatic limb to terminal
Ileum
• complications: protein calorie malnutrition, anemia, metabolic bone disease, fat-soluble
vitamin deficiency
Complications of Gastric Surgery
•most resolve within 1 yr
•important to note that morbidly obese patients usually do not present with the symptoms and signs
shown below;often times,the only presenting sign istachycardia
Alkaline Reflux Gastritis
•duodenal contents (bilious) reflux into stomach causing gastritis ± esophagitis
•treatment
medical H2-blocker, metoclopramide, cholestyramine (bile acid sequestrant)
surgical: conversion of Billroth 1 or II to Roux-en-Y
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Afferent Loop Syndrome
•accumulation of bile and pancreatic secretions causesintermittent mechanical obstruction and
distention of afferent limb
•clinical features
• early postprandial distention, RUQ pain, nausea, bilious vomiting, anemia
•treatment:surgery- (conversion to Roux-en-Y increases afferent loop drainage)
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GS29 General and Thoracic Surgery Toronto Notes 2023
Dumping Syndrome
• early: 15-30 min postprandial
» etiology
rapid emptying of hyperosmotic chyme leads to jejunal distention,stimulating release of
vasoactive hormones
clinical features
postprandial epigastric cramping, bloating, emesis, nausea, and vasomotor symptoms
(dizziness, palpitations, tachycardia,diaphoresis)
Liver
-
Stomach
treatment
frequent small meals high in fibre and protein,low in carbohydrates;avoidance of liquids
with meals
last resort is interposition of antiperistaltic jejunal loop between stomach and small bowel to
delay gastric emptying
• late: 3 h postprandial
etiology:hypoglycemia following postprandial insulin peak
• treatment:smallsnack 2 h after meals
Gallbladder Pancreas Bile luice
A. Alkaline Reflux Gastritis
1 Liver
Slijniciut
Blind-Loop Syndrome
• bacterial overgrowth of colonic Gram-negative bacteria in afferent limb
• clinical features
anemia/weakness,diarrhea,malnutrition, abdominal pain, and hypocalcemia
• treatment:broad-spectrum antibiotics and surgery (conversion to Billroth I)
Postvagotomy Diarrhea
• up to 25%
• bile salts in colon inhibit water resorption
• treatment: medical (cholestyramine) and surgical (reversed interposition jejunal segment)
Gallbladder Pancreas Obstruction
B. Afferent Loop Syndrome
'
Liver
^
V '
SMALL INTESTINE Stomach
Food Flow—i
——
Small Bowel Obstruction
Mechanical Small Bowel Obstruction
Gallbladder Pancreas Small Intestine
C. Dumping Syndrome Pathophysiology
• obstruction -> gas and fluid (swallowed or Cil secretions) accumulate proximal to site of obstruction
and distal decompression -> intestinal activity increases to overcome obstruction -» colicky pain and
diarrhea (initially)
Liver V — -x
Food Flow
Etiology
Table 14. Common Causes of SBO
Intraluminal Foreign Body Intramural Extramural (>85% of causes)
Crohn's
Radiation stricture
Neoplasm (adenocarcinoma, carcinoid,
lymphoma,sarcoma)
Adhesionsfrom previoussurgeries(75% SBO)
Incarcerated hernia
Peritoneal carcinomatosis
Intussusception
Gallstones (gallstone ileus)
Bcroars
Foreign Body Gallbladder Pancreas Chyme Bacteria
D. Blind Loop Syndrome
•AAST grading system for severity (Grade - “Operative Criteria”)
partial SBO - minimal intestinal distension with no evidence of obstruction
complete SBO with viable bowel - intestinal distension with transition point: no bowel
compromise
• complete SBO with compromised but viable bowel - intestinal distension with impending bowel
compromise
complete SBO with nonviable bowel or perforation and localized spillage - intestinal distension
with localized perforation or free fluid
small bowel perforation with diffuse peritoneal contamination - intestinal distension with
perforation,free fluid, and diffuse peritonitis
•closed-loop obstruction is when a segment is obstructed in two separate locations, creating a segment
with no proximal or distal outlet and can rapidly progress to complications and require immediate
abdominal exploration
Risk Factors
•prior abdominal or pelvic surgery (adhesions)
•abdominal wall or groin hernia
•personal history or increased risk of malignancy
•prior radiation
V
CutCNX
Liver
StomachC
Y
7
v
_
n
J
Gallblader PancreasColon
E. Postvagotomy Diarrhea
© WonsiShengWIO
Figure10.Complications of gastric
surgery
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GS30 General and Thoracic Surgery Toronto Notes 2023
• IBD
• history of foreign body ingestion
Clinical Features
• symptoms: colicky periumbilical abdominal pain, N/V, obstipation,delayed passage/inability to pass
flatus,inability to tolerate an oral diet
more feculent vomitus suggests more established obstruction because of bacterial overgr
passage of gas and/orstool that continues 6-12 h after onset of symptomssuggests partial rather
than complete obstruction
• inability to pass flatus is the most useful indicator
• signs:abdominal distention (most prominent if obstruction at distal ileum), hyperactive proceeding
to minimal bowel sounds, bloating, hypovolemia, hyperresonance with percussion
• strangulated obstruction:abdominal pain disproportionate to physical exam findingssuggest
intestinal ischemia
may have tachycardia,localized abdominal tenderness,fever, marked leukocytosis, and lactic
acidosis
Increased Risk ol Perforation with
Distention asseen on Abdomen
Imaging
. Small bowel >3cm
• Distal colon >6 cm
• Proximal colon >9cm
. Cecum z12 cm
owth
Important to know if chronic vs.acute.
Chronic distention is more likely to be
tolerated without perforation
•
Investigations
approach Patients
o
with NO Abdominal Surgery
History (“Virgin Abdomen")
Presenting with a SBO should have
surgery 7SAP (EXCEPTION:malignant
obstruction from history and imaging)
1.distinguish mechanical obstruction from ileus
2.determine likely and easily reversible etiology of obstruction
3.differentiate complicated (e.g.strangulated) obstruction
• imaging
AXR (3 views):triad of dilated small bowel (>3 cm in diameter), air-fluid levels on upright film,
paucity of air in colon (high sensitivity,low specificity as ileus and UK)
can present similarly)
* CT with IV contrast: discrete transition zone/point with proximal bowel dilation,distal bowel
decompression, and intraluminal contrast does not pass the transition zone
most importantly to rule out ischemic bowel/strangulation:pneumatosis intestinalis (free
air in bowel wall) and thickened bowel wall, air in portal vein, free intraperitoneal fluid, and
differential wall enhancements (poor uptake of IV contrast into the wall of the affected bowel)
• other (less common)
upper Gl series/small bowel series (if no cause apparent, i.e. no hernias, and no previous
surgeries)
serial CTs with oral contrast
may consider U/Sor MR1in pregnant patients
Patients with Abdominal Surgery
History (“Non-virgin Abdomen")
Adhesional SBOs resolve spontaneously
with NG tube decompression 70% of
time
Top 3Causes of SBO (in order)
• laboratory
may be normal early in disease course
• CBC, electrolytes, BUN, creatinine, lactate
creatinine and hematocrit to assess degree of dehydration
• may have fluid and electrolyte abnormalities with metabolic alkalosis due to frequent emesis
ifstrangulation:leukocytosis with left shift, elevated lactate (late signs)
ABC
Adhesions
Bulge (hernias)
Cancer (neoplasms)
Treatment Causes of SBO
• IV isotonic fluid resuscitation and urine output monitoring with catheter
• SBO related vomiting and decreased PO intake leads to volume depletion
• NG tube in the stomach for gastric decompression; decrease nausea, distention, and risk of aspiration
from vomiting
. NPO
• if partial SBO/Crohn’s/Carrinomatosis:conservative management with fluid resuscitation and NG
tube decompression
48 h of watchful waiting; if no improvement or develops complications,surgery
• for Crohn's patients, consider Gl consult for steroid management
• if no clinical features of ischemia:short course of conservative management with fluid resuscitation
and NG tube decompression with frequent re-examination by surgical team
duration of observation variesfrom hours to a few days
if SBO failsto resolve,or ifsymptoms of ischemia develop,then surgery
• if high-risk for ischemia based on clinicalsymptoms: urgent surgery to prevent irreversible ischemia
early postoperative SBO: if bowel function does not return within 3-5 d after surgery; usually
partial, extended conservative therapy (2-3 wk) with bowel rest, fluids, and TPN is appropriate
• immediate surgery if ischemia, necrosis, and perforation
• clinical signs: fever,leukocytosis, tachycardia, worsening pain, metabolic and lactic acidosis, and
tachypnea
radiologic signs:free air on radiographs or CT,closed-loop obstruction, abnormal course of a
mesenteric vessel, and high-density free fluid
SHAVING
Stricture
Hernia
Adhesions
Volvulus
IntussusceptionHBD
Neoplasm
Gallstones
n
L J
Prognosis
• related to etiology; mortality: non-strangulating <1%,strangulating 8% (25% if >36 h), ischemic = up
to 509
• surgical intervention associated with a lower risk of recurrence
Prevention
• open surgery hasfour-fold increase in risk of SBO in 5 yr compared to laparoscopic surgery
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GS31 General and Thoracic Surgery Toronto Notes 2023
Paralytic Ileus
Pathogenesis
• temporary, reversible impairment of intestinal motility;most frequently caused by:
abdominal operations, infections and inflammation, medications (opiates, anesthetics,
psychotropics), and electrolyte abnormalities
often seen for patients in the postoperative setting from intra-abdominal sepsis (perforated
appendicitis, diverticulitis, etc.)
» pathophysiology related to inhibitory splanchnic reflexes,inhibitory sympathetic activity,
inflammatory stress response, peptides (VIP,substance P,Calcitonin gene-related peptide
(CGRP))
• NOT the same as intestinal pseudo-obstruction
chronic pseudo-obstruction refers to specific disorders that affect the smooth muscle and
myenteric plexus, leading to irreversible intestinal dysmotility
Clinical Features
• symptoms and signs of intestinal obstruction without mechanical obstruction
» bowel sounds are diminished or absent (in contrast to initial hyperactive bowel sounds in SBO)
• pain is often diffuse and less frequently has the colicky pattern present in mechanical obstruction
passing gas isthe most useful indicator
• postoperative:gastric and small bowel motility returns by 24-48 h, colonic motility by 3-5 d
Investigations
• routine postoperative ileus: expected, no investigation needed
• if ileus persists or occurs without abdominal surgery
review patient medications(especially opiates)
» measure serum electrolyte to monitor for electrolyte abnormalities (including extended
electrolytes like Mg-- , Ca
^ \P043-)
creatinine and BUN
LITs
CT scan to rule out abscess or peritoneal sepsis, or to exclude mechanical obstruction
Treatment
• address underlying cause
• most important initial treatment: NPO + fluid resuscitation
• for prolonged ileus: NG tube decompression,TPN, and pain management
Intestinal Ischemia
Etiology
• acute
» arterio-oedusive mesenteric ischemia (AOM1) <ft
thrombotic, embolic, and extrinsic compression (e.g.strangulating hernia)
non-occlusive mesenteric ischemia (NOM1)
mesenteric vasoconstriction secondary to systemic hypoperfusion (preservessupply to vital
organs)
• mesenteric venous thrombosis(MVT)
« consider hypercoagulable state (l.e. rule out malignancy) and DVT (prevents venous outflow)
• chronic: usually due to atherosclerotic disease -look for CVD risk factors
• can lead to occlusion in vessels thatsupplies the small intestine and the large intestine
Clinical Features
• acute:severe abdominal pain out of proportion to physical findings, vomiting, bloody diarrhea,
bloating, minimal peritoneal signs early in course, hypotension,shock, and sepsis
• chronic: postprandial pain (from mesenteric angina), fear of eating, and weight loss
• common sites:SMA supplied territory, “watershed” areas of colon -splenic flexure,left colon,and
sigmoid colon
Investigations
• laboratory:leukocytosis (non-specific) and lactic acidosis (late finding)
amylase,lactate, CK, and ALP can be used to observe progress
• hypercoagulability workup ifsuspect venous thrombosis
• AXR: portal venous gas, intestinal pneumatosis, and free air if perforation
• contrast CT:thickened bowel wall, luminal dilatation, SMA or SMV thrombus, mesenteric/portal
venous gas, and pneumatosis
• CT angiography is the gold standard for acute arterial ischemia
Treatment
• fluid resuscitation, correct metabolic acidosis, NPO, NG tube decompression ofstomach, and
prophylactic broad-spectrum antibiotics;avoid vasoconstrictors and digitalis
• exploratory laparotomy/laparoscopy to assess extent of viability ± segmental resection of necrotic
intestine
if extent of bowel viability is uncertain, a second-look laparotomy 12-24 h later is mandatory
• angiogram, embolectomy/thrombectomy, bypass/graft, mesenteric endarterectomy, anticoagulation
therapy, and percutaneoustransluminal angioplasty ± stent
Pain “out of keeping with physical
findings” Is the hallmark of early
intestinal ischemia
An acute abdomen + metabolic acidosis
is bowel ischemia until proven otherwise
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GS32 General and Thoracic Surgery Toronto Notes 2023
Tumours of Small Intestine
BENIGN TUMOURS
• lOx more common than malignant
• usually asymptomatic until large
• most common sites: terminal Ileum and proximal jejunum
• polyps
adenomas
hamartomas
• 1
;
AP (see familial Colon Cancer Syndromes,GS42 )
• juvenile polyps
• other: leiomyomas, lipomas, and hemangiomas
Table 15. Malignant Tumours of the Small Intestine
Adenocarcinoma Carcinoid/GI NETNeuroendocrine Tumour
Lymphoma Metastatic
Usually SO Carcinoid Syndrome Symptoms - TO yr Mostcommon site of Gl
mclastases in patients
with metastatic melanoma
Epidemiology Highest incidence in
70sM>F
Usually non-Hodgkin’s
lymphoma
Crohn’s.celiac disease,
autoimmune disease,
immunosuppression,
radiation therapy,
and nodular lymphoid
hyperplasia
Classified based on embryologica!origin Usually distal ileum
(foregut. midgut,and hindgut)
Originate from gut cnlciochtomaffin cell patients with celiac
Appendix 46%,distal ileum 28%.
rectum17%
Increased incidence 50-60 yr
M>F
FDR
Flushing
Diarrhea
Right-sided heart failure Crohn’s. FAP,history
of CRC.HNPCC
Risk Factors Melanoma,breast,lung,
ovary,colon,andcervical
cancer
Originlocalion Usually in proximal
small bowel,
incidence decreases
distally
Hematogenous spread
from breast,lung,and
kidney
Direct extension from
cervix,ovaries,and colon
Proximal jejunum in
disease
ClinicalFeatures Early metastasis to
lymph nodes
80% metaslalic at
time of operation
Abdominal pain
(common)
K/V.anemia,Gl bleeding,jaundice,and Fatigue,weight loss,fever Obstruction and bleeding
weight loss (less common) malabsorption,abdominal
Often slow-growing
Usually asymptomatic,incidental finding constipation,and mass
Obstruction,bleeding,crampy
abdominal pain,and intussusception
Carcinoid syndrome (<10%)
Hot flashes,hypotension,diarrhea,
bronchoconslriction.and right heart
failure
Requires liver Involvement:lesion
secretes serotonin,kinins,and
vasoactive peptides directly to
systemic circulation (normally
inactivated by liver)
pain, anorexia, vomiting.
Rarely perforation,
obstruction,bleeding,and
intussusception
Investigations Cl abdomcn/pelvis Cl abdomen/pclvis
Endoscopy
Most found incidentally at surgery for Cl abdomcn/pelvis
obstruction or appendectomy
Cl thorax/abdomen/pelvis
Consider small bowel enterodysis to
look for primary
Serum chromograninAas a tumour
marker
Elevated 5-HIAA (breakdown product
of serotonin) In urine or increased 5-HT
in blood
Some nuclear medicine testing available
but should be done by endocrine
oncologist.Testing includes Galium
D01AIAIE and octreotidescans
Surgical resection
'
chemotherapy
Carcinoid syndrome treated with
octreotide
Metastatic risk 2% if sixe<1cm,90%
if >2 cm
low- grade: chemotherapy Palliation
with cyclophosphamide
High-grade:surgical
resection,and radiation
Palliative:somatostatin,
doxorubicin
5 yr survival 40%
Treatment Surgical resections
chemotherapy
Syr survival 25% (if
node positive)
5 yr survival 70%:20% with liver
melastases
Based on the Ki67 index
Prognosis Poor r T
L J
Indirect Inguinal Hernias:Rule of 5s
Staging System THM TNM Ann Arbor
5%lifetime incidencein males
5x more common than direct Inguinal
hernias
5-10x more common in males than
females
Generally occur by 5th decade of life
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GS33 General and Thoracic Surgery Toronto Notes 2023
Short Gut Syndrome
Inguinal Hernias Definition
• reduced surface area (length) of small bowel causing insufficient intestinal absorption leading to
diarrhea, malnutrition, and dehydration
Etiology
• due to surgical resection
• large amount of bowel at once (acute mesenteric ischemia, trauma, malignancies)
• cumulative resections (Crohn’s disease)
• in infant and paediatric patients, the most common causes are necrotizing enterocolitis, abdominal
wall defects, jejunal ileal atresia, and midgut volvulus
MO's don't Lie
MD: Medial to the inferior epigastric a.
-
Directinguinal hernia
U:Lateral to the inferior epigastric a. *
Indirect inguinal hernia
Inguinal Canal Walls -
MALT x 2
2 MRoof 2 muscles (internal
oblique, transversus
abdominis)
2 A Ant wall 2 aponeuroses (external
and internal oblique)
2 L Floor 2 ligaments (inguinal
and lacunar)
2 T Post wall 2T (transversalis fascia,
conjoint tendon)
Prognostic Factors
• residual small bowel length, residual colon length (reabsorption of water and electrolytes and some
reabsorption of nutrients),condition of the remnant small bowel (healthier bowel facilitate better
reabsorption), presence of ileocecal valve (delay transition into colon leading to more reabsorption)
• resection of ileum is less tolerated than resection of jejunum (ileum reabsorbs bile salt and vitamin
Bl2 )
Borders
o
of Hesselbach's Triangle
• Lateral: inferior epigastric artery
• Inferior:inguinal ligament
• Medial:lateral margin of rectus
sheath
Therapy
• medical
• IV fluids in acute management (initial 3-4 wk following resection) and TPN once stabilized to
replenish lost fluid and electrolytes in diarrhea
histamine 2-receptor antagonist or PP1 to prevent gastric acid secretion
antimotility agent to prolong transit time in the small intestine
consider octreotide to decrease G1 secretion and cholestyramine for bile acid absorption
• surgical: non-transplant
• to slow transit time:small bowel segmental reversal, intestinal valve construction, or electrical
pacing of small bowel
• to increase intestinal length:
• LILT'
(longitudinal intestinal lengthening and tailoring) procedure
• ST EP (serial transverse enteroplasty procedure) in dilated small bowels
• surgical:small bowel transplant
indication:life-threatening complication from intestinal failure or long-term T PN, including liver
failure, thrombosis of major central veins, recurrent catheter-related sepsis, and recurrentsevere
dehydration
Shotrldice Technique vs. Other Open Techniques
for Inguinal Hernia Repair
Cochrane 08 Syst Rev 2012:4:10001543
Purpose:1o evaluate the efficacy and safety of
the Shouldxe technique compared lo other non -
laparoscopic techniques.
Results Conclusions: 16 RCTsor quasi-ratidomued
Mis with 2566 hecnias|U21mesh:1608 norr-mesh).
The recurrence rate with Shonldxe was lagher
than mesh (08 3.80, 95% Cl 1.99-7.26) but lower
than non-mesh (OR 0.62, 95% Cl 0.45-0.85).There
was co difference in chronic pain or complications.
In conclusion,with respect tn recurrence rates.
Shouldice herniorrhaphy is the best non-mesh
technique, although infetiot to mesh . However, it
vsatso Roretime consuming andresultsiai slightly
longer postoperative hospital stays.
Abdominal Hernia
•see HM I us Hernia, ( iS23
Definition
•defect in abdominal wall causing abnormal protrusion of intra-abdominal contents long-term Results of a Randomiied Controlled
Trial of a Honoperative Strategy (Watchful
W ailing ) for Men with Minimally Symptomatic
Inguinal Hernias
inn Sorg 2013:258:508-514
Purpose: Ascertain ng the long-term crossover (00)
rate in patients with asymptomatic or minimally
symptomatic inguinal hernias undergoing watchfulwait«g (WW|at their primary treatment modality.
Background : i 2006 RCf comparing WIff with
routine inguinal heima icpoir, concluded that
WW was an acceptable option in the management
of male patients with minimal symptoms(JAMA
200629S(3)28S-292|.This study analyzesthe WW
group after 7 years of follow-up.
Conclusions:The estimated CO rale far the WW
cohort was 68%, while men older than 65 had a rate
of 79%.Therefore, while WW is a safe strategy,it is
.1 I -Kent!v. :! progress,ridelr : ve
surgical management will be indicated.
Epidemiology
•M:l
’
=9:l
•lifetime risk of developing a hernia: males 20-25%, females 2%
•frequency of occurrence:50% indirect inguinal, 25% direct inguinal, 8-10% incisional (ventral), 5%
femoral, and 3-8% umbilical
•most common surgical disease in males
Risk Factors
•activities which increase intra-abdominal pressure
obesity, chronic cough, asthma,COPD, pregnancy, constipation, bladder outlet obstruction,
ascites, and heavy lifting
•congenita] abnormality (e.g.patent processus vaginalis and indirect inguinal hernia)
•previous hernia repair, especially if complicated by wound infection
•loss of tissue strength and elasticity (e.g. hiatal hernia, aging, and repetitive stress)
•family history
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 orstraining
Investigations
•physical examination usually sufficient
•U/S ± CT (CT required for obturator hernias, internal abdominal hernias, and Spigelian and/or
femoral hernias in obese patients)
# L J
Outcomes of laparoscopic vs. Open Repair o!
Primary Ventral Hernias
JAMA Ssrg 2013:148:1043-1048
See LaTidmerk Genera I and thoracicSurgery Inals
table (or more information on outcomes of patents
electiWly cmfcrgo. ng laparoscopic ventral Hernia
repair (U7HR) vs. open ventral hernia repair (0VHR|
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GSM General and Thoracic Surgery Toronto Notes 2023
Classification
• complete: hernia sac and contents protrude through defect
• incomplete: partial protrusion through the defect
• internal hernia:sac herniating into or involving intra-abdominal structure
• external hernia:sac protrudes completely through abdominal wall
• strangulated hernia: vascular supply of protruded viscus is compromised (ischemia)
• requires emergency repair
• incarcerated hernia:irreducible hernia, not necessarily strangulated
• Richter’
s hernia:only part of bowel circumference (usually anti-mesenteric border) is incarcerated or
strangulated so may not be obstructed
a strangulated Richter'
s hernia may self-reduce and thus be overlooked, leaving a gangrenous
segment at risk of perforation in the absence of obstructive symptoms
• sliding hernia: part of wall of hernia sac formed by retroperitonealstructure (usually colon)
Inguinal Region (Male)
(eternal interior epigastric inguinal artery and vein
nng V
Rectus
abdominis
muscle \
Hesselbach'
s
L triangle .
Ingu
gen
IIIHI External
inguinal men)
ring Femoral
artery
Femoral Femoral Anatomical Types ring
• groin
indirect and direct inguinal, femoral
• 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
• other: Littre’
s (involving Meckel'
s), Amyand'
s (containing appendix), lumbar, obturator, peristomal,
umbilical,Spigelian (ventral hernia through linea semilunaris)
Spermatic
cord
Normal Anatomy
Complications
• incarceration
• strangulation
small, new hernias more likely to strangulate
• femoral > indirect inguinal > direct inguinal
intense pain followed by tenderness
intestinal obstruction, gangrenous bowel,sepsis
surgical emergency
DO NOT attempt to manually reduce hernia if septic or if contents of hernial sac gangrenous. This
will result in reduction of gangrenous contents and subsequent need for laparotomy Indimcl Hernia
Treatment
• surgical treatment (herniorrhaphy) is only to prevent strangulation and evisceration, for symptomatic
relief, for cosmesis;if asymptomatic can delay surgery.Data hasshown that prophylactic surgery does
not affect rate of strangulation in ASYMPTOMATIC patients.
• repair may be done open or laparoscopic and may use mesh for tension-free closure
• most repairs are now done using tension free techniques- a plug in the hernial defect and a patch over
it or patch alone
• observation is acceptable for small asymptomatic inguinal hernias
Postoperative Complications
• recurrence (15-20%)
risk factors:recurrent hernia, ages >50,smoking, BMI >25, poor preoperative functional
status(ASA 23-see Anesthesia. A4), associated medical conditions:T2DM, hyperlipidemia,
immunosuppression, and any comorbid conditions increasing intra-abdominal pressure
less common with mesh/“tension-free” repair
• scrotal hematoma (3%)
painful scrotal swelling from compromised venous return of testes
deep bleeding:may enter retroperitonealspace and not be initially apparent
difficulty voiding
• nerve entrapment
ilioinguinal (causes numbness of inner thigh or lateral scrotum)
« genital branch of genitofemoral (in spermatic cord)
• stenosis/occlusion of femoral vein
acute leg swelling
• ischemic colitis
• minimally invasive repair for ventral and umbilical hernia
r
Figure 11. Schematic of inguinal
(direct and indirect) and femoral
hernias +
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GS35 General and Thoracic Surgery Toronto Notes 2023
Groin Hernias
Robotic Inguinal vs.Transebdominal
Laparoscopic Inguinal Hernia Repair:the RIVAL
Randomired Clinical trial
JAMA Surg.2O20;1SS(5|:3B0- 3fi 7
Purpose:To deter- me whether a robotic approach
to inguinal hernia repair results m improved
postoperative outcomes compared with the
traditional laparoscopic inguinal hernia repairs.
Results:ttpieopeiatnre. t nreekand 30- day
assessmentsthere wtre no differences between
the groups on wound events,readmissions, pain, or
quahty ollife. However, the robotic appioach was
associated with increased cost,operative time,and
surgeon frustration compared to the laparoscopic
approach.
Conclusions: there is no benefit ol the robotic
appioach compared with the laparoscopic approach.
Table 16. Groin Hernias
Direct Inguinal Indirect Inguinal Femoral
Epidemiology 1% of all men Most common hernia in men and women Affects mostly females
M t
Etiology Acquired weakness of transvcrsalrs
fascia
"Wear and tear"
Increased intra abdominal pressure
Congenital persislenccof processus
vaginalis in 20% of adults
Pregnancy weakness of pelvic floor
musculature
Increased intra -abdominal pressure
Ihrough Hesselbach'striangle
Medial to inferior epigastric artery
Anatomy Originates in deep inguinal ring
lateral to inferior epigaslricartery
Usually does not descend into scrolal Often descends into scrotal sac (or labia
majora)
Into femoral canal, below inguinal
ligament but may override it
Medial to lemotal vein within femoral
canal
Surgical repair
sac
Surgical repair
3- 4% risk of recurrence
Surgical repair
«1% risk of recurrence
treatment
Prognosis
Table 17, Superficial Inguinal Ring vs. Deep Inguinal Ring*
Superficial Inguinal Ring Deep Inguinal Ring
Opening in external abdominal aponeurosis: palpable superior and
lateral to pubic tubercle
Medial border:medial crus of enter nal oblique aponeurosis
lateral border:lateral crusof external oblique aponeurosrs
Opening in transversalisfascia:palpable superior tomid-inguinal
ligament
Medial border: inferior epigastric vessels
Superior-lateral bolder:internal oblique and transversus abdominis
muscles
Roof:intercrural fibres Inferior border:inguinal ligament
'see BasicAnatomy Review.Figure 2.63
Appendix
Appendicitis
Epidemiology
• 6% of population, M>I
:
(1.4:1)
• 80% between ages 5-35
Psoas
/yfe major
1!
_!L :
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,fecalith, or obstructing neoplasm
other causes: parasites or foreign body
L A
V
/
Retrocecal
'
164%)
V
Ileal
' sub-ileal
<1% )
t 1
—"
Inferior (1%)
Pelvic (32%)
Paracolic
I2%r
~
liiacus muscle L
Obturator
internus
muscle
^
g Natalie Cormier 2015, after Wensi Shcng 2010,
•
Clinical
most reliable
Features
feature is progression of signs and symptoms o • low-grade fever (38‘G), rises if perforation
• abdominal pain then anorexia, N/V
• classic pattern: pain initially periumbilical;constant, dull, poorly localized, then well-localized pain
over McBurney’s 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
Figure 12. Appendix anatomy
• signs
inferior appendix: McBurney'
s sign (see sidebar), Rin sing'
s sign (palpation pressure to left
abdomen causes McBurney'
s point tenderness). McBurney’s sign is present whenever the opening
of the appendix at the cecum is directly under McBurney's point; therefore McBurney'ssign is
present even when the appendix is in different locations
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)
McBurney's Sign
Tenderness 1/3 the distance from the
ASIS to the umbilicus on the right side
r i
L.J
Complications +
• perforation (especially if >24 h duration)
• abscess, phlegmon
• sepsis
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GS36 General and Tlioracic Surgery Toronto Notes 2023
Investigations
• laboratory
mild leukocytosis with left shift (may have normal WBC counts)
higher leukocyte count with perforation
p-hCG to rule out ectopic pregnancy
urinalysis
• imaging
U/S: may visualize appendix, but also helps rule out gynaecological causes - overall accuracy 90-
94%, can rule in but CANNOT rule out appendicitis (if >6 mm, SENS/SEEC/NEV/PFV 98%)
• CT scan: thick wall, enlarged (>6 mm), wall enhancement, appendicolith, and inflammatory
changes- overall accuracy 94-100%, optimal investigation
AntibioticsversusAppendectomyfor Acnte
Appendicitis- Longer-Term Ontcomes
N EnglJ Ued 202T;38S|25|:2395. Epub 2021Oct 25
Purpose:Compare Ibe efficacy of antibioticsis.an
appendectomy for acute appendicitiswild respect to
long-term outcomes.
Method: Pe'
domned trial comparing antibiotic
treatment mth appendectomy in patients with
appendicitis.
Results: he 30-day general health status of
patientstreated with antibiotics was comparable to
the appendectomy group.However, 29 percentof
medially-treated patients required appendectomy by
90 days,longer-term data from thistrial nowconfirm
h gi rates of subsequent appendectomy after indial
medical therapy:40 percent at one year, 46 percental
two years,and 49 percent at threeand foot years.
Conclusions:Sutgery should continue to be
recommended foi uncomplicated appendicrtisand
antibiotic therapy should be reserved for thosewho
are medially unfit for or decline surgery.
Treatment
• hydrate,correct electrolyte abnormalities
• appendectomy (gold standard)
laparoscopic is standard
complications:intra-abdominal abscess, appendiceal stump leak
perioperative antibiotics: cefazolin + metronidazole, if uncomplicated perioperative dose is
adequate
• consider treatment with postoperative antibiotics for perforated appendicitis
• for patients who present with an abscess (palpable mass or phlegmon on imaging and often delayed
diagnosis with symptoms for >4-5d), consider radiologic drainage + antibiotics xl4 d ± interval
appendectomy once inflammation has resolved = (controversial)
• medical management with antibiotic therapy should be reserved for those who are unfit for or refuse
surgery
• colonoscopy in those >50 yr to rule out concurrent etiology (neoplasm)
Prognosis
• mortality rate: 0.09-0.24%
Inflammatory Bowel Disease
• see Gastroenterology', G22
Principles of Surgical Management
• medical management remainsfirst line, but surgery can alleviate symptoms, address complications,
and improve quality of life
• conserve bowel: resect aslittle as possible to avoid short gut syndrome
• perioperative management
optimize medical status: may require TEN (especially if >7 d NEC)) and bowel rest
hold immunosuppressive therapy preoperative, provide preoperative stress dose of corticosteroid;
if patient had recent steroid therapy, taper steroids postoperative
VTE prophylaxis:LMWH or heparin (IBD patients at increased risk of thromboembolic events)
Crohn’s Disease
•see Gastroenterology. G23
Treatment
•surgery is for symptom management; it is NOT curative, but over lifetime -70% of Crohn'
s patients
will have surgery
•indications for surgical management
failure of medical management
SBO (due to stricture/inflammation):indication in 50% ofsurgical cases
abscess,fistula (enterocolic, vesicular, vaginal, cutaneous abscess), quality of life, perforation,
hemorrhage, chronic disability, failure to thrive (children), and perianal disease
•surgical procedures
resection and anastomosis/stoma if active orsubacute inflammation, perforation,or fistula
• surgery should be attempted in the elective setting ideally off steroids
•resection margin only has to be free of gross disease (microscopic disease irrelevant to prognosis)
stricturoplasty - widens lumen in chronically scarred bowel: relieves obstruction without
resecting bowel (contraindicated in acute inflammation )
Complications of Treatment
•anastomotic leak
•dehydration
•short gutsyndrome (diarrhea,steatorrhea, malnutrition)
•fistulas
•gallstones (if terminal ileum resected, decreased bile salt resorption > increased cholesterol
precipitation)
•kidney stones (loss of calcium in diarrhea -> increased oxalate absorption and hyperoxaluria > stones)
Crohn
m's 3 Major Patterns
• Ileocecal 40% (RIOpain,fever,
weight loss)
• Small intestine 30% (especially
terminal ileum)
. Colon 25% (diarrhea)
Findings in Crohn’s
• "Cobblestoning” on mucosal surface
due to edema and linear ulcerations
• “Skip lesions": normal mucosa in
between
• "Creeping fat":mesentery infiltrated
by fat
• Granulomas:25-30%
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GS37 General and Thoracic Surgery Toronto Notes 2023
Prognosis
• recurrence rate at 10 yr:ileocolic (25-50%),small bowel (50%), colonic (40-50%)
• re-operation at 5 yr:primary resection (20%), bypass (50%),strictureplasty (10% at 1 yr)
• 80-85% of patients who need surgery lead normal lives
. mortality: 15% at 30 yr
Ulcerative Colitis
•see Gastroenterology.G25
Treatment
•indications for surgical management
failure of medical management (including inability to tapersteroids)
complications: hemorrhage, obstruction, perforation, toxic megacolon (emergency), failure to
thrive (children)
reduce cancer risk (1-2% risk per yr after 10 yr of disease)
•surgical procedures
proctocolectomy and ileal pouch-anal anastomosis (1PAA) ± rectal mucosectomy (operation of
choice)
proctocolectomy with permanent end ileostomy (if not a candidate for ileoanal procedures)
colectomy and 1FAA ± rectal mucosectomy
in emergency: total colectomy and ileostomy with Hartmann closure of the rectum,rectal
preservation
Complications of Treatment
•early:bowel obstruction, transient urinary dysfunction,dehydration (high stoma output),
anastomotic leak
•late:stricture,anal fistula/abscess, pouchitis, poor anorectal function, reduced fertility
Prognosis
•mortality: 5% over 10 yr
•total proctocolectomy will eliminate risk of cancer
•perforation of the colon is the leading cause of death from UC
LARGE INTESTINE
Large Bowel Obstruction
Mechanical Large Bowel Obstruction
Etiology
Top 3Causes of LBO (in order)
• Cancer (>60%)
. Volvulus (10-15%)
. Diverticulitis(10%)
Table 18. Common Causes of LBO
Intraluminal Intramural Extramural
Constipation
Foreign bodies
Adenocarcinoma
Diverticulitis (edema, stricture)
IBD stricture
Radiation stricture
Volvulus
Adhesions
Hernias (sigmoid colonin a large groin hernia)
In a patient with a clinical LBO consider
impending perforation when:
• Cecum i12 cm in diameter
• Tenderness present over cecum
Clinical Features (unique to LBO)
• open loop (10-20%)
• incompetent ileocecal valve allows relief of colonic pressure as contents reflux into ileum,
therefore clinical features similar to SBO
• closed loop (80-90%) (dangerous)
competent ileocecal valve,resulting in proximal and distal occlusions
massive colonic distention -» increased pressure in cecum -» bowel wall ischemia -> necrosis ->
perforation
n
L
Investigations
• GBG with differential, BUN, electrolyte panel, creatinine,CEA if patient is suspected to have
malignancy, and lactate for level of ischemia
• imaging: AXK and CT scan +
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GSM General and Thoracic Surgery Toronto Notes 2023
Treatment
• supportive management: IV fluids, gastrointestinal decompression
• surgical intervention (75% of cases)
volvulus: initial decompression with flexible sigmoidoscopy, operative reduction or sigmoid
resection dependent on severity
colorectal obstruction:ostomy alone (fecal diversion),colectomy with primary anastomosis, or
Hartmann procedure
• may pursue stenting as a bridge to surgery or palliation
Prognosis
• overall mortality: 10%
• cecal perforation t feculent peritonitis: 20% mortality
Table 19. Bowel Obstruction vs. Paralytic Ileus
SBO LBO Paralytic Ileus
Early,may be bilious
Colicky
Abdominal Distention (pros SBO).** (distal SBO)
Constipation
Bowel Sounds
N/V Late, may be feculent
Colicky
Present
Abdominal Pain Minimal or absent
Normal.Increased
Absent if secondary ileus
(delayed presentation)
Ait-fluid lewis
“ladder" pattern (plicae
circulares)
Proximal distention (>3 cm)
no colonic gas
Normal,increased (borborygmi)
Absent ilsecondary ileus (delayed presentation)
Decreased.absent
AXR Findings Air-fluid levels
“Picture frame"appearance
Proximal distention distal decompression
No small bowel air if competent ileocecal valve
Coffee bean sign (sigmoid volvulus)
Air throughoutsmall bowel
and colon
Functional Large Bowel Obstruction:Colonic PseudoObstruction (Ogilvie’s Syndrome)
Definition
• acute pseudo-obstruction
• distention of colon without mechanical obstruction in distal colon
• exact mechanism unknown, likely autonomic motor dysrcgulation
Associations
• most common: trauma, infection, and cardiac (MI, CHI'
)
• disability (long-term debilitation, chronic disease, bed-bound nursing home patients, and
paraplegia), drugs (narcotic use, laxative abuse, and polypharmacy), and other (recent orthopaedic
or neurosurgery, post-partum, electrolyte abnormalities including hypokalemia, retroperitoneal
hematoma, and diffuse carcinomatosis)
Clinical Features
• classically presents with abdominal distention (acute or gradual over 3-7 d)
• abdominal pain, N/V, constipation or diarrhea
• watch out for fever,leukocytosis, and presence of peritoneal signs(suggestive of colonic ischemia or
perforation)
Investigations
• AXR:cecal dilatation (if diameter £12 cm, increased risk of perforation)
Treatment
• treat underlying cause
• NFC), NG tube
• decompression: rectal tube,colonoscopy, neostigmine (cholinergic drug),orsurgical (ostomy/
resection)
• surgery (extremely rare): if perforation, ischemia, or failure of conservative management
Prognosis
• most resolve with conservative management
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GS39 General and Thoracic Surgery Toronto Notes 2023
Diverticular Disease
Definitions
• diverticulum:abnormal outpouching from the wall of a hollow organ
• diverticulosis: presence of multiple diverticula
• diverticulitis:inflammation of diverticula
• true (congenital) diverticuli:contain all layers of colonic wall,often right-sided
• false (acquired) diverticuli: contain mucosa and submucosa, often left-sided
FALSE DIVERTICULUM ,
(mucosal herniations) V
TRUE DIVERTICULUM
(full wall thickness) 11
Y,
Mucosa' x— Antimesentenc
tenia /
Circular muscle
I MesocolonMesenteric teniaSBR I
Figure 13. Diverticular disease -cross-sections of true and false diverticula
Diverticulosis
Epidemiology
• 5-50% of Western population, lower incidence in non-Western countries,M=F
• prevalence is age dependent: <5% by age 40, 30% by age 60, 65% by age 85
• 95% involve sigmoid colon (site of highest pressure)
Pathogenesis
• risk factors
lifestyle:diet (low-fibre, high fat, red meat), inactivity, and obesity
muscle wall weakness from aging and illness(e.g.Ehlers-Danlos, Marfan’s)
• high intraluminal pressures cause outpouching to occur at points of greatest weakness, most
commonly where vasa recta penetrate the circular muscle layer leading to an increased risk of
hemorrhage
Clinical Features
• uncomplicated diverticulosis:asymptomatic (70-80%)
• episodic abdominal pain (often LLQ), bloating,flatulence, constipation,diarrhea
• absence of fever/leukocytosis
• no physical exam findings or poorly localized LLQ tenderness
• complications:
diverticulitis (15-25%):25% of which are complicated (i.e. abscess,obstruction, perforation,
fistula)
bleeding (5-15%): PAINLESS rectal bleeding, 30-50% of massive LGIB
diverticular colitis(rare):diarrhea,hematochezia,tenesmus,and abdominal pain
Diverticulosis vs.Diverticulitis
Diverticulosis represents the presence of
diverticuli (bulging pouches) within the
colonic wall, whereas diverticulitis is the
inflammation of one or more diverticuli
Treatment
• uncomplicated diverticulosis: high fibre, education
• diverticular bleed
initially workup and treat as any LGIB
if hemorrhage does not stop, resect involved region
Diverticulitis
Epidemiology
• 95% left-sided in patients of Western countries, 75% right-sided in Asian populations
Pathogenesis
• erosion of the wall by increased intraluminal pressure or inspissated food particles -> inflammation
and focal necrosis-> micro or macroscopic perforation
• usually mild inflammation with perforation walled offby pericolic fat and mesentery; abscess,fistula,
or obstruction can ensue
• poor containment resultsin free perforation and peritonitis
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GS10 General and Thoracic Surgery Toronto Notes 2023
Clinical Features
• depend on severity of inflammation and whether or not complications are present; hence rangesfrom
asymptomatic to generalized peritonitis
• LLQ pain/tenderness (2/3 of patients) often for several days before admission
• constipation, diarrhea, N / V, and urinary symptoms (with adjacent inflammation)
• low-grade fever, mild leukocytosis, and occult or gross blood in stool rarely coexist with acute
diverticulitis
• complications (25% of cases)
• abscess: palpable, tender abdominal mass
fistula: colovesical (most common), coloenteric, colovaginal, and colocutaneous
colonic obstruction:due to scarring from repeated inflammation
perforation: generalized peritonitis(feculent vs. purulent)
• recurrent attacks rarely lead to peritonitis
Efficacy and Safety of Monantibiotic Outpatient
Treatment in M lid Acute Diverticulitis (DINAMO
study): A Multicentre, landomised, Open-label.
Noninferiority Trial
Ann Surg 2021;274(5):e435.
Background:In recent years,it hasshown no benefit
olantrkotntjAl!) in the treatrnentof uncomptcated
AD mhospitalited patients.
Methods:Prospective,nnlticentre. open-label,
noninferiority,randomized controlled trial.
Desalts: Differences in hospitaliiation rates,revisits,
and poor par n controlat 2 daysfollow- up were within
the non-inferiority margin.
Conclusions lit
of mild AD issafe and effectneand is not inferior to
current standard treatment
Investigations
• CT scan (test of choice)
very useful for assessment of severity and prognosis (97% sensitive, 99% specific)
• usually done with rectal contrast
increased soft tissue density within pericolic fatsecondary- to inflammation, diverticula
secondary to inflammation, bowel wall thickening,soft tissue mass (pericolic fluid, abscesses),
and fistula
10% of diverticulitis cannot be distinguished from carcinoma
. AXR, upright CXR
• localized diverticulitis(ileus,thickened wall, SBO, and partial colonic obstruction)
free air may be seen in 30% with perforation and generalized peritonitis
• colonoscopy or barium enema and flexible sigmoidoscopy (elective evaluation)
establish extent of disease and rule out other diagnoses (polyps and malignancy) AFTER
resolution of acute episode
Treatment
• uncomplicated: conservative management
• outpatient: clear fluids only until improvement. Avoid treatment with antibiotics for those with
uncomplicated acute diverticulitis
• hospitalize:ifsevere presentation, inability to tolerate oral intake,significant comorbidities,or fail to
improve with outpatient management
treat with NPO, IV fluids, and IV antibiotics (e.g. IV ceftriaxone + metronidazole)
• image-guided (CT) percutaneous drainage of abscesses reduces the urgency ofsurgical resection in
most patients
• surgery:
indications:
diverticulitis and
inflammation
Colostomy
unstable patient with peritonitis
Hinchey stage 3-4 (see Table 19)
after 1 attack if immunosuppressed
consider if recurrent episodes of diverticulitis(S3); recent trend is toward conservative
management of recurrent mild/moderate attacks
Resection of
diseasedarea
and closure
of distal
rectal stump
• procedures:
Hartmann resection (for unstable or complex cases)
• colon resection + colostomy and rectal stump > colostomy reversal in 3-6 mo
• for more stable patients with Hinchey stage 3 and 4 acute diverticulitis: colonic resection, primary
anastomosis + diverting loop ileostomy is becoming more common, with benefitsfor mortality
and morbidity
for Hinchey stage 3: laparoscopic peritoneal lavage with drain placement near the affected colon,
in addition to 4 antibiotics(NO resection), has been proposed
• complications:perforation,abscess,fistula, obstruction, hemorrhage,inability to rule out colon
cancer on endoscopy, or failure of medical management
Anastomosis -
in approximately s
:- 3mo
„
Figure 14.Hartmann procedure
Prognosis
• mortality rates:6% for purulent peritonitis,35% for feculent peritonitis
• recurrence rates:13-30% after first attack, 30-50% aftersecond attack
Table 20. Hinchey Staging and Treatment for Diverticulitis
Hinchey Stage Description Acute Treatment r i
1 L J
Phlegmonfsmall pericolic abscess
large abscess/fistula
Purulent peritonitis (ruptured abscess)
Feculent peritonitis
Medical
Medical, abscess drainage tresection with primary anastomosis
Resection or Hartmann procedure
Hartmann procedure
2
3
4
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GS41 General and ThoracicSurgery Toronto Notes 2023
Colorectal Neoplasms
Colorectal Polyps
Definition
• polyp: protuberance into the lumen of normally Hat colonic mucosa
sessile (flat) or pedunculated (on a stalk)
Epidemiology
• 30% of the population have polyps by age 50,40% by age 60,50% by age 70;M>F
Clinical Features
• 50% in the rectosigmoid region, 50% are multiple
• usually asymptomatic, do not typically bleed, tenesmus, intestinal obstruction, and mucus
• usually detected during routine endoscopy or familial/high-risk screening
Bowel lumen
-Bowel wall
v
Pathology
• non-neoplastic/non-adenomatous
hyperplastic: most common non-neoplastic polyp
mucosal polyps:small <5 mm, no clinical significance
hamartomas:juvenile polyps(large bowel), Peutz|
- eghersyndrome (small bowel)
malignant risk due to associated adenomas (large bowel)
low malignant potential-> mostspontaneously regress or autoamputate
inflammatory pseudopolyps:associated with IBD, no malignant potential
• submucosal polyps: lymphoid aggregates, lipomas, leiomyomas, and carcinoids
• neoplastic/adenomatous
adenomas: premalignant, considered carcinoma in situ if high-grade dysplasia
may contain invasive carcinoma (“malignant polyp” - 3-9%): invasion into submucosa
malignant potential related to histological type:villous > tubulovillous > tubular
Table 21. Characteristics of Tubular vs. Villous Polyps
OJanlea Wong 2003 J
Figure 15. Sessile and pedunculated
polyps
Tubular Villous
Comraon (60-80%)
Small(<2cm)
Pedunculated
less common(10%)
Large (usually>2 cm)
Sessile
Higher
tell sided predominance
Incidence
Size
Attachment
Malignant Potential
Distribution
Lower
(ven
Investigations
• colonoscopy with biopsy/resection (gold standard)
• CT colonography:increasing in availability;patientsstill require bowel prep and will require
colonoscopy if polyps are identified
• other: flexible sigmoidoscopy (if polyps are detected, proceed to colonoscopy for examination of entire
bosvel and biopsy)
Treatment
• indications:symptoms, malignancy or risk of malignancy (i.e. adenomatous polyps)
• endoscopic removal of entire growth
• indications forsegmental resection for malignant polyps:1) lymphovascular invasion; 2) tumour
budding; 3) positive resection margin; 4) poorly differentiated cells; 5) evidence of regional or distant
metastases on staging
most of these cases are usually discussed at multi-disciplinary’tumour boards
• follow-up endoscopy:
• every 5 yr: if low-risk polyp (<10 mm tubular adenoma or <10 mm sessile serrated without
dysplasia)
every 3yr: if high-risk polyp (3-10 tubular adenomas, >10 mm tubular or serrated polyp,
adenoma with villous features or high grade dysplasia, or sessile serrated with dysplasia)
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GSI2 General and Thoracic Surgery Toronto Notes 2023
Familial Colon Cancer Syndromes
FAMILIAL ADENOMATOUS POLYPOSIS
Epidemiology
• accountsfor <1% of colorectal cancers, affects males and females equally Referral Criteria for Genetic Screening
for APC
• To confirm the diagnosis of FAP
(in patients with >100 colorectal
adenomas)
• To provide pre-symptomatic testing
for individuals at risk for FAP (1st
degree relatives who are >10 yr)
• To confirm the diagnosis of
attenuated FAP (in patients with >20
colorectal adenomas)
Pathogenesis
• autosomal dominant inheritance, mutation in adenomatous polyposis coli (APC) gene
Clinical Features
• hundreds to thousands of colorectal adenomas usually by age 20 (by 40’s in attenuated TAP)
• virtually 100% lifetime risk of colon cancer (due to number of polyps)
• extracolonic manifestations
bile duct, pancreas,stomach, thyroid (large benign multinodular goitre), adrenal glands, and
small bowel
congenital hypertrophy of retinal pigment epithelium presents early in life in 2/3 of patients;97%
sensitivity
• variants
Gardner’ssyndrome: FAP + extra-intestinal lesions (sebaceous cysts, osteomas, desmoid
tumours)
• Turcot syndrome: FAP f CNS tumours (childhood cerebellar medulloblastoma)
Revised Bethesda Criteria for HNPCC
and Microsatellite Instability (MSI)
T umours from individuals should be
tested for MSI in the following situations:
• Colorectal cancer diagnosed in a
patient who is <50 yr
• Presence of synchronous,
metachronous, colorectal,or
other HNPCC-associated tumours,
regardless of age
• Colorectal cancer with the MSI-H
histology diagnosed in a patient who
is <60 yr
• Colorectal cancer diagnosed in one
or more first-degree relatives with an
HNPCC-related tumour,with one of
the cancers being diagnosed <50 yr
• Colorectal cancer diagnosed in two
or more first- or second-degree
relatives with FIN PCC-related
tumours, regardless of age
Investigations
• genetic testing (80-95% sensitive, 99-100% specific)
• if no polyposis found: annual flexible sigmoidoscopy from puberty to age 50, then routine screening
• if polyposis or APC gene mutation found: annual colonoscopy, consider surgery, and consider upper
endoscopy to evaluate for periampullary tumours
Treatment
• surgery indicated by ages 17-20
• total proctocolectomy with ileostomy or total colectomy with ileorectal anastomosis
• doxorubicin-based chemotherapy
• NSAIDs for intra-abdominal desmoids
HEREDITARY NON-POLYPOSIS COLORECTAL CANCER - LYNCH SYNDROME
Epidemiology
• most common inherited colorectal cancer susceptibility syndrome and accounts for 3% of colorectal
cancer diagnoses
Pathogenesis
• autosomal dominant inheritance, mutation in a DNA mismatch repair gene (MSH2,
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