Small and Large Bowel

Jejunum diameter up to 30mm (45mm in enteroclysis), ileum 25mm (35mm in enteroclysis). Folds are 2mm thick, 8mm deep, 4-7/inch in jejunum and 2-4/inch in ileum. Bowel wall 3mm.

Diffuse small bowel disease:

  • Dilatation indicates mechanical obstruction (transition point) or muscle dysfunction (diffuse; ileus, connective tissues diseases, malabsorption syndrome, chronic idiopathic pseudoobstruction).
  • Thickened folds indicates submucosal infiltration.
    • Uniform/straight/regular thickening from oedema or blood (usually thicker), may cause scalloping/thumbprinting. Diffuse oedema from hypoproteinaemia, CHF, portal HTN, lymphatic obstruction (lymphoma, radiation, mesenteric fibrosis, lymphangiectasis), Zollinger-Ellison syndrome, lactase deficiency. Short segment oedema from Crohn disease, eosinophilic gastroenteritis. Long segment haemorrhage from trauma, ischaemia, anticoagulation, bleeding diathesis, vasculitis (Henoch-Schonlein purpura, connective tisue disease, radiation, thromboangiitis obliterans).
    • Irregular/distorted/nodular thickening from cells or other non-fluid material. Proximal (duodenum, jejunum) from giardiasis, strongyloides, Whipple disease, eosinophilic gastroenteritis, Zollinger-Ellison syndrome. Distal (ileum) from lymphoma, Crohn disease, Yersinia, Campylobacter, Salmonella, TB, Behçet disease, CF, AIDS infections. Diffuse from lymphoma, polyposis syndromes, amyloidosis, histoplasmosis, systemic mastocytosis, Waldenstrom macrglobulinaemia, lymphoma.

Small bowel nodules:

  • Nodular lymphoid hyperplasia (2-4mm)
  • Lymphoma (>4mm)
  • Amyloidosis
  • Whipple diseas (1-2mm)
  • MAI
  • Lymphangiectasia
  • Systemic mastocytosis (<5mm)

Pneumatosis intestinalis – Gas in bowel wall. May be benign without clinical significance (likely if asymptomatic), bowel necrosis (ischaemia), mucosal disruption (ulcers, biopsy, trauma, enteric tubes, inflammatory bowel disease), mucosal permeability from immunosuppression (AIDS, transplantation, chemotherapy), alveolar disruption with dissection of gas along interstitium (COPD, asthma, CF, mechanical ventiliation, chest trauma). Cystic air bubbles or linear streaks (dependent areas), gas in mesenteric vessels or portal veins.

Lower GI haemorrhage may be caused by diverticula, angiodysplasia, carcinoma, polyp, rectal trauma/fissure/haemorrhoids; rarely duodenal ulcer, Meckel diverticulum, bowel ischaemia. Tc99-labelled RBC scan is sensitive to less than 0.1mL/min, CTA requires 0.3mL/min (may be intermittent hence need multiple scans), angiography requires 0.5-1mL/min (bleeding may be intermittent). Image when actively bleeding with CTA (NE, arterial and delayed/PV phases), only proceed to catheter angiography if positive. 75% will caese spontaneously with supporting measures (fluid resuscitation, reversal of anticoagulation). 1st line for upper GI haemorrhage (proximal to ligament of Treitz) is endoscopy (source identified in 95%); later CTA if required.

AXR – Fat planes include properitoneal (between peritoneum and abdominal wall), perivesical, psoas and perirenal fat planes. Fluid level in caecum seen in 20%. Spleen seen in 60%, psoas in 50%, bladder in 40%. Air-fluid levels distal to hepatic flexure are not normal.

Fluoroscopic Contrast Studies

Basic components:

  • Barium filling ± compression – Best with large amount of low-density contrast (to allow penetration). For strictures, contour abnormalities, polyps/filling defects.
  • Mucosal relief – Small amount contrast with partial collapse to best demonstrate folds.
  • Double/air contrast – High-density contrast (to coat mucosa) with gaseous distention. Distention should be enough to straighten folds, but not too much to flatten lesions; different levels of distention are ideal. For mucosal lesions and to accentuate areas of ridigity/stenoses. Gas may form bubbles, counter-acted with simethicone (in most barium and effervescent suspensions). Barium coating is improved with washing of barium bolus over the mucosa to remove mucous and debris. Good mocosal coating is characterised by homogeneous greyness (en-face view) which blends with a continuous smooth peripheral line (profile view of mucosa); area gastricae (stomach) or innominate lines (colon) may be seen. Patchy coating may simulate lesions.

Protrusions/elevations – Folds/haustra, polyps, inflammatory swellings or malignant tumours. Dependent surface filling defect with surrounding barium puddle (thicker surrounding density). Non-dependent surface etched in white (ring shadow) as the XR beam passes through the sides of the lesion that are covered with barium. Plaque-like lesions will not be seen on dependent surfaces as it is completely covered with barium, or only the central portion may be seen. Nondependent gradual sloping margins of lesions will be ill-defined.

  • Stalactite phenomenon – Droplet hanging from non-dependent protrusion, as a central density (surrounded by etched in white) or in profile.
  • Bowler hat sign – Lesion has acute angle with mucosal (eg polyp) consisting of trapped barium between the base and mucosa (brim) and curvilinear density at top of polyp (dome). Only seen on oblique, en-face is only a single ring shadow.
  • Mexican hat sign – Nondependent pedunculated polyp with outer head and inner stalk rings.
  • Submucosal lesions – Forms sharp right angles in profile; abrupt well-defined edges en-face. Mucosal folds fade out at the edge of the lesion.
  • Extrinsic mass – Indentation with white line in profile; ill-defined lucency en-face.

Depressions – Ulcers or diverticula. Dependent surface barium collection, may have radiating lucent folds or lucent halo (oedema or tumour); shallow ulcers may have empty craters (barium has escaped) with only the walls of crater shown as a ring shadow. Anti-dependent lesions are ring-shadows. Sharp outer border that fades inwards, (cf non-dependent protrusions that have sharp inner borders fade outwards); differentiation can be confirmed on profile views. Depressions be confirmed on dependent views after washing with Barium, demonstrating collection. May have associated interrupted folds. Filling defects within ulcers/erosions may represent blood clot. Double ring shadows may represent ulcers (inner neck and outer base) or ulcerated protrusions (inner ulcer, outer edge of protrusion).

The main barium pool (or smaller puddles) are used to wash the mucosa, for mucosal coating, fill ulcer caters; shallow pools will also demonstrate dependent filling defects. However it obscure dependent lesions (covering entirely) or non-dependent lesions (hiding the ring shadow). Compression may help to immerse nondependent lesions within the barium pool causing filling defects, and making them more apparent.


  • Barium-related:
    • Barium precipitation or flaking – May simulate diffuse ulceration.
    • Patchy mucosal coating
    • Stalactite phenomenon – From high viscosity.
    • Kissing artefact (apposition of bowel walls) – From insufficient gas separation, point of adherence produces an irregular outline.
  • Extraneous or foreign material – Gas bubbles, undissolved effervescent agent, adherent faecal material, extrinsic structures (eg bones, calcified lesions).
  • Barium flaking

Small Bowel Follow-Through (SBFT)


  • 500mL 42% Ba, lie on right, screen to proximal jejunum.
  • Supine views every 15-30min until reaches colon. Screen for motility, mobility, separation of bowel loops, mucosal pattern, luminal diameters. Spot views with compression at areas of interest.
  • Metoclopramide or barium/gastrograffin can be given to shorten transit time.
  • Transit time = beginning of gastric emptying to ileocaecal valve.

Malabsorption – Flocculation and segmentation of Ba column, Moulage phenomenon/sign (pooling/segmentation from hypotonic segments).

Barium Enema


  • Bowel preparation.
  • Insert rectal enema tube ± inflate retention balloon.
  • Induction of colonic hypotonia with glucagon (1mg IV, lasts 10-20min) or hyoscine (Buscopan).
  • Control/scout radiographs.
  • Instill barium (eg Polibar Plus) in prone position (lateral if anterior rectal pathology suspected eg rectovaginal fistula, Pouch of Douglas lesions) with partial opening of enema tube (rapid distention increases defecation urge). Turn patient to facilitate pasage: L oblique/lat (descending colon) ± slight Trendelenburg (splenic flexure), prone (transverse colon).
  • Barium pool images to check for filling defects ± posterior views.
  • Enema bag droped to floor to drain rectal pool (not sigmoid).
  • Room air or carbon dioxide intermittently insufflated. If patient is unable to turn easily to manipulate the barium pool (eg elderly, feble) then convert to single-contrast barium study only.
  • Double contrast images – Aim to demonstrate each surface of the colon with air contrast and barium pool with spot views. Different maneuvres of prone, supine, LPO, RPO, erect, recumbent, Trendelenburg. Ideally eliminate as much barium as possible on double-contrast views. Compression may be used to splay loops. Try to get adequate views of the sigmoid colon before contrast reaches the caecum and distal ileum (may obscure the loops). Only later turn patient R lat.
  • Overhead radiographs allow overview – Include R&L decubitus.
  • Views of the distal rectum after enema tube tip removal.
  • Postevacuation images can be obtained for fistulas or tracts

Obstruction and Pseudoobstruction

Small Bowel Obstruction (SBO)

Mechanical obstruction from obturation (mass in lumen), stenosis (intrinsic bowel lesion) or compression (extrinsic disease). Dilation from continued secretions, swallowed fluid/air/food then cessation of absorption. Stasis -> overgrowth of bacteria -> toxins -> mucosal injury. Distension and raised intraluminal pressure -> ischaemia (strangulated vs simple obstruction). Closed loop obstruction – obstruction at both ends of a loop, high risk of strangulation; caused by incarcerated hernias, volvulus. Dilated proximal loops cf distal loops (jejunum >3.5cm, ileum >3cm, distal ileum >2.5cm; rarely >5cm), air fluid levels (>25mm long, >5 in number or different heights in same loop), “string of beads/pearls” (gas trapped between valvulae conniventes), faecalisation. Causes include:

  • Adhesions – Postsurgical (75%) or postinflammatory. Fibrous bridges may allow internal herniation and closed loop obstruction. Fibrous adhesions may rarely be congenital.
  • Incacerated hernia (internal or external).
  • Intussusception – Telescoping of bowel of intussusceptum (prolapsing part) into the receiving intussusipiens. Once trapped it is propelled by peristalsis. May lead to obstruction, compression of vessels with infarction. In younger children usually no underlying anatomical defect, some associated with rotavirus; may be reduced by enema. In older children/adults usually caused by a lead point (intraluminal mass or tumour); usually requires surgery.
  • Volvulus
  • Malignancy (intrinsic or extrinsic)
  • Infarction
  • Gallstone ileus
  • Parasites (ascaris)
  • Foreign body (bezoar)
  • Meconium
  • Congenital stenosis


(Adynamic/paralytic/nonobstructive ileus). Ileus = “stasis”, includes obstruction and nonobstuctive ileus. From drugs (atropine, glucagon, opiates, barbiturates, phenothiazines), metabolic (diabetes, hypothyroidism, hypokalaemia, hypercalcaemia), inflammation (gastroenteritis and extra-intestinal), postoperative (usually resolves after 4-7 days), post-traumatic, ischaemia, post-spinal injury, vagotomy, diabetic neuropathy. Sentinal loop – segment of paralysed and dilated bowel next to inflammation.


3rd most common cause of colonic obstruction (10%). Rare in children (average 7yo) where it is caused by malrotation, constipation (mental retardation, Hirschsprung’s, CF, aerophagia). Redundant segment of freely movable bowel. Closed loop obstruction -> strangulation, ischaemia, nerosis, perforation

  • Sigmoid volvulus (2/3, 60-70yo) – Dilated sigmoid, inverted U, absent haustra, midline RUQ or LUQ, vertical dense line (apposed walls), absent gas in rectum, northern exposure sign (loop projects above transverse colon), whirl sign (twisted mesentery). Enema shows tapered beak at rectosigmoid jumction, corkscrew pattern mucosal folds at point ot torsion, shouldering (localised wall thickening at twist indicating chronicicity). From fibre (increase stool bulk and elongates colon), chronic constipation, obtundation (gaseous distension). Tx 50% chance of non-surgical decompression, 40% recurrence non-operative reduction. DDx functional megacolon (gross constipation without organic cause, dilated ahaustral gas or stool-filled colon), ogilvie syndrome (colon pseudo-obstruction of unkown cause, in unwell patients).
  • Caecal volvulus (1/3, young) – Twist distal to ileocaecal valve. Dilated ectopic caecum, apex -> mid or LUQ, kidney/coffee bean shape (indentation from ileocaecal valve), 1-2 hasutra, distended SB with collapsed large bowel. Caecal bascule – anterior folding in mid-abdomen possibly adhesion from previous surgery. From congenital defect in attachment, postpartum liggament laxity, colon distension. Tx colonoscopic reduction, surgery.
  • Transverse colon (2-4%) – Two air-fluid levels.
  • Splenic flexure (<1%) – Dilated, featureless loop in LUQ separate from stomach.
  • Compound volvulus (ileosigmoid knot, very rare) – Hyperactive ileum winds around narrow pedical of sigmoid. Dilated sigmoid in mid-abdomen -> RLQ, medial deviation of distal left colon. Strangulation and gangrene of SB within hours.


Inflammatory Bowel Disease (IBD)

Idiopathic inappropriate mucosal immue activation, not thought to be autoimmune but abnormal interactions of epithelium to intestinal microbes. F>M, 20s-40s, most common in Caucasians. Increasing incidence ?hygeine hypothesis (reduced enteric infections causing inadequately developed regulatory processes). Reduced incidence in areas with helminth infection. Smoking increases risk of Crohn disease, but reduces risk of UC. Perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) positive in 75% of UC, 10% of Crohn disease. Colitis-assiciated neoplasia risk increases sharply 10 years after disease onset, increased risk with pancolitis, frequency and severity of acute inflammation, primary sclerosing cholangitis.

Ulcerative Colitis (UC)

Inflammation with crypt abscesses, limited to mucosal and superficial submucosa. No granulomas. Granular mucosa (mucosal hyperaemia and oedema preceding ulceration), shallow stippled broad-based ulcerations which may be aligned along longitudinally (spread to cover entire mucosa). Islands of regenerating mucosa form pseudopolypswith tips of these fusing to form mucosal bridges. Later mucosal atrophy with lack of normal folds. No mural thickening, normal serosal surface and no strictures. Collar button ulcers (deeper crypt abscess extending deep in thickened oedematous mucosa, muscularis propria rarely involved). Inflammatory/hyperplastic polyps (small islands of inflamed mucosa), post-inflammatory polyps (mucosal tags in quiescent phases), filiform polyps (pos-tinflammatory polyps with wormlike appearance, usually in otherwise normal-appearing colon). Process is symmetric around lumen. Continuous confuent diffuse involvement extending proximally from rectum and limited to colon. SB almost always normal, but occasionally backwash ileitis in severe disease. Sharp demarcation with normal non-involved bowel. Complications and associations include:

  • Toxic megacolon – 2-5%, may be initial manifestation, most common cause of death. Inflammation damages muscularis propria, disturbing neuromuscular function leading to dilatation. High risk of perforation.
  • Massive haemorrhage.
  • Colorectal adenocarcinoma – High risk 1% per year.
  • Migratory spondyloarthritis – Mimicing ankylosing spondylitis, in 20%.
  • Uveitis and iritis in 10%.
  • Primary sclerosing cholangitis in 5% (more common that Crohn disease).
  • Increased risk of thromboembolic disease.

Crohn Disease

(Regional enteritis). Diarrhoea, pain, weight loss, fever with remission, relapse and progression. May involve any region of GIT, most commonly terminal ileum, ileocaecal valve, caecum; colon and TI in 55%, SB alone 30%, colon alone 15%, proximal SB without TI 3%. Rectum normal in 50% (cf UC), and if involved usually has deep ulcers and multiple fistulas to skin. Erosions, ulcerations, full-thickness transmural inflammation. Neutrophils infiltrate crypts forming crypt abscesses; cycles of destruction and regeneration distorts mucosal architecture. Noncaseating granulomas in 35%, in areas of active disease, uninvolved regions or mesenteric nodes; cutaneous granulomas – metastatic Crohn disease. Early aphthous ulcer’ (shallow 1-2mm usually surrounded by oedematous halo), later confluent deep linear/serpintine ulcerations (esp mesenteric border, often linear forming fissures between nodules of normal or elevated oedematous mucosa = ‘cobblestone pattern‘), thickened distorted folds, submucosal fibrosis with hypertrophy of the muscularis propria luminal narowing contractures and stenoses (strictures, string sign’ of contrast esp TI), pseudodiverticula (asymmetric fibrosis causing saccular outpouchings on other side), mesenteric involvement (ulceration may extend between leaves of mesentery, may be thickened and retracted). Fissures and fistulous tracts common. Asymmetric longitudinally and eccentric around lumen, skip lesions with normal intervening bowel is characteristic. Mestenteric fat extends around serosal surfaces (creeping fat). Complications and associations include:

  • Obstruction – Usually partial due to strictures or severe ulceration and spasm.
  • Fistula – Abnormal communication between 2 epithelial-lined organs, in 20%. Most ileocolic or ileocaecal, but can be enterocutaneous, enterovesical, colovesical.
  • Sinus tracts – From lumen to extraluminal mass.
  • Abscess and phelgmon – In mesentery, peritoneal cavity, retroperitoneum, abdominal wall.
  • Perforation – In 3%, most confined forming sinus tract or fistula.
  • Slight increased risk of carcinoma with prevalance ~0.5% (low risk).
  • Low risk of toxic megacolon.
  • Derranged absorption causing megaloblastic anaemia (vitamin B12 deficiency).
  • Increased risk of gallstones and renal stones.
  • Migratory spondyloarthritis – Mimicing ankylosing spondylitis, in 20%.

Indeterminate Colitis

Overlap between UC and Crohn disease in ~10% of IBD. No SB involvement, continuous colitis with histology or clinical features of Crohn disease. Later complications may ultimately establish the diagnosis.

Toxic Megacolon

Fulminant colitis with neuromuscular degeneration. Bowel wall like ‘wet blotting paper’. Caused by UC (75%, most common cause of UC mortality), pseudomembranous colitis, Crohns, amebiasis, ischaemic colitis, strongyloidiasis, bacillary dysentery, tyhpoid, cholera, Behçet’s syndrome. Precipitated by endoscopy, opiates, anticholinergics and antidiarrhoeal drugs, metabolic alkalosis, hypokalaemia and aerophagia. Dilated (>5.5cm, up to 15cm due to loss of muscle tone), transmural inflammation, ahaustral (normal haustra exludes megacolon), thickwalled (subserosal and omental oedema), deep ulcerations that may extend to serosal surface with mucosal islands/pseudopolyps, large areas of denuded mucosa, pericolic fat line, and air-fluid levels, usually transverse colon, pneumatois coli, irregular nodular wall. Cx perforation, abscess, peritonitis, mortality 20%. Tx colectomy. Barium studies should be avoided due to risk of perforation.


(Caecitis). Neutropenic immunocompromised patients with systemic symptoms, bloody diarrhoea, RLQ pain. ?Combination of ischaemia, infection (CMV, Pseudomonas aeruginosa), mucosal haemorrhage and ?neoplastic infiltration. Potentially fatal. Concentric marked thickening of caecum and ascending colon, prominent pericolic stranding. At risk of ischaemia.

Cathartic Colon

Neuromuscular incoordination from chronically increased muscle activity by laxatives (castor oil, bisacodyl, senna), usually after at least 15yrs. Predominantly ascending colon, may cause dilatation or smooth pseudostrictures (spasm), patulous ileocaecal valve, shortening, effaced mucosa with absent haustrations.

Diversion Colitis

Colitis in the diverted/unused segment of colon esp UC. Mucosal erythema, friability, numerous mucosal lymphoid follicles resembling IBD. ?Due to changes in luminal microbes and diversion of faecal stream providing nutrients to epithelial cells.

Behçet Disease

Small vessel vasculitis affecting eyes (iridocyclitis), joints (mild arthritis), skin, CNS, GIT with mucocutanoeous ulcerations, vesices and pustules. GIT most commonly ileocaecal with aphthous erosions, deep ulcerations, stenosis, fistulas. Cx perforation, peritonitis.

Infectious Enterocolitis

Bacterial infections:

  • Yersinia enterocolitica and pseudotuberculosis – G-positive bacillus from contaminated pork/milk/water. Self-limited in 8-12/52 involving terminal ileum, appendix and ascending colon with aphthous ulcers, nodules up to 10mm, wall and fold thickening with effacement (oedema). May have cause nodular lymphoid hyperplasia during resolution stage.
  • Typhoid/enteric fever – Salmonella typhi and paratyphi endemic in India, Mexico, Philippines, Pakistan, Haiti. Contaminated food/water. Enlarged Peyer’s patches in terminal ileum, enlarged nodes, oval ulcers along axies of ileum that may perforate, splenomegaly. Typhoid nodules (foci of parenchymal necrosis replaced with macrophages) in liver, bone marrow, lymph nodes. Colonisation may cause gallstones.
  • Camylobacter jejuni – Comma-shaped flagellated G-neg. Acute self-limited colitis, usually lasts only 1-2/52, but commonly relapses. May cause autoimmune reactions with reactive arthritis (esp patients with HLA-B27), erythema nodosum, Guillain-Barre syndrome.
  • (Nontyphoid) Salmonella – G-neg bacilli in contaminated food. Self-limited colitis.
  • Shigella – G-neg bacilli, intraceuular proliferation. Damages surface epithelium with haemorrhage, ulceration, occasionally pseudomembranes. Most prominently descending colon, occasionally ileum. Uncommonly causes Reiter syndrome (sterile arthritis, urethritis, conjunctivitis in HLA-B27 positive men 20-40yo), haemolytic-uraemic syndrome
  • Escheriscia coli – G-neg bacilli normal colinisation, most nonpathogenic. Groups causing colitis include enterotoxogenic (ETEC, traveller’s diarrhoea), enterohaemorrhagic (EHEC, bloody diarrhoea, haemolytic-uraemic syndrome), enteroinvasive (EIEC self-limited colitis), enteroaggregative (EAEC).
  • Pseudomembranous colitis (antibody-associated colitis/diarrhoea) – Pseudomembrane of necrotic debris and overgrowth of Clostridium difficile, in colon and occasionally SB. Caused by antibiotics (change in bowel flora), ischaemia (esp postsurgery), radiation, long-term steroids, shock, obstruction. Dilated colon (may be marked with toxic megacolon), marked wall thickening (~15mm, with halo or target appearance), nodular thickening of haustra, thumbprinting, accordian sign (intraluminal contrast trapped between nodular wall thickening in stripes), superficial ulcers, mild pericolic stranding (less than expected for wall thickening), ascites (in 35%). Patchy distribution with sparing of rectum.
  • Whipple disease – Rare systemic disease, Tropheryma whippelii (Whipple bacilli) G-positive actinomycete causing malabsorption, lymphadenopathy, CNS. Organism-laden macrophages cause lymphatic obstruction in small bowel lamina propria and nodes (causing malabsorption). Irregularly thickend folds esp jejunum, tiny 1mm sand-like nodules spread diffusely or in small groups (suggestive), intralumional fluid but no significant dilatation. Low/fat-density mesenteric nodes is characteristic. Macrophageas can also accumulate in synovial membranes of joints, cardiac valves, brain etc.
  • Cholera – Vibrio cholerae comma-shaped G-neg endemic to India and Bangladesh, contaminated drinking water. Noninvasive in small intestine with watery diarrhoea.

Viral gastroenteritis:

  • Norovirus (norwalk-like virus) – ~50% of all gastroenteritis outbreaks, mostly affecting small bowel.
  • Rotavirus – Most common severe childhood diarrhoea. Selectively infects and destroys enterocytes in small bowel. Vaccines now available.
  • Adenovirus – Second most common pediatric diarrhoea, also affects immunocompromised patients.

Parasitic enterocolitis:

  • Ascariasis – Ingestion of food/water contaminated with eggs of roundworm Ascaris lumbricoides esp Asia and Africa. Hatch in SB, larvae penetrate wall and migrate to lungs where they molt and grow, may also form hepatic abscesses. Migrate to bronchi and trachea before being swallowed again, mature in SB/jejunum where they grow up to 15-35cm. Ova excreted in faeces. Large bolus of worms may obstruct or cause intussusception. Seen on XR in 70% as round and tubular densities outlined by gas. Barium ingested by worms may be seen as long string-like lines in intestinal tracts, outlined by linear filling defect.
  • Strongyloides – Larvae in faecally contaminated soil penetrate unbroken skin, migrate to lungs, swallowed and mature into adult worms in intestine. Ova can hatch in intestines with larvae penetrating mucosa (autoinfection). Oedematous folds, spasm, dilated proximal duodenum, diffuse mucosal ulceration.
  • Amebiasis – Entamoeba histolytica common in SA, Central/South America, Asia where 5% harbor amebae. Contaminated food/water ingested, cyst capsule dissovled in SB releasing trophozoites that migrate to colon (esp caecum, rectum) and burrow into mucosa -> small abscesses, may spread throughout body. Aphthous ulcers, deep ulcers, asymmetric and skip areas. TI spared. Cx strictures, amebomas (hard mass of granulation tissue mimiking neoplasm), toxic megacolon, fistulas. Amebic liver abscess may cause diaphragmatic perforation, pleural effusion, thoracic disease. May also spread to kidneys and brain.
  • Giadiasis (most common pathogenic parasitic infection) – Giardia lamblia in faecally contaminated water/food, unfilted water supplies (cysts resistant to chlorine). Duodenum/jejunum, symptomatic if invades wall (pain, diarrhoea, malabsorption); distorted thickened folds, hypermotility and spasm, increased secretions.


AIDS-Related Enterocolitis

AIDS predisposes to lymphoma, Kaposi sarcoma, opportunistic infections. Usually with CD4 count <200, from CMV, cryptosporidum or HIV itself. Most commonly right colon with wall thickening, ulceration.

  • Cryptosporidium and Isospora belli – Protozoa infesting proximal intestine causing cholera-like diarrhoea. Thickend folds, marked intraural fluid.
  • CMV – SB, colon, lungs, liver, splen. Mucosal ulceration with bleeding, perforation, thickened folds, loop separation, ulcers, fistula.
  • MAI – Lung liver, spleen, bone marrow, LN, GIT. Thickend nodular folds, sandlike mucosal pattern, adenopathy, focal liver and splenic lesions.
  • Candida
  • Amoeba
  • Giadia
  • Strongyloides
  • Herpes simplex
  • Campylobacter


Chronic diarhoea, steatorrhoea, weight loss, anorexia, distention. Most commonly pancreatic insufficiency, coeliac disease, Crohn disease. Abnormality in intraluminal digestion (breakdown of proteins, carbohydrates, fats), terminal digestion (hydrolysis of carbohydrates and peptides in emzymes in brush border of small bowel mucosa), transepithelial transport (across epithelium) or lymphatic transport of absorbed lipids. Secretory diarrhoea is isotonic stool persisting during fasting; osmotic from hypertonic unabsorbed luminal solutes; malabsorptive from failed nutrient absorption releived by fasting; exudative from inflammation.

Cystic fibrosis has absense of epithelial CF transmembrane conductance regulator (CFTR) with defective intestinal chloride secretion and thus bicarbonate/sodium/water secretion resulting in luminal dehydration. This causes duct obstruction with chronic autodigestion of the pancreas and exocrine pancreatic insufficiency.

Coeliac Disease

(Nontropical/coeliac sprue, gluten-sensitive enteropathy). Malabsorption, steatorrhoea, weight loss. Autoimmune reaction to gluten (wheat, rye, oats, barley) insoluble protein, damaging the mucosal epithelium. Prevalence 0.5-1%, most present 30-60yo, M=F but women present 2-3x more due to demand for iron and vitamins. May be associated with type 1 diabetes, thyroiditis, Sjogren syndrome. Increased intraepithelial lymphocytes, crypt hyperplasia and villous atrophy (loss of mucosal brush border reducing surface areas and hence malabsorption) with mucosal flattening esp D2-prox jejunum. Submucosa, muscularis and serosa normal. Dilated SB, normal/thin folds. Reversal of the jejunoileal fold pattern with reduced folds/inch in jejunum but incresed in ileum (>/=5; jejunization of the ileum). Fluid excess in ileum. Transient intussusceptions. Enlarged mesenteric LN. Increased risk of T-cell lymphoma and adenocarcinoma.

Tropical Sprue

Exclusively tropics where it is endemic. Similar changes and malabsorption as coeliac disease, but total villous atrophy is uncommon and tends to involve distal small bowel (with folate and B12 deficiency). No definite causal organism identified. Responds to folate and antibiotics.

Lactose Intolerance

Deficiency of lactase (disaccharidase) in jejunum. Congenital deficiency is AR, rare. Acquired deficiency from down-regulation of lactase gene expression, common in Chinese, Native Americans, Africa-Americans. Secondary lactase deficiency with alcoholism, Crohn disease, drugs (eg neomycin). Nondigested lactose (from milk) increases intraluminal fluid and distention, but normal folds.

Infiltrative Diseases

Eosinophilic Gastroenteritis

Proximal SB, almost always associated gastric antrum. Usually associated with other allergy, self-limiting but freqently reccurs. Intense eosinophilic infiltration in lamina propria causing distorted thickening of walls and folds, luminal narrowing, separation between loops.


Progressive collagen deposition with atrophy of muscularis and flaccid atonic dilated bowel. Most commonly affects the oesophagus with dilated distal 2/3, shortening due to fibrosis, GOR. Duodenum > jejunum > ileum. Malabsorption. Valvulae conniventes normal/thin. Hide-bound appearance (pathognomonic) of thin folds tethered together due to longitudinal > circular muscle contraction. Accorian sign – evenly spaced mucosal folds in the duodenum. Excessive mesenteric border contraction -> antimesenteric mucosal sacculations.


Extracellular infiltration of amorphous amyloid throughout body tissues. Primary, or secondary to multiple myeloma, RA or TB. Most systemic, 10-20% localised. Deposition throughout SB wall esp small vessels -> ischaemia, infarction. Deposition in muscularis impairs motility. Diffuse irregualr thickened folds, nodules. No dilatation or hypersecretion.

Systemic Mastocytosis

Proliferation of mast cells in skin (urticaria pigmentosa), bones (osteoblastic change in 70%), LN, GIT, hepatosplenomegaly. Bowel wall and fold thickening, nodules up to 5mm.


True diverticula contain all 3 layers or the bowel wall, lined by mucosa nd communicate with the lumen. Most commonly jejunal mesenteric border. Mucosal outopuchings between leaves of mesentery. Commonly multiple. Usually asymptomatic, but stasis may cause bacterial overgrowth, deconjugation of bile salts and malabsorption (vitamin B12 deficiency, megaloblastic anaemia). Cx obstruction, acute diverticulitis, haemorrhage, volvulus. Most have small neck smaller than opuch, diverticula lack mucosal folds and don’t contract (lack of muscle).

False diverticular are herniations of mucosa through muscularis propria.

Pseudodiverticula are outpouchings along antimesenteric border with lack/attenuated muscularis propria, secondary to disease, esp Crohn diseae, scleroderma. Fibrosis and contraction of mesenteric border causes pleating and sacculatiosn of unsupported antimesenteric border.

Meckel Diverticulum

2% of population, M:F 2:1, if symptomatic usually by 2yo (only ~4% are symptomatic). ~2 inches (2-8cm) long, antimesenteric border of ileum, usually within 2ft (85cm) of ileocaecal valve (may be up to 2m). From failed involution of the vitelline duct (lumen of developing gut -> yolk sac). True diverticulum with all layers. Tip may be attached to umbilicus via remant of vitelline duct. Ectopic gastric mucosa in 60%, positive for Tc99m; peptic secretions may cause ulceration and bleeding. Cx intussusception, volvulus perforation.

Diverticular Disease

Acquired herniation of mucosa and muscularis mucosae through muscularis propria (false diverticula, lacking all 3 elements) creating 0.5-10 mm sacs alongside the taeniae coli, anywhere in colon but more common in sigmoid. From elevated intraluminal pressure due to exaggerated peristaltic contractions in spasmotic movements and reduced stool bulk (low fibre diet, hence much less common in Japan). Mucosa penetrates through regions of focal muscle wall discontinuities (penetrating nerves and vasa recta), which in other parts of the bowel are reinforced by the external longitudinal layer (non-circumferential 3 bands of taeniae coli in colon). Diverticulosis when diverticulae are multiple. Some sacs are reducible, disappearing with complete luminal filling. Rare <30yo, 50% of >60yo. Thickening of muscularis propria (circular muscle), bowel shortening with crowding of circular muscle bundles, spiked irregular luminal outline, muscle dysfunction (pain, tenderness without inflammation). May cause bleeding. Diverticulitis in 20%.

Diverticulitis – Inflammation of diverticula, occasionally with perforation, intramural/localised pericolic abscess. Deformed diverticular sacs, localised wall thickening, pericolic stranding/abscess, extravasation into abscess/fistula, narrowed lumen with tapered margins, double track sign (barium tracking parallel to lumen often connecting perforated sacs). Cx obstruction, bleeding (more commonly diverticulosis than diverticulitis), peritonitis, sinus tract and fistula (bladder, vagina, skin). May appear similar to carcinoma, follow-up may be required.

Neoplasm and Hyperplasia

Extrinsic masses can simulate intrinsic disease, include:

  • Endometriosis – Multiple varibale sized implants on sigmoid and rectum, cul-de-sac. Sharply defined, compressing, not usually circumferential.
  • Benign or malignant pelvic masses. Invaded colon may show wall thickening, separation of folds, spiculation, angulations, narrowing, serosal plaques.
  • Extrinsic inflammation – Mass effect, asymmetrical tethering, spiculation.


Protrusions from mucosa. Filling defect in barium pool or etched in white. May be pedunculated with stalk or sessile. Bowler hat sign when oblique with coating of body and recess at base. Those <5mm are almost always hyperplastic (malignant risk 0.5%), 5-10mm 90% adenomas (risk 1%), 10-20mm usually adenomas (risk 10%), >20mm 1/2 are malignant.

  • Hyperplastic polyps (90%, metaplastic polyp) – Mucosal proliferations ?from dealyed shedding of surface epithelial cells. Round, sessile, almost all <5mm, usually at crests of mucosal folds. No malignant potential except in polyposis syndromes. Most commonly rectosigmoid.
  • Adenomatous polyps (10%, adenomas) – Premalignant neoplasms with core of connective tissue. In almost 50% of those 50yo. Epithelial dysplasia. Most don’t progress into adenocarcinomas. 4mm to large (10% are >10mm with 10% risk of malignancy), may be pedunculated (fibrovascular stalk) or sessile. Tubular (pedunculated with small rounded/tubular glands), tubulovillous or villous (larger sesslie with slender villi, higher risk of malignant transformation) depending on architecture.
  • Hamartomatous/juvenile polyp (1%) – Common cause of PR bleeding in children, most <5yo. Isolated polyps commin, in up to 2% of children. Proliferation of all 3 mucosal layers (epithelium, lamina propria, muscularis) with smooth muscle core covered by mature glandular epithelium. Most pedunculated. characteristic cystic spaces. No risk of malignant transformation. My be sporadic or syndromic.
  • Inflammatory polyps (0.5%, pseudopolyps, false polyps) – Multiple, associated with chronic inflammation esp IBD.

Polyposis Syndromes

Multiple polypoid lesions. DDx metastases, lymphoma, nodular lymphoid hyperplasia, Kaposi sarcoma, carcinoid tumours.

Familial adenomatous polyposis (FAP) – 2/3 inherited (AD with high penetrance, mutation of the adenomatous polyposis coli APC gene), 1/3 spontaneous. Tubulovillous adenomas carpeting the entire colon (with few in SB esp ampulla of Vater and stomach) starting by 20yo. >100 polyps required for diagnosis. Colorectal cancer in almost all patients, usually by 30yo. Most treated with total colectomy. Increased risk of SB carcinomas, thyroid carcinoma, mesenteric fibromatosis.

  • Gardner syndrome – Also associated with cortical thickenineg of ribs and long bones, skull osteomas, supernumerary teeth, exostoses of mandible, dermal fibromas, desmoids, epidermal cysts, thyroid tumours.
  • Turcot syndrome – Also associated with CNS tumours (medulloblastomas, gliobastomas).

Hamartomatous polyposis syndromes.

  • Peutz-Jeghers syndrome – Rare AD, multiple hamartomatous polyps in SB (most common), colon and stomach, occasionally bladder and lungs. Characteristic melanin freckles on face, palmar fingers and toes, mucous membranes. Mostly in jejunum, usually pedunculated, up to 40mm. At risk of intussusception, adenocarcinoma (2-20% from coexisting adenomatous polyps), other malignancy (breast, pancreas, uterus, ovary).
  • PTEN hamartoma tumour syndrome (PHTS) – Group of disorders with mutation in tumour suppressor gene PTEN. Includes Cowden syndrome, BRRS (Bannayan-Riley-Ruvalcaba syndrome with macocephaly, multiple lipomas, haemangiomas, GI hamartomatous polyps), Proteus syndrome (congenital malformations, hemihypertrophy, hamatomatous overgrowths, naevi and hyperostoses).
    • Cowden syndrome (multiple hamartoma syndrome) – AD, mostly Caucasians. Multiple hamartomas including hamartomatous polyposis of GIT, macrocephaly, goiter and thyroid adenomas. All patients have mucocutanoues lesions with facil papules, oral papillomas, palmoplantar keratoses. Increased risk of breast cancer, follicular thyroid cancer, endometrial cancer, bladder TCC.
  • Juvenile polyposis syndrome (JPS) – >3-5 juvenile polyps in the colorectum.
  • Cronkhite-Canada syndrome – Nonhereditary, onset >50yo, unknown aetiology. Polyps throughout stomach, SB and colon. Associated with nail atrophy, brownish skin pigmentation, alopecia. Watery diarrhoea and protein-losing enteropathy.
  • Others diseases with increased risk of hamartomatous polyps include MEN2b, NF1, basal cell naevus syndrome (Gorlin syndrome).

Hereditary non-popyposis colorectal cancer (HNPCC, Lynch syndrome) – Increased risk of colorectal, endometrial, stomach, ovarian, ureter, brain, SB, hepatobiliary and skin cancers. Colon cancers at a younger age, often right colon. Mutation of gene involved in repair of DNA replication errors with microsatellite instability (indicating mutated mismatch repair gene also seen in other colon cancers).


Small bowel adenocarcinoma (uncommon) – More common in duodenum (50%) and proximal jejunum. Most symptomatic at presentation esp mass. Increased risk with adult celiac disease, Crohn disease, Peutz-Jeghers syndrome. Infiltrating producing strictures (typical ‘apple-core’ with abrupt edges to thickened wall), polypoid or ulcerating. Cx bleeding. obstruction, intussusception. Poor prognosis 20% at 5yr. Metastases by intraperitoneal seeding, LN, liver.

Colorectal adenocarcinoma – 50% in rectum/rectosigmoid area, 25% sigmoid, 25% remainder of colon. Proximal tumours are often large exophytic polypoid, rarely causing obstruction, presenting with iron-deficiency anaemia. Distal tumours tend to be annular causing napkin-ring/apple-cre constrictions and obstruction. 15% of all cancer-related deaths (second to lung cancer), peak 60-70yo, M slightly >F, more common in developed countries. Increased risk with low fibre intake, high refined carbohydrates and fat; ?due to altered intestinal microbiota. The adenoma-carcinoma sequence (80%) is from consecutive mutations of the APC, p53 and other genes. Microsatellite instability (DNA repair gene) skips this sequence (eg HNPCC). 20% have second tumour at diagnosis (usually adenoma or other carcinoma), 5% have second colorectal carcinoma (same time or subsequently). Increased risk with UC, Crohn, FAP, HNPCC, Peutz-Jeghers syndrome. Types include annular constricting (most, raised everted edges, ulcerated mucosa), polypoid (frondlinke villous carcinoma) or infiltrating scirrhous (rare, except in UC). Polypoid tumour >10mm, apple-core lesion (irregular thickening and narrowing, shouldering), cystic/necrotic/haemorrhagic areas (esp when large). Obstruction, oedema or ischaemia may thicken uninvolved proximal colon. Direct invasion through wall into pericolic fat, adjacent organs. Pericolic linear stranding indicates extension through wall. Metastases to LN (>10mm), liver and elsewhere. Intraperitoneal seeding may occur. Cx obstruction (common), perforation, intussusception, abscess, fistula. Local staging best with transrectal/colonoscopic US. Recurrence at operative site near anastomosis, in draining LN, peritoneal cavity or liver/metastases.


  • Low anterior resection (LAR) – resection along the circumferential resection margin (CRM), ie mesorectal fascia.
  • Ultra low anterior resection (ULAR) – extension of the resection into intersphincteric plane.
  • Abdominoperoneal resection (APR) – resection of rectum and anus, leaving a permanent end colostomy.
  • Neoadjuvant chemoradiotherapy – given for T3b, CRM, node positive disease or prior to APR.

Rectal MRI

Distance from anal verge to level of pelvic floor + distance to inferior part of tumour <5cm lower third, 5-10cm middle third and >10cm upper third. Measure length of tumour and describe clockface circumferential extension (lithotomy position with 12 o’clock anterior, 3 o’clock left). Distance/involvement of the tumour to the peritoneal reflection and anal sphincter should be described.

AJCC TNM Staging

  • Tumour. Ax and Cor T2 should be obliqued along the tumour.
    • Tis – Intramucosal or invasion of lamina propria.
    • T1 – Past lamina propria into submucosa. Villous adenoma may have a vascular stalk which breaches the muscularis (ie not T2 diseae).
    • T2 – Invades muscularis propria (loss of normal dark T2 line)
    • T3 – Through muscularis propria into pericolorectal tissues. Tumour is triangular/nodular, whereas desmoplastic is thin linear. T3 disease is usually at the mid-point of the tumour.
      • T3a <1mm beyond muscularis propria
      • T3b 1-5mm – 85% 5yr survival
      • T3c 5-10mm – 55% 5yr survival
      • T3d >15mm
    • T4 – Invades to involve the peritoneal reflection (4a) or invades/adherant to other organs/structures (4b).
  • Regional lymph nodes – Includes draining nodes within the mesorectal fascia (circumferential resection margin). Pelvic sidewall nodes outside the mesorectum is metastatic disease. Nodes are normal if oval and homogeneous <10mm. Any irregular contour, heterogeneity or low T2 signal is suspicious. Tumeral deposits are <3mm, nodes are >3mm.
    • N0 – No regional nodes.
    • N1 – 1-3 regional nodes. .
    • N2 – >/= 4 nodes.
  • Distant metastases
    • M0 – No metastases.
    • M1 – Distant metastases limited to one organ (1a) or >1 organ/site or peritoneum (1b).

Anal complex staging should be given for low rectal tumours. Axial and coronal T2 should be obliqued along the anal canal.

  • Stage 1 – partial thickness involvement of internal anal sphincter (muscularis propria)
  • Stage 2 – full thickness
  • Stage 3 – invades into intersphincteric space
  • Stage 4 – invades or <1mm from puborectalis

Measure shortest distance from the CRM (circumferential resection margin) to any T3/4 disease, LN, tumeral deposits or EMVI. The CRM is involved if <1mm.

Extramural vascular invasion (EMVI) – only occurs with T3/T4 disease. Abnormal intermediate T2 signal within vessels (normally dark T2 flow void ) or nodular thickening.

Staging of response to chemoradiation:

  • TRG 1: complete radiologic response with no evidence of any abnormality
  • TRG 2: >75% response with no obvious residual or minimal residual tumour. Mucinous change/response is T2 hyperintensity in tumour that was initially non-mucinous or heterogeneously mucinous. Fibrotic response is low T2 signal with loss of volume.
  • TRG 3: mix of fibrotic/mucinous resopnse and viable tumour
  • TRG 4: slight response (<25%), but mostly residual tumour
  • TRG 5: no response, same appearances as original tumour.

Tumours of the Anal Canal

Upper 1/3 lined by columnar rectal epithelium, middle 1/3 by transitional epithelium, lower 1/3 stratified squamous; carcinomas may hence be glandular or squamous. Basaloid tumours (cloacogenic carcinomas) are derived from immature cells in the basal layer of transitional epithelium. Pure squamous cell carcinomas are associated with HPV infection.


~1/3 of SB tumours. Low grade malignancy, from endocrine cells (enterochromaffin/Kulchitsky cells) in mucosa which produce serotonin and bradykinins. 20% in SB (esp ileum where they are commonly multiple). Carcinoid syndrome in 7% if liver metastases (liver inactivates the vasoactive substances) with flushing, cramps, diarrhoea. Primary lesion usually <15mm, mural nodule or intraluminal polyp, occasional central calcification. Luminal narrowing, fold and wall thickening, mesenteric mass (separating bowel loops), sunburst radiating mesenteric fibrosis (drawing loops together). Cx stricture, obstruction, infarction (fibrosis of vessels), intussusception. May locally recur or metastases to LN, liver, lung.

Gastrointestinal Stromal Tumour (GIST)

20-30% in SB, tend to be more aggressive than gastric GIST. Almost all mesenchymal tumours of GIT (true leuomyomas and leiomyosarcomas very rare), less common in colon cf stomach/SB. May also primarily arise in mesentery or omentum. Obstruction or bleeding. Submucosal mass with smooth mucosa, tends to ulcerate when >20mm, homogeneous HU similar to muscle. Malignant GIST tend to be >50mm, heterogeneous, prominent necrosis and haemorrhage. LN metastases uncommon. Calcification uncommon.


GIT involvement mostly SB esp distal ileum (more lymphoid tissue), less commonly stomach, caecum, rectum anus. Most B-cell NHL. Multiple in 10-25%. Increased risk with AIDS. Diffuse infiltration, exophytic mass, polypoid mass or multiple nodules. Aneurysmal dilatation due to replacement of muscularis and destruction of autonomic plexus without fibrosis (hence obstruction uncommon). Circumferential long segment wall, effacement of folds, narrowed widened or normal lumen, cavitation with fluid and debris, polypoid mass, eccentric wall thickening, shallow ulceration, rarely multiple variable-sized nodules. When in the mesentery causes straight and regular fold thickening from lymphatic obstruction; when infiltrates the bowel wall causes irregular nodular distorted fold thickening. Homogeneous with limited enhancement (cf prominent enhancement in GIST, adenocarcinoma). Mesenteric confluent mass may encase multiple loops, sandwich sign – sparing rind of fat around vessels. Adenopathy, hepatosplenomegaly.

  • Burkitt lymphoma – Aggressive with rapid doubling time, poor prognosis, children and young adults. Bulky tumour esp ileocaecal areas.
  • AIDS-related lymphoma – Aggressive, high-grade NHL, similar findings to other SB lymphoma. Adenopathy DDx: Kaposi sarcoma, MAI.

Nodular Lymphoid Hyperplasia

Enlarged lymphoid follicles. Peyers patches are normal aggregations of lymphoid follicles in the distal small bowel (ileum, not seen in the jejunum). Associated with hypogammaglobulinaemia esp low IgA. Diffuse uniform small 2-4mm nodules evenly distributed, may involve entire SB. If confined to TI and proximal colon is usually incidental, ?recent virus. If >5mm is associated with allergic, infectious and inflammatory disorders. May be associated with intussusception.


Common, via:

  • Peritoneal seeding – Serosa, mesenteric border, esp TI caecum and ascending colon due to flow of fluid from LUQ to RLQ. From ovaries, colon, stomach, pancreas.
  • Haematogenous spread – Antimesenteric border where vessels branch. From melanoma, lung, breast, colon, embryonal testicular carcinoma.


More common in ileum, caecum, ascending colon. From submucosal fat. Most asymptomatic incidental, may cause bleeding or intussusception. Smooth, well-defined, elliptical 10-30mm, change shape with compression.


Solitary, submucosal polypoid. Mostly jejunum. 2/3 present with bleeding. Occasional calcified phlebolith.


Acute Appendicitis

Lifetime risk 7%, most commonly adolescents/young adults, M slightly > F. Obstructed appendiceal lumen (in 50-80% by faecolith, gallstone, tumour or mass of worms) with continued mucosal secretions causing dilation, raised pressure imparing venous drainage, mucosal ulceration. Bacterial infection -> gangrene, perforation with abscess. Most abscesses are walled off, occasionally free perforation and pneumoperitoneum. Slow graded compression US or CT. Noncompressible appendix >6mm (outer wall to outer wall), hyperenhancing, adjacent echogenic stranding, calcified shadowing appendicolith (seen on XR in 14%, from laminated calcium with lucent around lucent nidus of inspissated faeces), discontinuous wall, caecal lumen deformed, localised ileus. Inflammatory mass is >20HU, liquefied abscess <20HU, those >30mm generally requires surgery or drainage. Complete contrast filling of appendix to tip excludes appendicitis.

Mucocoele of the Appendix

Distension of all or portion of appendix by sterile mucous, obstructed by appendicolith, foreign body, adhesions or tumour. Some caused by mucinous cystadenoma or cystadenocarcinoma of appendix. Continous mucus secretion causes up to 150mm well-defined cystic mass, may have peripheral calcification. Rupture may cause pseudomyxoma peritonei with gelatinous implants throught peritoneum, adhesions and mucinous ascites.

Appendiceal Neoplasms

  • Carcinoid (85%) – Most common location for carcinoid tumour (60%). Most near tip, round/nodular up to 25mm, solitary. Less likely to metastasize than elsewhere in GIT, carcinoid syndrome rare, mesenteric reaction usually absent.
  • Adenomas – Usually associated with FAP; isolated adenomas usually mucinous cystadenomas with mucocoele.
  • Adenocarcinoma – Rare, usually in setting of appendicitis in older adult. Soft tissue mass within or replacing appendix.


Ischaemic Bowel Disease

Due to collaterals and arcades, slowly progressing loss of blood supply from one artry (CA/SMA/IMA) is compensated. Acute occlusion may cause long-segment ischaemia. Mucosal infarction is limited by the muscularis mucosa; mural infarction involves mucosa and submucosa; transmural involves all 3 layers. Mucosal/mural usually from acute/chronic hypoperfusion; transmural from acute obstruction. Occlusion from atherosclerosis (esp origin), aortic aneurysm, hypercoagulable state, OCP, emboli (cardiac vegetation, aortic atheroma). Hypoperfusion from heart failure, shock, dehydration or vasoconstrictive drugs. Vasculidities include polyarteritis nodosum, Henoch-Shonlein purpura, Wegener granulomatosis. Venous occlusion is uncommon, from hypercoagulable states, invasive neoplasm, cirrhosis, trauma, extrinsic mass.

Epithelial cells are relatively resistant to initial trasient hypoxic injury; second phase of reperfusion injury causes the greatest damage. Watershed zones are most susceptible, including splenic flexure, rectosigmoid colon. Intestinal capillaries run from crypts to the surface before making a hairpin turn at the surface into venules; protects deeper crypts and epithelial stem cells but leaves surface epithelium vulnerable which atrophies/necroses and sloughes; crypts may be hyperproliferative. Mucosal/mural infarctions may repair if corrected or adequate collaterals form. Infarction may be continuous, but more commonly segmental/patchy. Mucosa is haemorrhagic, ulcerated, dark red/purple. Areas of transmural infarction are well-demarcated from normal bowel, congested dusky/purple-red. Venous occlusion result in less abrupt transitions. Gaseous distention, thickened mucosal folds with thumbprinting, intramural or portal venous gas, poor enhancement of bowel wall, engorged mesenteric vessels. Characterstic target appearance of bowel end-on with low density submucosal oedema. Mucosal breakdown may lead to septicaemia with high mortality.

Radiation Enterocolitis

The small bowel is the most radiosensitive organ. Slowly progressive end-arteritis causes ischaemia, fibrosis. Segmental thickened folds, impaired peristalsis, spiculation, ulceration. Fibrosis -> rigid featureless bowel, dense mesentery, tapered strictures, adhesions, fistulas. Healing may cause pseudopolyps and postinflammatory polyps.


Gross dilatation of lymphatics in mucosa and submucosa. Primary from congenital obstruction, associated with asymmetric limb oedema, doesn’t tend to present until young adult with protein-losing enteropathy, diarrhoea, infections. Secondary obstruction from radiation, CHF or mesenteric LN enlargement. Diffuse fold thickening worse in the jejunum, increased intraluminal fluid, tiny 1mm nodules (distended villi). DDx Whipple disease.


Most common in caecum and ascending colon >60. ?Normal distention and contraction intermittently occluding submucosal veins penetrating through the muscularis propria (causing focal dilatation and tortuosity of overlying veins), degenerative vascular changes, and/or developmental element. Distorted tangled dilated mucosal and submucosal veins with kinking replace normal mucosa and only thin layer of covering epithelium, no associated mass. Chronic bleeding -> anaemia, but may be acute massive (20% of major lower GI bleeds).


5% of population, from persistently elevated venous pressure in the haemorrhoidal plexus from straining (constipation) and venous stasis of pregnancy. Venous hypertension is relieved by the formation of porto-systemic collaterals. External haemorrhoids are located below the anorectal line (inferior haemorrhoidal plexus); internal in the distal rectum (superior haemorrhoidal plexus). Thin-walled dilated submucousal vessels.

Perianal Sepsis

Supralevator abscess not seen at EUA.