General Surgery GI Flashcards
Midgut structures, arterial supply, venous drainage and innervation
structures: jejunum, ileum, cecum, large intestine up to left colic flexure
supplied by superior mesenteric artery
drained by superior mesenteric vein to portal system
innervated by lesser (T10-T11) and least (T12) splanchnics from sympathetic system and vagus nerve from parasympathetic system
Hindgut structures, arterial supply, venous drainage and innervation
structures: descending colon, sigmoid colon, rectum, anal canal
supplied by inferior mesenteric artery
drained by inferior mesenteric vein to portal system
innervated by lumbar splanchnics (L1-L2) from sympathetic system and pelvic splanchnics (S2-S4) from parasympathetic
Division of the compartment of greater sac
greater sac divided by transverse, ascending and descending colon into supra colic compartment, infra colic compartment, right paracolic gutter and left paracolic gutter
the infra colic and supra colic compartment communicate via paracolic gutters
Jejenum vs ileum
wall, caliber: jejunum have thicker walls with larger diameter whereas ileum have thinned walls with smaller diameter
location: jejunum located in upper left quadrant whereas ileum is located in lower right quadrant
vascularity: jejunum have greater vascularity so it appears darker and more red whereas ileum have lesser vascularity so it appears lighter and more pink
vasa recta: vasa recta is long in jejunum and short in ileum
mesenteric fat: jejunum have less mesenteric fat and ileum have more mesenteric fat
circular folds: jejunum have tightly packed circular folds whereas ileum have sparse circular folds and absent circular folds distally
intestinal villi: jejunum have more numerous and prominent villi whereas ileum have less numerous and less prominent villi
lymphoïde mode follicules: jejunum have no aggregates (no Peyer’s patches) whereas ileum contain Peyer’s patches
Arterial supply of jejenum vs ileum
both jejunal and ileal arteries are branches from superior mesenteric artery (15-18 arteries in total)
jejunum / ileum artery -> arcade -> vasa recta
jejunum have fewer, larger arteries that loops and have longer vasa recta (straight arteries) than ileum
What is the ileoceacal junction
ileum terminates by partly invaginating into cecum, forming the ileocecal valve
How to locate the appendix
appendix location can vary, it is usually localized by tracing to origin of taenia coli
Blood supply of midgut
mid gut supplied by superior mesenteric artery (SMA) at L1 level
superior mesenteric artery have branches to feed small intestines and branches to feed large intestines
all of branches of SMA that course toward the left are jejunal arteries and ileal arteries supply small intestines
branches of SMA that course toward the right include ileocolic artery (with ileal and colic branches), appendicular artery, right colic artery and middle colic artery that supply the large
intestines
the ileocolic artery split into ileal and colic branches that supply ascending colon
appendicular arteries is a branch of ileocolic artery that supply the appendix
the right colic artery is a branch of SMA that supply the ascending colon
middle colic artery is a branch of SMA that supply the transverse colon
Venous drainage of midgut
midgut drained by superior mesenteric vein (SMV), which drain to the portal vein (portal system)
SMV branches are paired and travel with arteries with same name (jejunal veins, ileal veins, ileocolic vein, right colic vein, middle colic vein, appendicular vein)
the SMV and its branches are always anterior to its correspondent SMA and its branches
large intestine intraperitoneal and retroperitoneal components
large intestines include cecum, appendix, ascending colon, transverse colon, descending colon and sigmoid colon
cecum, appendix, transverse and sigmoid colon are intraperitoneal and covered by mesentery
ascending colon, descending colon and rectum are retroperitoneal
What are the taenia coli
taenia coli = 3 strips of longitudinal muscle extending length of large colon
the longitudinal muscle names are taenia libera, taenia omentalis and taenia mesocolica
pulling force of taenia coli result in haustra (sacculated appearance that look like pouches)
taenia coli unite at base of appendix and then splay out to form outer wall of rectum
Locations of longitudinal taenia muscles
taenia omentalis is underneath the greater omentum
taenia libera is anterior
taenia mesocolica is posterior
what are epiploic appendages
epiploic appendages are small pouches of peritoneum filled with fat along the colon
what are semilunar folds
semilunar folds are ridges inside the large intestine between taenia coli that separate the haustra
rectosigmoid junction landmarks
- located anterior to S3 vertebra
- termination of sigmoid mesocolon (mesentery)
- colon traits (taenia coli, haustra, appendages) end at rectosigmoid junction
- taenia coli stop being distinct bands, flare out and become continuous muscle layer covering the rectum
Rectum, its components and pouches
rectum is part of the large intestine that is retroperitoneal and fixed
ampulla of rectum is the inferior dilatation of rectum
lowest extent of peritoneal cavity forms a pouch
rectovesival pouch between rectum and bladder in male
rectouterine pouce between rectum and uterus in female
drainage of excess peritoneal fluid and peritoneal dialysis at these pouches
where is the anorectal junction roughly located
pelvic diaphragm
anal canal and its components
in anal canal, interior (mucosa) and exterior (skin) surfaces are divided by pectinate line
anal columns are longitudinal ridges that elevate, which is due to superior rectal artery and vein
anal sinuses are grooves between anal columns that secrete mucus
Embryological origin, innervation, arterial supply, venous drainage and lymphatic drainage of tissue above the pectinate line (visceral)
Endoderm
Autonomic: distension sensation
Superior Rectal A. (IMA)
Superior Rectal V. (IMV –> Portal drainage)
Visceral pattern (internal iliac lymph nodes –> chyle cistern)
Embryological origin, innervation, arterial supply, venous drainage and lymphatic drainage of tissue below the pectinate line (body wall/somatic)
Ectoderm
Somatic: pain sensation (inferior rectal N.)
Inferior Rectal A. (from internal iliac artery)
Middle/inferior rectal V. (int iliac V. –> IVC, caval drainage)
Body wall drainage pattern (superficial inguinal lymph nodes –> body wall)
Branches of inferior mesenteric artery
1 = IMA
2 = left colic artery, a branch of IMA, supplies left part of transverse colon and descending colon
3 = sigmoid arteries (usually 2 or 3 arteries), branches of IMA, supply sigmoid colon
4 = superior rectal artery, a continuation of IMA after sigmoidal arteries are given off
blue arrows = marginal artery of Drummond that anastomose between SMA and IMA along length of entire large colon
marginal artery encircles the entire colon
Venous drainage of hindgut
hindgut drained by inferior mesenteric vein (IMV), which drain to the portal vein (portal system)
IMV branches are paired and travel with arteries with same name (right colic vein, sigmoidal veins, superior rectal vein)
IMV and its branches are always posterior to the correspondent IMA and its branches
Lymphatic drainage of midgut and hindgut
lymph nodes generally associated with arteries (nodes along arteries) to bypass portal venous system
this is unique to GI, where lymph usually follows veins elsewhere in the body
small intestine lymph follows arterial lymph nodes to chyle cistern to thoracic duct
large intestine lymph follows arterial lymph nodes to chyle cistern to thoracic duct
anal canal lymph superior to pectinate line follow arterial lymph node to chyle cistern to thoracic duct (gut drainage pattern)
anal canal lymph inferior to pectinate line drain to superficial inguinal lymph nodes (body wall drainage pattern)
Overall Regulation of GI System
3 types of regulation of GI system
1) Nervous system control
autonomic innervation (sympathetic and parasympathetic)
as a rule, sympathetic always inhibit GI function and parasympathetic always stimulate GI function
enteric nervous system
2) Endocrine control
secretion of hormones into bloodstream
e.g. secretin, CCK, somatostatin, VIP, gastrin
3) Paracrine control
secretion of signalling molecule into interstitial for communication between nearby cells
Role of CCK and Secretin
CCK and secretin are hormones released by duodenum
fatty chyme stimulate release of CCK
acidic chyme stimulate release of secretin
CCK inhibit gastric emptying, stimulate pancreatic growth, stimulate release of pancreatic enzyme and stimulate release of bile from gallbladder
secretin stimulate release of basic pancreatic fluid and basic bile
CCK and secretion potentiate each other’s effect
Overview of digestion and absorption
1) Mouth
mastication
saliva
2) Stomach
pepsin
gastric acid secretion
intrinsic factor
3) Liver
bile acid
4) Pancreas bicarbonate amylase protease lipase / colipase
5) Duodenum, jejunum
water and electrolyte absorption
nutrient absorption
90% of digestion and absorption occur in duodenum
6) Terminal ileum
bile salt transport
vitamin B12 absorption
absorption of fat soluble vitamins
7) Colon
water absorption
bacterial fermentation of disaccharide into short chain fatty acids and acids (CO2, methane)
short chain fatty acids are used by colonic epithelium or metabolized by liver
Digestion and absorption of proteins
1) Digestion in stomach
proteins denatured in gastric acid
pepsinogen (secreted by chief cells in stomach) is activated in gastric acid to pepsin, which cleave protein into peptides
2) Digestion in duodenum
pancreatic proteases cleave peptides into oligopeptides (2-6 amino acids) and amino acids
trypsin, chymotypsin, elastase and carboxypeptidase
duodenum mucosal enzyme enterokinase cleave and activate trypsin, which then cleave and activate chymotrypsin
brush border enzymes cleave oligopeptides into tri-peptides, dipeptides and amino acids
aminopeptidase, carboxypeptidase, dipeptidase
3) Absorption in small intestine
amino acids are absorbed into enterocytes by co-transport with Na
dipeptides and tripeptides are absorbed into enterocytes by co-transport with H+ and hydrolyzed into amino acids inside the cell
4) Absorption into blood
amino acids leave epithelial cell by facilitated diffusion, which then enter capillary blood in villi to hepatic portal vein to liver
Digestion and absorption of carbohydrates
1) Digestion in mouth salivary amylase (secreted by salivary glands) break starch (amylose and amylopectin) into oligosaccharides disaccharide (lactose and sucrose) and monosaccharides (glucose and fructose) go through mouth, esophagus and stomach without any digestion
2) Digestion in duodenum
pancreatic amylase further break starch into oligosaccharides (maltose, maltotriose, dextrin)
3) Digestion in small intestine
brush border enzyme (lactase, maltase and sucrase) break disaccharide (lactose, maltose and sucrose) into monosaccharides (glucose, fructose, galactose)
4) Absorption in small intestine
monosaccharide absorbed into enterocytes
glucose and galatose are absorbed into enterocytes via co-transport with Na
fructose enter enterocytes by facilitated diffusion
all monosaccharides leave epithelial cells via facilitated diffusion, which then enter capillary blood in villi to hepatic portal vein to liver
Digestion and absorption of fat
1) Mixing in mouth and stomach
fat (triglyceride, phospholipid and cholesterol) are crushed and mixed in mastication within the mouth and stomach
small amount of fat broken by gastric lipase
2) Emulsification to fat droplets in duodenum bile salts (secreted by liver into gallbladder) that emulsify (surround) fat, to break it down into fat droplets and make it soluble in water
3) Digestion in duodenum
pancreatic lipase cleave triglyceride into fatty acids and a monoglyceride
pancreatic phosphlipase break phospholipids into fatty acids and lysophosphatidylcholine
pancreatic cholesterol esterase break cholesterol into sterol
4) Emulsification to micelle in duodenum
cleaved fatty acids, monoclygeride, choline and sterol are emulsified by bile salt into micelles
5) Absorption of micelle in small intestine (mainly duodenum and jejunum)
fatty acids leave micelle and diffuse into enterocytes
in enterocytes, fatty acids and monoglycerides are reformed into triglycerides, which are packaged with triglycerides, cholesterol, phospholipids and protein to form chylomicron (a
lipoprotein particle)
chylomicron exit enterocyte by exocytosis and enter lacteals in villi, where they enter the lymphatics
short chain fatty acids and glycerol are absorbed directly into blood stream and do not enter the lymph system
bile salts are absorbed in ileum
6) Transport from lymph into blood
lymphatics carry chylomicron to thoracic duct, where it enters the blood stream to the liver
Hernia epidemiology
affects more commonly males than females, males have 25% lifetime risk of hernia whereas females have 2% lifetime risk of hernia
50% hernias are indirect inguinal hernia; 25% hernias are direct inguinal hernia; 5% hernias are femoral hernias
most common hernias in male and female are indirect inguinal hernia, but male are more predisposed to indirect hernia due to opening of inguinal canal
females are more pre-disposed to femoral hernias
Hernia risk factors
increased intra-abdominal pressure
body habitus that increase intra-abdominal pressure: obesity, pregnancy, ascites
activities that increased intra-abdominal pressure: chronic cough, constipation, straining on urination / defecation, heavy lifting
congenital abnormality (patent processus vaginalis)
previous history of hernia and hernia repair
Hernia anatomical classification
A) Internal hernia
B) External hernia
1) groin hernia
a) indirect inguinal hernia: herniation originating from deep inguinal ring lateral to inferior epigastric artery descending into scrotal sac or labia majora
b) direct inguinal hernia: herniation through Hesselbach’s triangle, medial to inferior epigastric artery usually does not descent into scrotal sac
“MD don’t LIe” = Medial to inferior epigastric artery is the Direct hernia; Lateral to inferior epigastric artery is the Indirect hernia
c) pantaloon hernia: combined direct and indirect groin hernia with peritoneum draped over inferior epigastric vessels
d) femoral hernia: herniation into femoral canal below inguinal ligament medial to femoral vein within femoral canal
femoral hernia have highest risk of incarceration and strangulation
2) epigastric hernia
epigastric hernia: defect in linea alba above umbilicus causing hernia
3) incisional hernia
incisional hernia: ventral hernia at site of wound closure
4) other types of hernia
Littre’s: hernia involving Meckel’s
Amyand’s: hernia containing ruptured appendix
lumbar hernia
obturator hernia
parastomal hernia
umbilical hernia
Spigelian hernia: ventral hernia through linea semilunaris
Hernia complications
incarceration, where hernia cannot be reduced
strangulation, where an irreducible hernia have ischemia
strangulation of hernia can cause intestinal obstruction, necrotic bowel, sepsis
strangulated hernia is a surgical emergency
Hernia clinical presentation
History:
swelling or fullness at hernia site, mass of variable size, hernia enlarges with coughing / lifting / straining and disappears in supine position
aching sensation radiating into area of hernia, tender at end of day relieved with supine position or with reduction
abdominal fullness, burning / gurgling / aching sensation
no pain or tenderness on palpation of hernia
incarcerated hernia: painful enlargement of previous hernia, irreducible either spontaneously or manually through defect, may have symptoms of bowel obstruction (nausea &
vomiting, distended abdomen, constipation, obstipation)
strangulated hernia: irreducible hernia with increasing pain and tenderness, symptoms of bowel obstruction (nausea & vomiting, distended abdomen, constipation, obstipation), fever,
chills
Physical Exam (of Groin Hernia):
on inspection, bulges at femoral or inguinal areas with patient standing while straining down
in male, palpation by invaginating loose skin of scrotum with index finger up into inguinal canal to feel for any palpable herniation descending onto finger while patient strains down or
coughs
in female, palpation with open hand over groin area to detect impulse of hernia descending during straining or coughing
incarcerated hernia: irreducible hernia
strangulated hernia: fever, distended abdomen, peritonitis
Hernia diagnosis
usually physical exam sufficient for diagnosis of hernia
may use ultrasound or CT to aid in diagnosis of hernia
CT useful for diagnosis of obturator hernia, internal abdominal hernia, Spigelian femoral hernia in obese patients
Hernia management for non-incarcerated non-strangulated hernias
a) small, minimally symptomatic, first occurrence hernia
surgical repair is not necessary and patients can be followed expectantly
if no surgical repair, then patients counselled on symptoms of incarceration and strangulation, so that they can seek prompt healthcare evaluation
b) all other hernia
surgical repair (herniorrhaphy) for all other hernias
symptomatic, large or recurrent hernia should have surgical repair within 1 month of detection
surgical repair of hernia to prevent incarceration and strangulation; or to treat symptoms; or for cosmesis
surgical repair can be open or laparoscopic, depending on surgeon preference, usually uses mesh for tension-free closure
repair can be done with plug in hernia defect with patch over it or patch alone
Post-surgical complications of hernia surgery
recurrence (15-20% risk), which is less common with mesh / tension-free surgical repair
scrotal hematoma (3% risk) from compromised venous return of testes
nerve (ilioinguinal or genital branch of genitofemoral) entrapment
stenosis or occlusion of femoral vein, causing acute leg swelling
ischemic colitis
Hernia management for acutely incarcerated or strangulated hernia
acutely incarcerated hernia have risk of subsequent strangulation, so patients should undergo attempts at reduction followed by surgical repair
strangulated hernia should undergo emergent surgical repair
hernia definition
hernia = fascial defect resulting in protrusion of a viscus into an area in which it is not normally contained
complete hernia definition
complete hernia = hernia sac and contents protrude through defect
incomplete hernia definition
incomplete hernia = partial protrusion through defect
internal hernia definition
internal hernia = sac herniating into or involving intra-abdominal structure
external hernia definition
external hernia = sac protruding completely through abdominal wall
sliding hernia definition
sliding hernia = part of wall of hernia formed by protruding viscus
ex. sliding hernia where cecum forms part of hernia wall
Richter’s hernia definition
Richter’s hernia = only part of circumference of bowel (usually anti-mesenteric border) is incarcerated or strangulated, so may not cause bowel obstruction
What is Hesselbach’s triangle
Anatomical triangle formed by 3 borders:
medial border = lateral margin of rectus abdominis
lateral border =
inferior epigastric artery
inferior = inguinal ligament
Most common complication of hernia repair
most common complication of hernia repair include hematoma, penile ecchymosis, scrotal ecchymosis, wound infection, chronic pain
Types of IBD
many types of inflammatory bowel disease including
Crohn’s disease (CD): relapsing transmural inflammation and ulceration of GI tract anywhere from mouth to anus
Ulcerative colitis (UC): inflammation and ulceration of rectum extending proximally to large bowel
other IBD include microscopic colitis, diversion colitis, radiation colitis, drug induced colitis, indeterminate colitis
Epidemiology of IBD
highest incidence and prevalence of IBD in Europe and North America
bimodal age distribution, with 1st peak at age 20-30 and 2nd peak at age 60
highest prevalence in Caucasian and African American
lowest prevalence in Asians and Hispanics
Pathophysiology of IBD
aetiology of IBD unknown, but hypothesized to be a multifactorial disease
genetic predisposition, dysregulation in mucosal immune system and environmental trigger cause chronic inflammation in GI tract, resulting in IBD
UC vs CD overall severity
overall, CD is worse than UC, because CD has many complications (e.g. peri-anal disease, obstructions) and it can affect any part of the GI tract
Crohn’s location
rectal bleeding
diarrhea
abdominal pain
fever
palpable mass
recurrence after surgery
endoscopic features
Histologic features
Radiologic features
Complications
Colon cancer risk
Location- any part of GI tract
Small bowel + colon 50%
Small bowel only 30%
Colon only 20%
rectal bleeding uncommon
diarrhea less prevalent
abdominal pain post-prandial/colicky
fever common
palpable mass frequent (25%) RLQ
recurrence after surgery common
endoscopic features
Discrete aphthous ulcers
Patchy lesions
Pseudopolyps
Histologic features Transmural distribution with skip lesions Focal inflammation Sometimes non caseating granulomas Deep fissuring + aphthous ulcerations Strictures Glands intact
Radiologic features
cobblestone mucosa
frequent strictures and fistulae
AXR: bowel wall thickening “string sign”
Complications
Strictures
Fistulae
Perianal disease
Colon cancer risk increased if >30% of colon involved
UC location
rectal bleeding
diarrhea
abdominal pain
fever
palpable mass
recurrence after surgery
endoscopic features
Histologic features
Radiologic features
Complications
Colon canc
Locationisolated to large bowel
always involves rectum, may progress proximally
rectal bleeding very common (90%)
diarrhea frequent small stools
abdominal pain pre-defecatory urgency
fever uncommon
palpable mass rare (if present, likely cecum full of stool)
recurrence after surgery none-post colectomy
endoscopic features Continuous diffuse inflammation Erythema Friability Loss of normal vascular pattern Pseudopolyps
Histologic features Mucosal distribution Continuous disease (no skip lesions) Granulomas absent Gland destruction, crypt abscess
Radiologic features
Lack of haustra
Strictures rare and suggests complicating cancer
Complications
Toxic megacolon
Colon cancer risk increased except in proctitis
Common presentation of IBD
Symptoms abdominal pain, frequent bowel movement, diarrhea bloody stools urgency failure to thrive or weight loss
Extraintestinal manifestations of IBD
Derm- erythema nodosum, pyoderma grangenosum, perianal skin tags, oral mucosal lesions, psoriasis
Rheum
Peripheral arthritis, ank spondylitis, sacroiliitis
Ocular
Uveitis (vision threatening), episcleritis (benign)
Hepatobiliary
Cholelithiasis, PSC, fatty liver
Urologic
Calculi, ureteric obstruction, fistulae
Others VTE vasculitis osteoporosis vitamin deficiencies (B12, ADEK) Cardiopulmonary disorders Pancreatitis (rare)
Most of these are more common in CD except sacroiliitis (equal)
Complications of IBD, their pathophysiology, clinical presentation, diagnosis and treatment
- Toxic Megacolon:
most commonly in UC
pathophysiology: inflammation result in colonic paralysis and obstruction with high risk of perforation
clinical presentation: fever, tachycardia, leukocytosis, peritoneal signs on abdominal exam
treatment: fluid resuscitation, NG tube, IV Solumedrol, immediate surgical colectomy
2. Bowel Perforation
pathophysiology: perforation of intestinal content into abdominal cavity, resulting in bacterial infection and peritonitis
clinical presentation: fever, chills, nausea & vomiting, severe abdominal distention, peritoneal signs on abdominal exam
diagnosis: free gas / air under diaphragm on X-ray
treatment: fluid resuscitation, IV antibiotics, surgery
3. Dysplasia
pathophysiology: IBD leads to dysplasia, which increase risk of colorectal carcinoma
clinical presentation: dysplasia associated lesion or mass (DALM) on endoscopy
treatment: surveillance colonoscopy, prophylactic colectomy in high risk patients
Crohn’s disease epidemiology
incidence 1-6/100,000, prevalence 10-100/100,000
common in Caucasian and Ashkenazi Jews
M=F
Crohn’s disease clinical presentation
recurrent abdominal cramps, diarrhea and weight loss
most commonly affect terminal ileum and ascending colon
ileitis: vomiting, post-prandial pain, RLQ mass
fistula, fissure, abscess
Crohn’s disease investigations
colonoscopy with biopsy
CT enterography for involvement of small bowel
elevated ESR and CRP
Crohn’s disease management
non-pharmacological: smoking cessation
anti-diarrheal: Loperamide (Imodium), Diphenoxylate (Lomotil)
mild CD: 1) antibiotics (Metronidazole or Ciprofloxacin); and 2) 5-ASA (5-Aminosalicyclic acid)
moderate CD: 1) steroid Prednisone or Budesonide; and 2) immune-modulator Azathioprine (AZA; Imuran), 6-Mercaptopurine (6-MP) or Methotrexate (MTX)
severe CD: surgery and / or biologics Infliximab (Remicade) or Adalimumab
surgery indicated in complications of fistula, obstruction, abscess, perforation, bleeding and medically refractory disease
Ulcerative colitis epidemiology
incidence 2-10/100,000, prevalence 35-100/100,000 (more common than Crohn’s)
M=F
inflammation to rectum or left colon more common
Ulcerative colitis clinical presentation
chronic abdominal cramps / pain with defecation, diarrhea and rectal bleeding
may have tenses, urgency, incontinence
systemic symptoms include fever, anorexia, weight loss and fatigue in severe cases
Ulcerative colitis clinical classification
mild UC: <4 stools / day and nothing else
moderate UC: >4 stools / day with minimal signs of toxicity (fever, tachycardia, anemia, high ESR)
severe UC: >6 stools / day and signs of systemic toxicity (fever, tachycardia, anemia, high ESR)
fulminant UC: >10 stools / day; continuous bleeding requiring blood transfusion; systemic toxicity (fever, tachycardia, anemia, high ESR); abdominal tenderness and distension; and
colonic dilation on abdominal plain film
Ulcerative colitis investigation
sigmoidoscopy with mucosal biopsy for diagnosis, which can be substituted with CT colonography
Ulcerative colitis management
total colectomy for refractory & severe UC, colonic stricture, life-threatening UC complications (severe bleeding, toxic megacolon, impending perforation), dysplasia or carcinoma
mild UC: 1) 5-ASA
moderate UC: 1) 5-ASA; and 2) steroid Prednisone or Budesonide
severe UC: 1) surgery; and 2) Cyclosporine
consider adding immunomodulator AZA or 6-MP; or biologics Infliximab for moderate to severe UC
General indications for surgery in IBD
severe disease: intractable symptoms and failure to respond to medical therapy, extra-intestinal manifestations, chronic disability, failure to thrive in children, poor quality of life
GI emergencies: toxic megacolon, bowel perforation, uncontrolled hemorrhage, bowel obstruction
structural abnormalities: fistula, stricture
infectious: abscess
malignancy: pre-cancerous lesions, colorectal cancer
General principles of surgery in IBD
surgeries can alleviate symptoms, address complications and improve quality of life
principle of to conserve as much bowel as possible (i.e. resect as little as possible to avoid short gut syndrome)
perioperative management:
a) optimize medical status with bowel rest, which may require TPN if >7 days of NPO
b) hold immune suppressive therapy pre-op, provide pre-op stress dose of corticosteroid if patient had recent steroid therapy, taper steroids post-op
c) DVT prophylaxis
Surgery in Crohn’s Disease specific indications
structural lesions (stricture, fistula): bowel resection and anastomosis (or stoma if active inflammation, perforation, fistula)
small bowel obstruction due to stricture or inflammation: bowel resection and anastomosis
stricture: stricturoplasty (widening of lumen in bowel stricture)
abscess: surgical incision and drainage
peri-anal disease: appropriate surgical treatment for types of peri-anal disease
Surgery in Crohn’s Disease complications
small bowel resection -> short bowel syndrome
short bowel syndrome if functional small intestine <50% or <200cm
short bowel syndrome = malabsorption disorder due to surgical removal of small intestine resulting in diarrhea, steatorrhea, malnutrition
symptoms: abdominal pain, diarrhea, steatorrhea, weight loss, malnutrition, fatigue
vitamin A, D, E, K, folic acid, B12, Ca, Mg, iron, zinc deficiency
hypo calcium increases risk of kidney stones
ileal resection -> watery diarrhea, steatorrhea, gall stones
<100cm resection cause watery diarrhea due to impaired bile salt absorption treated with cholestyramine or anti-diarrheal (Loperamide)
>100cm resection cause steatorrhea due to reduced mucosal surface area for fat absorption and bile salt deficiency treated with fat restriction and medium chain triglycerides
decreased bile absorption -> increased risk of gallstone
any abdominal surgery -> fistula, adhesions
Surgery in Crohn’s Disease prognosis
post surgical removal, 10 year recurrence rate: 25-50% in ileocolic region, 50% in small bowels, 50% in large bowels
proportion requiring re-operation due to recurrence: primary resection have 20% re-operation, bypass have 50% re-operation, stricturoplasty have 10% re-operation
80-85% of patients who require surgery will lead normal lives
post surgery, 15% mortality risk at 30 years
Surgery for UC indications
severe to fulminant UC: total colectomy with ileal pouch - anal anastomosis
can resect only portion of colon that is pathologic (e.g. proctocolectomy, rectal mucosectomy)
decrease colorectal cancer: total proctocolectomy
in surgical emergencies: total colectomy and ileostomy with Hartmann closure of rectum, rectal preservation
Complications of surgery in UC
early: anastomotic leak, dehydration from high stoma output, bowel obstruction, transient urinary dysfunction
late: stricture, anal fistula / abscess, pouchitis, poor anorectal function, infertility
Surgery for UC prognosis
post surgery, 5% mortality risk at 10 years
IBS epidemiology
prevalence of 20% in North America
females > males
IBS pathophysiology
likely due to visceral hypersensitivity with possible psychological or environmental trigger
IBS clinical presentation
GI symptoms: chronic abdominal pain or discomfort; chaotic defecation (period of normal bowel movement punctuated by episodes of constipation and / or diarrhea)
abdomen exam: unremarkable
80% IBS cases improve over time and have normal life expectancy
IBS diagnosis
diagnosis based on symptoms alone (Rome criteria) see Tony’s page 118
IBS subtypes
subtype of IBS based on consistency of stool and percentage of time
IBS-C = IBS with mainly constipation
IBS-D = IBS with mainly diarrhea
IBS-M = mixed IBS with some constipation or diarrhea
IBS-U = untyped IBS
IBS investigations
if benign history and physical exam, diagnosis clinically on Rome 3 criteria and no investigations required
additional investigations to be considered:
blood work: CBC, TSH, albumin, CRP, tTG
stool C & S O & P, fat excretion
sigmoidoscopy
Management of IBS
1) make positive diagnosis of IBS
comfort / reassure patient, address patient concerns and establish patient-doctor relationship to enhance placebo effect (most effective treatment)
explain, support, aim for realistic goals
2) diet and lifestyle advice balanced and healthy diet exercise dietary fiber or fiber supplement for constipation if lactose intolerance, restrict diary if food intolerance, eliminate food from diet reduce sorbitol, reduce fructose avoid caffeine and alcohol
3) if suspected psychological trigger (anxiety, depression or phobia)
behavioural therapy
drugs
consider relaxation therapy, biofeedback, hypnosis, stress reduction
4) if severe symptoms, drugs to address the symptoms
pain: anti-spasmodic before meals (Hyoscine, Pinaverium, Trimebutine), tricyclic antidepressants (TCA), selective serotonin re-uptake inhibitor (SSRI)
diarrhea: Loperamide, Diphenoxylate, cholestyramine
constipation: osmotic or other laxatives
What is a peptic ulcer
defect (erosion, ulceration) of inner mucosal lining that penetrate muscularis mucosal layers of the stomach (gastric ulcer) or duodenum (duodenal ulcer)
Etiology of peptic ulcer
gastric acid is necessary for ulcer to form, but it does not cause peptic ulcer
1) H. pylori infection
H. pylori infection cause 60% gastric ulcer and 90% duodenal ulcer
2) NSAID
NSAID cause 35% gastric ulcer and 7% duodenal ulcer
3) gastric cancer
other: physiologic stress induced in severely ill patients, Zollinger-Ellison syndrome, chemotherapy or radiation ulcer, alcohol, CMV infection, ischemia, idiopathic
Peptic ulcer clinical presentation
GI symptoms: asymptomatic (70% cases), nausea, dyspepsia (classically worse with food in gastric ulcer and better with food in duodenal ulcer)
abdominal exam: usually benign exam, may have epigastric tenderness
Complications of peptic ulcers pathophysiology, symptoms, presentation, treatment
1) Upper GI Bleed (10-15% cases)
pathophysiology: erosion of ulcer into blood vessel (classically gastroduodenal artery by duodenal ulcer), causing upper GI bleeding
symptoms: hemetemesis, melena
treatment: ABC, fluid resuscitation, IV PPI, endoscope injection of epinephrine / cauterization / hemoclip, interventional radiology angiography with embolization / coiling, surgery if
severe or recurrent bleeding
2) Perforation (2% cases)
pathophysiology: erosion through entire lining, resulting in perforation through stomach or duodenum
symptoms: acute onset severe abdominal pain
abdominal exam: peritoneal signs
imaging: free air on X-ray (70% cases) or abdominal CT
treatment: surgery
3) Obstruction (2% cases)
pathophysiology: ulcer can cause inflammation & swelling or can heal & scar, which obstruct the GI tract, classically at gastric outlet by duodenal ulcer
symptoms: nausea & vomiting, abdominal pain, obstipation, constipation
abdominal exam: distended abdomen, succussion splash on auscultation, may have peritoneal signs if ischemia or perforation
treatment: NG decompression, correct fluid & electrolyte imbalance, high dose PPI therapy, surgery
4) Fistula / Penetration (<1% cases)
pathophysiology: ulcer can penetrate to adjacent organs, forming a fistula connecting the 2 organs
ulcer in duodenum can penetrate into pancreas, causing pancreatitis
gastric ulcer can penetrate into liver or colon, causing perforation
General indications for gastric and duodenal ulcer surgery
unresponsive to medical treatment (including endoscopy)
hemorrhage
perforation
obstruction
Peptic ulcer surgery procedures
gastrectomy = removal of portion of stomach usually with reconstruction (Billroth 1, Billroth 2, Roux-en-Y)
Billroth 1 = removal of pylorus and anastomosis of proximal stomach to duodenum
Billroth 2 = (removal of antrum and pylorus of stomach with) anastomosis of greater curvature of stomach to jejunum
Roux-en-Y = proximal segment of stomach anastomosis with jejunum, distal stomach to duodenum anastomosis with jejunum
vagotomy = transection or removal of portion of vagus nerve to decrease gastric secretion
pyloroplasty = widening of pylorus to facilitate gastric emptying
gastrojejunostomy = anastomosis between dependent portion of stomach to jejunum to facilitate gastric emptying
suture ligation = oversew of an vessel to stop bleeding
Pauchet procedure = distal gastrectomy extending along lesser curvature to include ulcer
Complications of peptic ulcer surgery
fistula, commonly gastrocolic, gastrojejunal fistulas
dumping syndrome
post-vagotomy diarrhea
afferent loop syndrome
Specific indications for surgery for gastric ulcer
unresponsive to medical treatment (including endoscopy)
perforation
gastric dysplasia or carcinoma, usually based on endoscopic biopsy
failure to heal completely after medical treatment (due to risk of malignancy)
any hemorrhage (due to high risk of hemorrhage for gastric ulcer compared to duodenal ulcer)
Types of gastric ulcers
type 1 gastric ulcer (most common) = along lesser curvature near function of fundus and antrum
type 2 gastric ulcer = combined gastric and duodenal ulcer
type 3 gastric ulcer = prepyloric ulcer
type 4 gastric ulcer = high along lesser curvature close to gastroesophageal junction
Gastric ulcer surgery procedures
removal of ulcer:
type 1 ulcer requires distal gastrectomy with (Billroth 1 or 2) reconstruction
type 2 or 3 ulcer requires antrectomy and vagotomy with (Billroth 1 or 2) reconstruction
type 4 ulcer requires subtotal gastric resection or Pauchet procedure with Roux-en-y reconstruction
perforation: partial gastrectomy to include ulcer
hemorrhage: partial gastrectomy with (Billroth 1 or 2) reconstruction; or ulcer excision with trundle vagotomy and pyloroplasty
Surgery for duodenal ulcer specific indications
unresponsive to medical treatment (including endoscopy)
perforation
failure to heal completely after medical treatment (due to risk of malignancy)
hemorrhage (large amount of blood loss >8 units, rate of bleeding, hemodynamic instability)
Duodenal ulcer surgery procedures
perforation: oversew ulcer (plication) and omental (Graham) patch
hemorrhage: oversewing of ulcer and pyloroplasty
obstruction: antrectomy / distal gastrectomy; or vagotomy with drainage
elective surgery to reduce acid secretion: vagotomy, gastrectomy
Treatment for peptic ulcer
no dietary recommendation
acid suppression: proton pump inhibitor (PPI) or histamine 2 receptor antagonist (H2RA)
if test positive for H. Pylori, eradication regimen:
1st line = triple therapy (PPI + Amoxicillin + Clarithromycin)
2nd line = quadruple therapy (PPI + bismuth + Tetracycline +
Metronidazole)
discontinue NSAID if possible
for gastric ulcer, repeat endoscopy after resolution to confirm that gastric ulcer healed (unhealing gastric ulcer suggests malignancy)
What structure separates upper from lower GI bleed
Mouth to ligament of Treitz to anus
Upper GI bleed epidemiology
upper GI bleed constitute majority (75%) of GI bleed
commonly affects males more than females
incidence increase with age
associated with mortality rate of ~10% (higher than lower GI bleed)
usually majority (80%) of upper GI bleed are self limited
Upper GI bleed causes
from most common to less common causes:
1) peptic ulcer in 50% of cases
2) varices (esophageal or gastric) in 15% of cases
due to liver disease: portal hypertension, cirrhosis
3) arterial venous malformation (angiodysplasia) in 5% of cases
4) Mallory Weiss tears (tears at gastroesophageal junction from severe vomiting, retching or coughing) in 5% of cases
5) tumours in 5% of cases
6) erosions in 5% of cases
Upper GI bleed clinical presentation
generally, upper GI bleed is more likely to present with hemodynamic instability due to rich blood supply of upper GI tract
Symptoms
hematemesis (bright red blood worse than coffee grounds)
melena from digested blood
increased bowel movement
blood is a laxative
increased frequency is indicator of rapidity of bleeding
hemodynamic symptoms
pre-syncope or syncope
orthostatic dizziness, lightheadedness
chest pain or dyspnea due to hypo perfusion of heart
hematochezia (red blood per rectum) i.e. massive rectal bleeding
hematochezia usually a sign of lower GI bleed, but can occur with brisk upper GI bleed
patient with upper GI bleed and hematochezia usually are hemodynamically unstable
if rectal bleeding, use NG tube lavage to rule out a brisk upper GI bleed, frank blood aspirated from NG lavage suggest brisk upper GI bleed and should be followed by EGD
other symptoms depend on cause: nausea, vomiting, dysphagia, heart burn, abdominal pain
Lower GI bleed epidemiology
lower GI bleed constitute minority (25%) of GI bleed
associated with mortality rate of 2% (lower than upper GI bleed)
Lower GI bleed causes
from most common to less common:
1) diverticular bleed in 33% of cases
2) colon cancer in 20% of cases
3) angiodysplasia in 10% of cases
4) ischemic colitis
5) brisk upper GI bleed
6) other inflammatory or ulcer causes
inflammatory bowel disease, ischemic bowel, vasculitis, infectious, radiation induced, NSAID induced
7) anorectal bleeding in 5% of cases
fissures, hemorrhoids
usually very small amount of blood (e.g. on toilet paper)
Lower GI bleed clinical presentation
hematochezia (red blood per rectum)
blood can be bright red blood or dark / maroon
bright red blood suggest left colon as source
dark or maroon suggest distal small bowel or right colon as source
blood can be mixed inside stool or covering outside of stool
blood covering outside of stool suggest perianal source
blood mixed inside stool suggest right colonic source
change in bowel movement
increased frequency due to cathartic effect of blood
decreased form / consistency (diarrhea)
melena
melena usually a sign of upper GI bleed, but can occur in lower GI bleed if the source is the distal small bowel, cecum or right colon
patient with lower GI bleed and melena usually are hemodynamically stable with very slow bleeding
other symptoms depend on cause: fever, chills, weight loss, abdominal pain or cramps, fecal urgency, tenesmus, fecal incontinence
angiodysplasia and diverticular bleeding usually not painful
ischemic colitis very painful
What can mimic melena
iron pills and bismuth (Peptol Bismol) can mimic melena
Upper GI bleed symptoms, signs and labs
Symptoms - hematemesis, melena, usually acute
Signs - tend to be hemodynamically unstable, NG lavage of blood from suction
Labs - High [BUN x 10] : Cr ratio (>1.5)
Lower GI bleed symptoms, signs and labs
Symptoms - hematochezia, usually chronic
Signs - tend to be hemodynamically stable, no NG lavage findings
Labs - Equal [BUN x 10] : Cr ratio (~1)
Empiric upper GI bleeding management
if upper GI bleeding, then empiric IV PPI, IV somatostatin and pro kinetics
a) empiric IV PPI to treat possible peptic ulcer until EGD performed
PPI stabilize ulcer and promote clotting, shown to decrease need for endoscopic therapy and decrease risk
e.g. Esomeprazole 50mg IV bolus BID or Pantoprazole 40mg IV bolus BID
b) empiric IV somatostatin (Octreotide) to treat possible variceal bleed
somatostain vasoconstricts splanchnic arteries to decrease portal hypertension and thus decrease bleeding
e.g. Octreotide 50mcg bolus followed by 50mcg / hr infusion
c) prophylactic antibiotic therapy for patients with cirrhosis
prophylactic antibiotic can be any of the following
Ciprofloxacin 400-1000mg mg IV for 7 days
Ceftriaxone 1g IV daily for 7 days
d) pro kinetics (metoclopramide (Maxeran) or IV erythromycin) to prepare for EGD
pro kinetics clear UGI tract of blood for better visualization with scope
e.g. Erythromycin 3mg/kg IV over 20-30 minutes done 30-90 minutes prior to endoscopy
Indications for urgent EGD
EGD urgent if any of the following
a) hemodynamically unstable shock (systolic <100, heart rate >100, orthostatic hypotension) hemoglobin <80 requires >2 packs of RBC transfusion hematemesis
b) hematochezia in suspected upper GI bleed
c) suspected varices
d) serious comorbidity (malignancy or cirrhosis)
EGD is non-urgent in young and healthy patient with minimal bleeding
Upper GI bleed EGD should be done when
within 24h
Management if unclear if upper or lower GI bleed
treat empirically with medication (IV PPI, IV somatostatin, pro kinetics) as upper GI bleed
do EGD first, then colonoscopy
Lower GI bleed colonoscopy should be done when
if lower GI bleeding, wait for bleeding to stop and then do colonoscopy
generally lower GI bleed less severe, so colonoscopy is not urgent
colonoscopy mainly diagnostic and not therapeutic, because it is difficult to identify source
Alternatives to scope to find and stop bleeding
endoscopy always 1st line treatment for bleed
if endoscopy fails to identify source or failed to stop bleeding, then angiography (by interventional radiology) or RBC scan
Surgery
intra-operative enteroscopy by surgery
surgery = oversewing bleeding vessel and resection of bleeding segments within GI tract (e.g. vagotomy with pyloroplasty, partial gastrectomy)
EGD endoscopic therapy for GI bleeding
endoscopy is diagnostic and therapeutic
endoscopy is definitive bleeding management for GI bleed
many methods for hemostasis by EGD
1) injection
injection of vasoconstrictor (epinephrine), saline, sclerosants or tissue adhesives
2) thermal therapy
electrocoagulation
laser photocoagulation
3) mechanical therapy
hemoclips, rubber bands
closure of vessel
What is angiography and sensitivity and specificity
angiography is diagnostic and therapeutic done by IR
catheter through femoral artery to abdominal aorta and its branches
can inject dyes to find bleeding site
lower sensitivity, but higher specificity (can rule in)
can perform therapy by embolization
What is RBC scan and sensitivity and specificity
RBC is diagnostic but not therapeutic
patient infused with radioactive tagged RBC
high sensitivity, but lower specificity (can rule out)
Indications for surgery to stop upper or lower GI bleeding
hemodynamic instability including hypovolemic shock despite vigorous resuscitation
prolonged bleeding with transfusion requirement >3 units
failure of medical management
recurrent hemorrhage after initial stabilization procedure with >2 attempts of endoscopic hemostasis
peritonitis, suggestive of perforation
Causes of acute abdomen
causes of bowel obstruction
small bowel obstruction: adhesion post abdominal surgery, hernia, malignancy (metastasis to small bowel)
large bowel obstruction: malignancy (colorectal cancer and metastasis), diverticular stricture, colonic volvulus
causes of peritonitis
inflammation / infection: pancreatitis, appendicitis, diverticulitis, pelvic inflammatory disease, large intra-abdominal abscess
bowel perforation
bowel obstruction
vascular: intra-abdominal hemorrhage (e.g. aortic aneurysm rupture, trauma, surgery, ectopic pregnancy), ischemic colitis
Bowel obstruction pathophysiology
1) disruption of normal flow of intestinal contents cause upstream proximal intestinal dilatation and downstream distal decompression
proximal intestinal dilatation may cause bowel perforation
2) obstruction and dilatation may interrupt blood supply causing bowel ischemia via strangulation of blood supply or bowel wall inflammation
3) bowel wall edema from venous congestion and disruption of normal bowel absorption function from interruption of intestinal contents cause increased intra-luminal fluid and fluid loss into peritoneal cavity as well as electrolyte disturbance
Complications of bowel obstruction
strangulating obstruction (10% of bowel obstruction), which is a surgical emergency
bowel perforation -> sepsis
hypovolemia from third spacing of fluids
Clinical presentation of strangulating bowel obstruction
cramping pain -> continuous ache
GI bleed (hematemesis, melena)
fever
tachycardia
hypotensive shock
peritoneal signs
leukocytosis
Types of bowel obstruction
small bowel obstruction = obstruction at small bowel
large bowel obstruction = obstruction at large bowel
pseudo-obstruction / ileus = obstruction due to dysfunctional peristalsis
Clinical presentation of SBO: N/V abdo pain abdo distension constipation other bowel sounds AXR findings
N/V early, may be bilious
abdo pain colicky
abdo distension + (prox)< ++ (distal)
constipation +
other sometimes visible peristalsis
bowel sounds normal, increased or absent if secondary ileus
AXR findings air fluid levels, 'ladder' pattern (plicae circularis) proximal distension (>3 cm) + no colonic gas
Clinical presentation of LBO: N/V abdo pain abdo distension constipation other bowel sounds AXR findings
N/V late, may be feculent
abdo pain colicky
abdo distension ++
constipation +
other sometimes visible peristalsis
bowel sounds normal, increased (borborygmi), absent if secondary ileus
AXR findings
air fluid levels
‘picture frame’ appearance
proximal distension + distal decompression
no small bowel air if competent ileocecal valve
coffee bean sign
Clinical presentation of paralytic ileus: N/V abdo pain abdo distension constipation other bowel sounds AXR findings
N/V present
abdo pain minimal or absent
abdo distension +
constipation +
other
bowel sounds decreased, absent
AXR findings
air throughout small bowel and colon
What is borborygmi
a rumbling or gurgling noise made by the movement of fluid and gas in the intestines.
Bowel obstruction investigations
Labs:
if emesis, venous blood gas, which may show metabolic alkalosis
if suspected strangulation, lactate and LDH, which may be elevated in ischemia
Imaging:
Upright chest X-ray for free air under diaphragm, suggestive of bowel perforation
abdominal X-ray (3 views, AP, lateral decubitus, upright) may show dilated bowel loops, air fluid levels
abdominal CT can confirm obstruction and determine structural cause for obstruction
upper GI series / small bowel series for small bowel obstruction if no apparent cause
rectal water soluble Gastrografin enema
Small vs large bowel obstruction on abdominal xray
abdominal series enough to diagnose small bowel obstruction 60% of time
obstructed small bowel:
- plicae circularis that go the whole way across the intestine
- have a thicker wall (white line border)
- located in middle of abdomen
- smaller in diameter
- supine abdomen X-ray: distended loop of small bowel and collapsed colon
increased risk of perforation if small bowel diameter >3cm - normal (unobstructed) small bowel is not clearly visible on X-ray, because it is white and loops around one another
obstructed large bowel
1. striae that do not go all the way across the intestine
- have thinner wall (no white line border)
- located around the abdomen
- larger in diameter
bowel obstruction diagnosis
diagnosis confirmed by abdominal series X-ray (supine, upright, left lateral decubitus) and CT (if still unclear on abdominal X-ray)
bowel obstruction general management
- stabilize patient
- NPO, suck (NG tube) and drip (IV fluids)
NG tube to relieve vomiting, prevent aspirations and decompress small bowel
IV fluid resuscitation due to fluid loss in intestine and peritoneal cavity - correct electrolyte abnormalities
- Foley catheter to monitor fluid output
- surgery for correctable cause or non-resolving cases
Small bowel obstruction top 3 causes
top 3 causes = ABCs
1) A = adhesion (from previous abdominal surgery)
2) B = bulge i.e. hernia (incarcerated / strangulated)
3) C = cancer, commonly metastasis to small bowel (e.g. melanoma)
Intraluminal causes of SBO
Intussusception
Gallstones
Intramural causes of SBO
Crohn’s
Radiation stricture
Adenocarcinoma
Extramural causes of SBO
Adhesions
Incarcerated hernia
Peritoneal carcinomatosis
Clinical presentation of small bowel obstruction
symptoms: nausea & vomiting, bloating, diffuse cramp abdominal pain, constipation, obstipation (not passing gas)
abdominal exam: distended abdomen, high pitched bowel sound, hyper-resonant / tympanic abdomen, no localized tenderness, no peritoneal signs
Mortality in small bowel obstruction
mortality: <1% in uncomplicated small bowel obstruction; 10% with strangulation; 50% with ischemia
Small bowel obstruction labs
CBC: normal or slightly high WBC
electrolytes: low Cl, low K, metabolic alkalosis due to vomiting
Indications for surgery in SBO
small bowel obstruction with history of abdominal / pelvic surgery with no resolution in 2-3 days
small bowel obstruction with no previous surgery and no evidence of carcinomatosis
complete bowel obstruction
complications: strangulation, perforation
Indications for conservative management in SBO
small bowel obstruction with history of abdominal / pelvic surgery for the first 2-3 days (70% chance of spontaneous resolution)
Crohn’s disease
recurrent small bowel obstructions
carcinomatosis
majority of small bowel obstruction will resolve in 12-24 hours with conservative treatment
LBO top 3 causes
top 3 causes
1) colorectal cancer
2) diverticular stricture
3) colonic volvulus (5-10% of large bowel obstruction)
LBO intraluminal causes
Constipation
LBO intramural causes
Adenocarcinoma
Diverticulitis
IBD stricture
Radiation stricture
LBO extramural causes
Volvulus
Adhesions
LBO clinical presentation
history: history or presentation of colorectal cancer (melena, blood per rectum, change in bowel habit, decreased caliber of stool, incomplete emptying, soiling underwear)
same presentation as small bowel obstruction
LBO mortality
mortality: 10% in uncomplicated large bowel obstruction; 20% with perforation and feculent peritonitis
LBO investigations
1) Abdominal X-ray
dilated colon
increased risk of perforation if distal colon >6cm; proximal colon >9cm; cecum >12cm
distinguish between closed loop vs. open loop
closed loop (80-90% cases) = competent ileocecal valve blocking air in colon from entering small bowel
small bowel is not dilated in closed loop
closed loop has a high risk of ischemia -> necrosis -> perforation and is a surgical emergency
open loop (10% cases) = incompetent ileocecal valve allowing air in colon from entering small bowel small bowel dilated in open loop
2) Abdominal CT
abdominal CT can differentiate between causes of large bowel obstruction by visualization of site and structural cause for obstruction
3) Colonoscopy
colonoscopy can assess for cancer
LBO management
if closed loop obstruction, then urgent surgery to correct underlying cause
if sigmoid volvulus, then colonoscopy decompression followed by delayed surgical sigmoid resection, or surgical reduction if colonoscopic decompression
unsuccessful
What is the pathophysiology of a contained perforation
full thickness perforation of well wall but free spillage of intestinal contents and air is prevented because a nearby organ walled off the perforated area
What is the pathophysiology of a free perforation
perforation of bowel wall resulting in leakage of intestinal contents and air into the peritoneal space, which cause infection and inflammation of the peritoneal cavity
(peritonitis)
Bowel perforation management
1) stabilize patient, ensuring ABC
aggressive fluid resuscitation (boluses 2L NS or RL IV) to maintain blood pressure and hydration status
correct any electrolyte abnormalities
monitor fluid status
2) empiric antibiotic coverage
broad IV antibiotic coverage for intestinal flora (gram negatives and anaerobes), which can be any of the following
Ceftriaxone + Metronidazole OR
Piperacillin-Tazobactam
3) surgery as definitive treatment to correct perforation and underlying cause
exploratory laparotomy, closure of perforation (e.g. resection of perforated bowel segment and anastomosis), peritoneal wash
Toxic megacolon causes
inflammatory: ulcerative colitis, Crohn’s disease
infectious: bacterial colitis (C. difficile, Salmonella, Shigella, Campylobacter), vital colitis (cytomegalovirus), parasite (E. histolytica)
mechanical: volvulus, diverticulitis, ischemic colitis, obstructing colon cancer
Toxic megacolon pathophysiology
extension of inflammation into smooth muscle layer of colon bowel wall causing paralysis of peristalsis, resulting in dilatation of colon increasing risk of bowel perforation
Toxic megacolon clinical presentation
symptoms: abdominal distention, abdominal tenderness, diarrhea, hematochezia
vitals: may be septic (fever, tachycardia, hypotension, tachypnea)
abdominal exam: distended abdomen, peritoneal signs (rigidity, guarding, rebound tenderness) if perforation
Toxic megacolon mortality
mortality: 25-30% mortality rate
Toxic megacolon imaging
abdominal X-ray: dilated colon (>12cm in right colon, >6cm in transverse colon, >9cm in left colon), loss of haustra, thumb printing sign
abdominal CT with IV contrast: visualization of underlying cause of toxic megacolon
Toxic megacolon diagnosis
patient diagnosed with toxic megacolon if patient has all of the following criteria
- some systemic manifestations: fever, tachycardia, hypotension, altered level of consciousness, leukocytosis, anemia, fluid and electrolyte imbalance
- radiologic evidence of dilated colon
Toxic megacolon management
1) stabilize patient
2) prevent worsening of colon dilatation
NPO, NG tube
stop constipation agents
3) empiric antibiotic coverage
broad IV antibiotic coverage for intestinal flora (gram negatives and anaerobes), which can be any of the following:
Ceftriaxone + Metronidazole or
Piperacillin-Tazobactam
4) treat underlying cause
aggressive treatment of underlying disease
e.g. systemic steroids in inflammatory bowel disease
e.g. antibiotic therapy for infectious colitis
5) monitoring
monitor with serial abdominal X-rays
6) surgery if indicated
surgery = subtotal colectomy and end ileostomy (may have 2nd operation for re-anastomosis later)
Indications for surgery in toxic megacolon
worsening or persistent systemic toxicity or colon dilation after 48 to 72 hours
severe hemorrhage
bowel perforation
high lactate and WBC
Volvulus definition
volvulus = rotation of a bowel segment about its mesenteric axis
Volvulus most common type
sigmoid (65%) > Cecum (30%) > transverse colon (3%) > splenic flexure (2% case)
Volvulus risk factors
elderly, where age predisposes to stretching and elongation of bowel high fibre diet chronic constipation laxative abuse pregnancy bedridden institutionalization congenital hypermobile cecum
Volvulus clinical presentation
symptoms: nausea & vomiting, colicky abdominal pain, obstipation, constipation
abdominal exam: distended abdomen, may have peritoneal signs
Volvulus imaging
abdominal X-ray: signs of large bowel obstruction
sigmoid volvulus = coffee bean with central cleft pointing to LLQ
cecal volvulus = coffee bean with central cleft pointing to RLQ
omega sign, bent inner tube sign
abdominal CT: can diagnose volvulus not visualized on abdominal X-ray
barium enema: ace of spades or birds beak sign
Volvulus management
a) sigmoid volvulus
non-surgical: flexible sigmoidoscopy decompression and insertion of rectal tube past obstruction, followed by subsequent elective surgery due to 50-70% recurrence if no surgery
surgical: left hemi-colectomy + ileotransverse colonic anastomosis
b) cecal volvulus
non-surgical: colonoscopy detorsion and decompression
surgical: right hemi-colectomy and ileotransverse colonic anastomosis
What is tenesmus
sense of incomplete emptying in rectum
Physical exam for peri-anal disease should include
inspection of peri-anal area
DRE
proctoscope (anoscope) for examination of inner anal canal
rigid sigmoidoscope for examination of rectum
Visualization characteristics of hemorrhoids
pain, lump, painless bleeding
Visualization characteristics of anal/colorectal cancer
lump, bleeding mixed with faeces
Visualization characteristics of anal fissure
pain with bowel movement, bleeding on toilet paper
Visualization characteristics of peri-anal abscess
lump, pain, signs of infection (skin swelling, erythema, tenderness, warmth, fluctuance), drainage
Peri-anal disease differential diagnosis
mechanical: anal fissure
infection: peri-anal / ischiorectal abscess, pilonidal sinus, anal herpes, peri-anal warts
neoplastic: anal cancer, colorectal cancer, colorectal polyps
vascular: peri-anal hematoma, hemorrhoids
Hemorrhoids epidemiology
5-30% prevalence in general population
Hemorrhoids risk factor
pregnancy
spinal injured population
Hemorrhoids anatomy
hemorrhoids are part of the normal human anatomy
in normal anatomy, hemorrhoids are cluster of cushion
made of vascular tissue, smooth muscle and connective tissue lined by epithelium of anal canal
hemorrhoids contain many arterio-venous channels
hemorrhoid cushions located an right anterior, right posterior and left lateral, acting as conformable plug that contribute to resting anal pressure and continence
cushions at 3, 7, 11 o’clock position when examining patient in lithotomy position
there are external and internal hemorrhoids
external hemorrhoids arise from external hemorrhoidal plexus below the pectinate line covered by squamous epithelium somatic innervation, so can feel pain drain by inferior rectal vein to IVC
internal hemorrhoids
arise from superior and middle hemorrhoidal plexus
above the pectinate line
covered by columnar epithelium
sympathetic innervation, so cannot feel pain
drain through superior rectal vein to portal system
Hemorrhoids pathophysiology
hemorrhoids only cause symptoms when they swell and prolapse
1) swelling of hemorrhoid cushions
increased anal resting pressure (from straining, prolonged toilet time or inadequate fiber) may cause hemorrhoid swelling
2) swelling dilate and engorge the arteriovenous plexus inside hemorrhoid
long term blood engorgement can cause thrombosis of hemorrhoids
3) engorged arteriovenous plexus stretch suspensory muscle and may lead to prolapse of hemorrhoid through anal canal or bleeding through erosion
Hemorrhoids clinical presentation
symptoms mainly from stretched suspensory muscle and engorged arteriovenous plexus
internal hemorrhoids: swelling, rectal fullness, pruritus, prolapse, painless rectal bleeding (bright red coating stool at end of defecation or drip into toilet)
prolapsed internal hemorrhoids: mild fecal incontinence, mucus discharge, wetness, sensation of fullness in peri-anal area
external hemorrhoids: swelling, pain after bowel movement, itchiness, peri-anal mass
thromboses external hemorrhoids: acute pain, hard lump that cannot be pushed back inside, may leave pari-anal skin tag after resolution within 2 weeks
DRE: tender palpable hemorrhoids if thrombosed
Internal hemorrhoids classification
management depend on grading of internal hemorrhoid
grade 1: cushion protrude into lumen of anal canal, which is only visualized on anoscope
grade 2: prolapse beyond external sphincter, but spontaneously reduce
grade 3: prolapse beyond sphincter and require manual reduction
grade 4: irreducible prolapse
Hemorrhoids diagnosis
hemorrhoids are a diagnosis of exclusion
all suspected hemorrhoids should be scoped (anoscopy) to rule out fissure, fistula, abscess, anal cancer, colorectal cancer, rectal varices
Hemorrhoids management
1) conservative treatment (for all hemorrhoids)
lifestyle modification: Sitz bath, improved anal hygiene, avoid constipation & diarrhea, increased fibre & fluid intake
topical treatment: topical treatment to alleviate pain, which include local anesthetics Parmoxine (Anusol), corticosteroids, vasoconstrictor, antiseptics, protectants
2) non-surgical treatment (grade 2 internal hemorrhoids)
rubber band ligation
sclerotherapy (injection of agent to form scar)
3) surgical treatment (grade 3-4 internal hemorrhoids)
surgery is most effective and have lowest recurrence but have the highest complication rate
surgery = hemorrhoidectomy or stapled hemorrhoidectomy or Doppler guided hemorrhoidal artery ligation
Hemorrhoid surgery indications
refractory to non-surgical treatment
large external hemorrhoids or mixed internal-external hemorrhoids with significant prolapse
grade 3 or 4 hemorrhoids
Hemorrhoid surgery complications
fecal incontinence
Treatment of thrombosed hemorrhoids
if within first 2 days of thrombosis, then surgical decompression, otherwise medical treatment as above
Perianal abscess risk factors
smoking diabetes type 2 obesity male previous episode of peri-anal abscess
Perianal abscess causes
moss commonly crypto glandular abscess
other causes: Crohn’s disease, tuberculosis, actinomycosis, lymphogranuloma venereum, radiation, leukemia
Perianal abscess pathophysiology
1) anal crypts at pectinate line become obstructed
the anal glands drained by crypts are also obstructed
2) glandular secretion become static, resulting in infection
usually bacterial infection by e. coli, proteus, streptococcus, staphylococcus, bacteroides, anaerobes
3) infection lead to formation of pus and abscess
over time, abscess may drain pus through spontaneously formed sinus tracts from abscess to epithelium layer of skin or anal canal
Perianal abscess common comorbid entity
over time, 50% abscess will have fistula
Location of anal duct infection
from most common to least common location: perianal (60% cases), ischiorectal (20% cases), inter-sphincteric (5% cases), supra-levator (5% cases)
ischiorectal abscess = abscess in ischiorectal fossa
inter-sphincteric abscess = abscess in inter-sphincteric groove between internal and external sphincter
supra-levator abscess = abscess above levator ani muscle
horseshoe abscess = ischiorectal abscess around anal canal
Perianal abscess clinical presentation
symptoms: dull peri-anal discomfort or pain out of proportion, pruritus, pain with defecation / sitting, purulent discharge, constitutional symptoms (fever, chills)
signs: rectal exam may show signs of infection (skin erythema, swelling, tenderness, warmth), fluctuate and tender mass, may have drainage through sinus
DRE: palpable inter-sphincteric abscess or sinus tracts
Perianal abscess investigation
CT or MRI if suspected non-palpable abscess or deep abscess (i.e. not peri-anal) to differentiate ischio-rectal abscess vs. inter-sphincteric abscess vs. supra-levator abscess
Perianal abscess diagnosis
peri-anal abscess diagnosed based on clinical history and physical exam
Perianal abscess management
incision and drainage of abscess, which is more effective in OR than ER
consider fistulotomy in horseshoe abscess
antibiotics Cephalexin PO indicated if diabetic, immunocompromised, valvular heart disease or important cellulitis
Fistula-in-Ano (Anal Fistula) definition
fistula = abnormal connection (tract) connecting 2 epithelial surfaces
fistula in ano is a hollow tract connecting an internal opening inside the anal canal to an external opening in peri-anal skin
Fistula-in-Ano (Anal Fistula) causes
anal fistula almost always caused by previous anorectal abscess that drained to the peri-anal skin
other causes include: post-operative incision & drainage of abscess, trauma, malignancy, radiation proctitis
Fistula-in-Ano (Anal Fistula) location
based on Parks classification
Intersphincteric fistula (Parks Type 1)
Transphincteric fistula (Parks Type 2)
Suprasphincteric fistula (Parks Type 3)
Extrasphincteric fistula (Parks Type 4)
Fistula-in-Ano (Anal Fistula) clinical presentation
previous history of painful and swollen abscess that drained spontaneously or surgically
symptoms: peri-anal discharge, pain, swelling, may have rectal bleeding, diarrhea, skin excoriation
inspection of entire perineum: external opening in perianal skin
DRE: induration, palpable fibrous sinus tract
Fistula-in-Ano (Anal Fistula) investigations
no investigations needed for diagnosis
ultrasound, CT or MRI indicated only if complex peri-anal inflammation (e.g. Crohn’s disease)
Fistula-in-Ano (Anal Fistula) diagnosis
diagnosis based on inspection of tract opening on peri-anal skin with history of previous abscess drainage
What is Goodsall’s Rule
For anorectal fistulas
fistula with anterior external opening (on skin) follow straight tracts
fistula with posterior external opening (on skin) follow curved path to internal opening at midline (primary opening in crypt)
Fistula-in-Ano (Anal Fistula) management
surgical intervention under anesthesia sealing the fistula (any of the options below)
fistulotomy, which is surgical unroofing of fistula tract from external to internal opening, allowing drainage and healing by secondary intention
fibrin sealant
insertion of Seton (string threaded through fistula)
fistula plug
mucosal advancement flap (flap of muscle covering external fistula tract opening)
Anal fistula surgical complications
recurrence
fecal incontinence
Anal fistula post-op care following surgery
Sitz baths
Irrigation and packing to ensure healing proceeding from inside to outside
Anal fissure definition
tear in the anoderm distal to the pectinate line
Anal fissure epidemiology
risk factors include local trauma (passage of hard stool, prolonged diarrhea, vaginal delivery, anal sex)
Anal fissure causes
midline fissure: trauma that stretch anal mucosa
non-midline fissure: Crohn’s disease, neoplasm, infection (tuberculosis, syphilis, HIV)
Anal fissure midline pathophysiology
1) stretching of anal mucosa beyond its normal capacity
2) stretching tears the anal mucosa, exposing the internal sphincter and forming the fissure
3) the internal sphincter undergo spasm due to damage
4) spasm of internal sphincter pulls apart the edges of the fissure
5) spasm decrease blood flow from posterior portion
Anal fissure clinical presentation
symptoms: painful rectal bleeding (on toilet paper), pain with bowel movement, pruritus
inspection of anus: fissure in posterior midline (90% cases) or anterior midline (10% cases), chronic fissure (anal ulcer) triad of fissure + sentinel skin tags + hypertrophied papillae
DRE: sphincter spasm
Anal fissure treatment
1) Conservative treatment
prevent constipation and straining: stool softener, bulking agents
symptomatic relief: Sitz bath
relaxation of internal anal sphincter to promote healing: topical calcium channel blocker, topical nitroglycerin, botox
2) Surgical treatment
lateral internal sphincterotomy to relieve sphincter spasm to increase blood flow and promote healing
fissurectomy
anal advancement flap
surgery increase risk of fecal incontinence
Peri anal complications of Crohn’s Disease
~40% of patients with Crohn’s disease have peri-anal disease, which can include any of the following
anal fissure
peri-anal abscess and anal fistula
recto-vaginal fistula
anal stenosis
hemorrhoids
adenocarcinoma, which can occur in fistula tracts
peri-anal skin excoriation, skin tags
Anal tumours anatomy
anal tumors classified based on anal canal vs. anal margin
anal margin = below / distal to anal verge
anal canal = above / proximal to anal verge
inner lining of anal canal is mucosa, which give rise to anal cancer (squamous cell carcinoma)
glands and ducts are found under mucosa in anal canal, which give rise to adenocarcinoma
rectum = columnar cells -> transitional zone = transitional cells -> below dentate line = squamous cells -> outside anal verge = skin cells
Types of anal tumours
types of anal tumor can be differentiated based on appearance on inspection or pathology from biopsy
1) Benign tumors inflammatory polyps lymphoid polyps hypertrohied anal papillae skin tags anal warts (condylomas) adnexal tumor leiomyoma granular cell tumor hemangioma lipoma Schwannomas
2) Malignant tumors pre-cancerous lesions: anal intraepithelial neoplasia squamous cell carcinoma adenocarcinoma skin: basal cell carcinoma, melanoma GI stromal tumor
Anal tumour by anatomical position
anal canal tumors: anal intraepithelial neoplasia, polyp, squamous cell carcinoma, adenocarcinoma
anal verge tumors: Bowen’s disease (squamous cell carcinoma), Paget’s disease (adenocarcinoma), squamous cell carcinoma, basal cell carcinoma, Kapok’s sarcoma, giant condyloma
Anal cancer epidemiology
uncommon cancer, but incidence increasing
common in elderly (age >60)
Anal cancer risk factors
HPV (type 16 and 18)
inflammatory bowel disease (Crohn’s)
sexual activity (increased sexual partners)
HIV, especially in men who have sex with men
chronic immunosuppression
smoking
family history of anal or colorectal cancer
Anal cancer types
majority of anal cancer are squamous cell carcinoma
anal cancer can also be adenocarcinoma, basal cell carcinoma, lymphoma, melanoma, kaposi’s sarcoma or giant condyloma
Anal cancer clinical presentation
anal cancer presents similar to hemorrhoid
rectal bleeding (bright red blood, usually on toilet paper) in 45% cases
anarectal pain or sensation of rectal mass in 30% cases
change in bowel habits: constipation, diarrhea or different caliber of stool
prolapsing sensation
lump near anus
fecal incontinence
itching or discharge from anus
constitutional symptoms: weight loss
inspection from rectal exam or scope (anoscopy, rigid sigmoidoscopy) can show a rough, bulky and friable mass (which is different from hemorrhoids that are smooth)
Anal cancer investigations
Rigid sigmoidoscopy or anoscopy
Colonoscopy
CT colonography
Anal cancer diagnosis
usually diagnosis based on pathology of biopsy via endoscope (anoscopy or rigid sigmoidoscopy)
Anal cancer management
surgery only if stage 1 (T1N0M0)
chemotherapy with radiotherapy for almost all anal cancer (Nigro regimen)
5-FU
mitomycin or cisplatin
intermediate dose of radiotherapy
abdominal perineal resection if patient has any of the following:
recurrent disease that is resistant to chemotherapy and radiation is not recommended
persistent disease
