Radiology Review Manual
6th Edition

Gastrointestinal Tract
Differential Diagnosis of Gastrointestinal Disorders
Acute Abdomen in Child
  • Intussusception
  • Appendicitis
  • Obstruction (previous surgery, hernia)
  • Acute gastroenteritis
  • Basilar pneumonia
Gastrointestinal Hemorrhage
Mortality: approx. 10%
  • Barium examination should be avoided in acute bleeders!
Source:
  • UPPER GASTROINTESTINAL HEMORRHAGE
    • = bleeding site proximal to ligament of Treitz
    • @ Esophagogastric junction
      • Esophageal varices (17%): 50% mortality
      • Mallory-Weiss syndrome (7–14%): very low mortality
    • @ Stomach
      • Acute hemorrhagic gastritis (17–27%)
      • Gastric ulcer (10%)
      • Pyloroduodenal ulcer (17–25%)
      Mortality: <10% if under age 60; >35% if over age 60
    • @ Other causes (14%):
      • visceral artery aneurysm, vascular malformation, neoplasm, vascular-enteric fistula
      Average mortality: 8–10%
    • Rx:
      • Transcatheter embolization (method of choice) abundant collaterals except for postoperative stomach
      • Intraarterial vasopressin infusion (0.2–0.4 U/min)
      Prognosis: controls 73% of gastric mucosal bleeding; high recurrence rate
  • LOWER GASTROINTESTINAL HEMORRHAGE
    • = bleeding site distal to ligament of Treitz
    • @ Small intestine
      • tumor (eg, leiomyoma, hemangioma, metastases), ulcers, diverticula (eg, Meckel diverticulum), inflammatory bowel disease (eg, Crohn disease), vascular malformation, visceral artery aneurysm, aortoenteric fistula
    • @ Colorectal (70%)
      • — massive bleeding
        • Diverticula (most common): hemorrhage in 25% of patients with diverticulosis; spontaneous cessation of bleeding in 80%; recurrent bleeding in 25%
        • Colonic angiodysplasia (2nd most common cause) = most common vascular lesion; self limiting
        • Biopsy
      • — low-rate bleeding
        • Inflammatory bowel disease
        • Benign/malignant tumor
        • Mesenteric varices
    • Rx:
      • Intraarterial vasopressin infusion
        Prognosis: 90% initial control rate; in 30% recurrent bleeding
      • Transcatheter embolization
        • Requires superselective catheterization using microcatheters + microembolic agents
        Cx: 25% risk of bowel infarction + stricture
Gastrointestinal Bleeding in Infant
  • Peptic ulcer
  • Varices
  • Ulcerated Meckel diverticulum
Gastrointestinal Bleeding in Child
  • Meckel diverticulum
  • Juvenile polyp
  • Inflammatory bowel disease
  • Clotting disorder
  • Arteriovenous malformation
Intramural Hemorrhage
  • VASCULITIS
    • Henoch-Schönlein purpura
  • TRAUMA
  • COAGULATION DEFECT
    • Anticoagulant therapy
    • Thrombocytopenia
    • Disseminated intravascular coagulation
  • DISEASES WITH COAGULATION DEFECT
    • Hemophilia
    • Leukemia, lymphoma
    • Multiple myeloma
    • Metastatic carcinoma
    • Idiopathic thrombocytopenic purpura
  • ISCHEMIA (often fatal)
    • abdominal pain
    • melena
Site: submucosal/intramural/mesenteric
  • “stacked coin”/“picket fence” appearance of mucosal folds (due to symmetric infiltration of submucosal blood)
  • “thumbprinting” = rounded polypoid filling defect (due to focal accumulation of hematoma in bowel wall)
  • separation + uncoiling of bowel loops
  • narrowing of lumen + localized filling defects (asymmetric hematoma)
  • no spasm/irritability
  • mechanical obstruction + proximal distension of loops
Prognosis: resolution within 2–6 weeks
GI Abnormalities In Chronic Renal Failure And Renal Transplantation
  • @ Esophagus
    • Esophagitis: candida, CMV, herpes
  • P.754

  • @ Stomach & duodenum
    • Gastritis
      • thickened gastric folds (38%)
      • edema + erosions
      • Cause:
        • imbalance of gastrin levels + gastric acid secretion due to
          • reduced removal of gastrin from kidney with loss of cortical mass
          • impaired acid feedback mechanism
          • hypochlorhydria
        • opportunistic infection (eg, CMV)
    • Gastric ulcer (3.5%)
    • Duodenal ulcer (2.4%)
    • Duodenitis (47%)
  • @ Colon
    • More severely + frequently affected after renal transplantation
    • Progressive distention + pseudoobstruction
      Contributing factors: dehydration, alteration of diet, inactivity, nonabsorbable antacids, high-dose steroids
    • Ischemic colitis
      • primary disease responsible for end-stage renal disease (eg, diabetes, vasculitis)
      • trauma of renal transplantation
    • Diverticulitis
      Contributing factors: chronic obstipation, steroids, autonomic nervous dysfunction
    • Pseudomembranous colitis
    • Uremic colitis = nonspecific colitis
    • Spontaneous colonic perforation
      Cause: nonocclusive ischemia, diverticula, duodenal + gastric ulcers
  • @ Pancreas
    • Pancreatitis
      Cause: hypercalcemia, steroids, infection, immunosuppressive agents, trauma
  • @ General
    • GI hemorrhage
      Cause: gastritis, ulcers, colonic diverticula, ischemic bowel, infectious colitis, pseudomembranous colitis, nonspecific cecal ulceration
    • Bowel perforation (in 1–4% of transplant recipients)
    • Opportunistic infection
      Organism: Candida, herpes, CMV, Strongyloides
    • Malignancy
      • skin tumors
      • lymphoma
Enteropathy
Protein-Losing Enteropathy
  • DISEASE WITH MUCOSAL ULCERATION
    • Carcinoma
    • Lymphoma
    • Inflammatory bowel disease
    • Peptic ulcer disease
  • HYPERTROPHIED GASTRIC RUGAE
    • Ménétrier disease
  • NONULCERATIVE MUCOSAL DISEASE
    • Celiac disease
    • Tropical sprue
    • Whipple disease
    • Allergic gastroenteropathy
    • Gastrocolic fistula
    • Villous adenoma of colon
  • LYMPHATIC OBSTRUCTION
    • Intestinal lymphangiectasia
  • HEART DISEASE
    • Constrictive pericarditis
    • Tricuspid insufficiency
Malabsorption
  • = deficient absorption of any essential food materials within small bowel
  • PRIMARY MALABSORPTION
    • = the digestive abnormality is the only abnormality present
    • Celiac disease = nontropical sprue
    • Tropical sprue
    • Disaccharidase deficiencies
  • SECONDARY MALABSORPTION
    • = occurring during course of gastrointestinal disease
    • enteric
      • Whipple disease
      • Parasites: hookworm, Giardia, fish tapeworm
      • Mechanical defects: fistulas, blind loops, adhesions, volvulus, short circuits
      • Neurologic: diabetes, functional diarrhea
      • Inflammatory: enteritis (viral, bacterial, fungal, nonspecific)
      • Endocrine: Zollinger-Ellison syndrome
      • Drugs: neomycin, phenindione, cathartics
      • Collagen disease: scleroderma, lupus, polyarteritis
      • Lymphoma
      • Benign + malignant small bowel tumors
      • Vascular disease
      • CHF, agammaglobulinemia, amyloid, abetalipoproteinemia, intestinal lymphangiectasia
    • gastric
      • vagotomy, gastrectomy, pyloroplasty, gastric fistula (to jejunum, ileum, colon)
    • pancreatic
      • pancreatitis, pancreatectomy, pancreatic cancer, cystic fibrosis
    • hepatobiliary
      • intra- and extra-hepatic biliary obstruction, acute + chronic liver disease
Roentgenographic Signs in Malabsorption
  • SMALL BOWEL WITH NORMAL FOLDS + FLUID
    • Maldigestion (deficiency of bile salt/pancreatic enzymes)
    • Gastric surgery
    • Alactasia
  • SMALL BOWEL WITH NORMAL FOLDS + WET
    • Sprue
    • Dermatitis herpetiformis
  • P.755

  • DILATED DRY SMALL BOWEL
    • Scleroderma
    • Dermatomyositis
    • Pseudoobstruction: no peristaltic activity
  • DILATED WET SMALL BOWEL
    • Sprue
    • Obstruction
    • Blind loop
  • THICKENED STRAIGHT FOLDS + DRY SMALL BOWEL
    • Amyloidosis (malabsorption is unusual)
    • Radiation
    • Ischemia
    • Lymphoma (rare)
    • Macroglobulinemia (rare)
  • THICKENED STRAIGHT FOLDS + WET SMALL BOWEL
    • Zollinger-Ellison syndrome
    • Abetalipoproteinemia: rare inherited disease characterized by CNS damage, retinal abnormalities, steatorrhea, acanthocytosis
  • THICKENED NODULAR IRREGULAR FOLDS + DRY SMALL BOWEL
    • Lymphoid hyperplasia
    • Lymphoma
    • Crohn disease
    • Whipple disease
    • Mastocytosis
  • THICKENED NODULAR IRREGULAR FOLDS + WET SMALL BOWEL
    • Lymphangiectasia
    • Giardiasis
    • Whipple disease (rare)
Small Bowel Nodularity with Malabsorption
mnemonic: What is His Main Aim? Lay Eggs, By God
  • W hipple disease
  • I ntestinal lymphangiectasia
  • H istiocytosis
  • M astocytosis
  • A myloidosis
  • L ymphoma, L ymph node hyperplasia
  • E dema
  • B lood
  • G iardiasis
Abdominal Mass
Abdominal Mass in Neonate
  • RENAL (55%)
    • Hydronephrosis (25%)
    • Multicystic dysplastic kidney (15%)
    • Polycystic kidney
    • Mesoblastic nephroma
    • Renal vein thrombosis
  • GENITAL (15%)
    • Ovarian cyst
    • Hydrometrocolpos
  • GASTROINTESTINAL (15%)
    • Duplication
    • Volvulus
    • Cystic meconium peritonitis
    • Mesenteric cyst
  • NONRENAL RETROPERITONEAL (10%)
    • Adrenal hemorrhage
    • Neuroblastoma
    • Teratoma
  • HEPATOBILIARY (5%)
    • Hemangioendothelioma
    • Choledochal cyst
    • Hydrops of gallbladder
Abdominal Mass in Infant &Child
  • RENAL (55%)
    • Wilms tumor (22%)
    • Hydronephrosis (20%)
    • Cystic renal mass
    • Congenital anomaly
  • NONRENAL RETROPERITONEAL (23%)
    • Neuroblastoma (21%)
    • Teratoma
  • GASTROINTESTINAL (18%)
    • Appendiceal abscess (10%)
    • Hepatobiliary (6%)
  • GENITAL (4%)
    • Ovarian cyst/teratoma
    • Hydrometrocolpos
Abnormal Intraabdominal Air
Abnormal Air Collection
  • Abnormally located bowel
    • Chilaiditi syndrome (= colon interposed between liver and chest wall), inguinal hernia
  • Pneumoperitoneum
  • Retropneumoperitoneum
    • perforation of duodenum/rectum/ascending + descending colon, diverticulitis, ulcerative disease, endoscopic procedure
  • Gas in bowel wall
    • gastric pneumatosis, phlegmonous gastritis, endoscopy, rupture of lung bulla
  • Gas within abscess
    • located in subphrenic, renal, perirenal, hepatic, pancreatic space, lesser sac
  • Gas in biliary system = pneumobilia
  • Gas in portal venous system
Pneumoperitoneum
Cause:
  • DISRUPTION OF WALL OF HOLLOW VISCUS
    • trauma
    • iatrogenic perforation
    • diseases of GI tract
      • Perforated gastric/duodenal ulcer
      • Perforated appendix
      • Ingested foreign-body perforation
      • Diverticulitis (ruptured Meckel diverticulum/sigmoid diverticulum, jejunal diverticulosis)
      • Necrotizing enterocolitis with perforation
      • P.756

      • Inflammatory bowel disease (eg, toxic megacolon)
      • Obstruction† (gas traversing intact mucosa): neoplasm, imperforate anus, Hirschsprung disease, meconium ileus
      • Ruptured pneumatosis cystoides intestinalis† with “balanced pneumoperitoneum” (= free intraperitoneal air acts as tamponade of pneumatosis cysts thus maintaining a balance between intracystic air + pneumoperitoneum)
      • Idiopathic gastric perforation = spontaneous perforation in premature infants (congenital gastric muscular wall defect)
  • THROUGH PERITONEAL SURFACE
    • transperitoneal manipulation
      • Abdominal needle biopsy/catheter placement
      • Mistaken thoracentesis/chest tube placement
      • Endoscopic biopsy
    • extension from chest†
      • Dissection from pneumomediastinum (positive pressure breathing, rupture of bulla/bleb, chest surgery)
      • Bronchopleural fistula
    • rupture of urinary bladder
    • penetrating abdominal injury
  • THROUGH FEMALE GENITAL TRACT†
    • iatrogenic
      • Perforation of uterus/vagina
      • Culdocentesis
      • Rubin test = tubal patency test
      • Pelvic examination
    • spontaneous
      • Intercourse, orogenital insufflation
      • Douching
      • Knee-chest exercise, water skiing, horseback riding
  • INTRAPERITONEAL
    • Gas-forming peritonitis
    • Rupture of abscess
Note† = asymptomatic spontaneous pneumoperitoneum without peritonitis
  • air in lesser peritoneal sac
  • gas in scrotum (through open processus vaginalis)
  • Large collection of gas:
    • abdominal distension, no gastric air-fluid level
    • “football sign” = large pneumoperitoneum outlining entire abdominal cavity
    • “double wall sign” = “Rigler sign” = “bas-relief sign”
      • = air outlining the luminal + serosal surface of the bowel wall with patient in supine position (usually requires >1,000 mL of free intraperitoneal gas + intraperitoneal fluid)
      • [Leo Rigler (1896–1979), radiologist in Minneapolis, USA]
    • “telltale triangle sign” = triangular air pocket between 3 loops of bowel
    • depiction of diaphragmatic muscle slips = two or three 6–13-cm long and 8–10-mm wide arcuate soft-tissue bands directed vertically inferiorly + arching parallel to diaphragmatic dome superiorly
    • outline of ligaments of anterior inferior abdominal wall:
    • “inverted V sign” = outline of both lateral umbilical ligaments (containing inferior epigastric vessels)
    • outline of medial umbilical ligaments (obliterated umbilical arteries)
    • “urachus sign” = outline of middle umbilical ligament
  • RUQ gas (best place to look for small collections):
    • single large area of hyperlucency over the liver
    • oblique linear area of hyperlucency outlining the posteroinferior margin of liver
    • doge’s cap sign = triangular collection of gas in Morison pouch (posterior hepatorenal space)
    • outline of falciform ligament = long vertical line to the right of midline extending from ligamentum teres notch to umbilicus; most common structure outlined
    • ligamentum teres sign = air outlining fissure of ligamentum teres hepatis (= posterior free edge of falciform ligament) seen as vertically oriented sharply defined slitlike/oval area of hyperlucency between 10th and 12th rib within 2.5–4.0 cm of right vertebral border 2–7 mm wide and 6–20 mm long
    • ligamentum teres notch = inverted V-shaped area of hyperlucency along undersurface of liver
    • “saddlebag/mustache/cupola sign” = gas trapped below central tendon of diaphragm
    • parahepatic air = gas bubble lateral to right edge of liver
Iatrogenic Pneumoperitoneum
  • Laparotomy/laparoscopy (58%)
    • absorbed in 1–24 days dependent on initial amount of air introduced and body habitus (80% in asthenic, 25% in obese patients)
    • After 3 days free air should be followed with suspicion!
  • Leaking surgical anastomosis
  • Peritoneal dialysis
  • Feeding tube placement
  • Endoscopic perforation
  • Enema tip injury
  • Use of gynecologic instruments
  • Vigorous respiratory resuscitation
  • Diagnostic pneumoperitoneum
Spontaneous Pneumoperitoneum
  • Peptic perforation
  • Ischemia
  • Bowel obstruction
  • Toxic megacolon
  • Inflammation: appendicitis, tuberculosis, necrotizing enteroccolitis
Traumatic Pneumoperitoneum
  • Blunt trauma
  • Penetrating trauma:
    • Perforating foreign body (eg, thermometer injury to rectum, vaginal stimulator in rectum)
    • Compressor air directed toward anus
Miscellaneous Causes of Pneumoperitoneum
  • Drugs: steroids, NSAID
  • Pneumatosis coli/intestinalis
  • Entry through female genital tract: douching, sexual intercourse, insufflation
P.757

Pseudopneumoperitoneum
  • = process mimicking free air
  • ABDOMINAL GAS
    • gastrointestinal gas
      • Pseudo-wall sign = apposition of gas-distended bowel loops
      • Chilaiditi syndrome
      • Diaphragmatic hernia
      • Diverticulum of esophagus/stomach/duodenum
    • extraintestinal gas
      • Retroperitoneal air
      • Subdiaphragmatic abscess
  • CHEST
    • Pneumothorax
    • Empyema
    • Irregularity of diaphragm
  • FAT
    • Subdiaphragmatic intraperitoneal fat
    • Interposition of omental fat between liver + diaphragm
Pneumoretroperitoneum
Cause:
  • Traumatic rupture (usually duodenum)
  • Perforation of duodenal ulcer
  • Gas abscess of pancreas (usually extends into lesser sac)
  • Urinary tract gas (trauma, infection)
  • Dissected mediastinal air
  • kidney outlined by gas
  • outline of psoas margin ± gas streaks in muscle bundles
Pneumatosis Intestinalis
  • = PNEUMATOSIS CYSTOIDES INTESTINALIS = BULLOUS EMPHYSEMA OF THE INTESTINE = INTESTINAL GAS CYSTS = PERITONEAL LYMPHOPNEUMATOSIS
  • Cause:
    • Attributed to at least 58 causative factors!
    • BOWEL NECROSIS/GANGRENE
      • Most common + life-threatening cause!
      Pathogenesis: damage + disruption of mucosa with entry of gas-forming bacteria into bowel wall (cysts contain 50% hydrogen = evidence of bacterial origin)
      • necrotizing enterocolitis, ischemia + infarction (mesenteric thrombosis), neutropenic colitis, sepsis, volvulus, emphysematous gastritis, caustic ingestion
    • MUCOSAL DISRUPTION
      Pathogenesis: increased intestinal gas pressure leads to overdistension and dissection of gas into bowel wall
      • intestinal obstruction:
        • pyloric stenosis, annular pancreas, imperforate anus, Hirschsprung disease, meconium plug syndrome, obstructing neoplasm
      • intestinal trauma:
        • endoscopy ± biopsy, biliary stent perforation, sclerotherapy, bowel surgery, postoperative bowel anastomosis, penetrating/blunt abdominal trauma, trauma of child abuse, intracatheter jejunal feeding tube, barium enema
      • infection/inflammation:
        • peptic ulcer disease, intestinal parasites, tuberculosis, peritonitis, inflammatory bowel disease (Crohn disease, ulcerative colitis, pseudomembranous colitis), ruptured jejunal diverticula, Whipple disease, systemic amyloidosis
    • INCREASED MUCOSAL PERMEABILITY
      Pathogenesis: defects in lymphoid tissue of bowel wall allows bacterial gas to enter bowel wall
      • immunotherapy:
        • graft-versus-host disease, organ transplantation, bone marrow transplantation
      • others:
        • AIDS enterocolitides, steroid therapy, chemotherapy, radiation therapy, collagen vascular disease (scleroderma, systemic lupus erythematosus, periarteritis dermatomyositis), intestinal bypass enteropathy, diabetes mellitus
    • PULMONARY DISEASE
      Pathogenesis: alveolar rupture with air dissecting interstitially along bronchovascular bundles to mediastinum + retroperitoneally along vascular supply of viscera
      Cause: Chronic obstructive pulmonary disease (chronic bronchitis, emphysema, bullous disease of lung), asthma, cystic fibrosis, chest trauma (barotrauma from artificial ventilation, chest tube), increased intrathoracic pressure associated with retching + vomiting
    Path: (a) microvesicular type = 10–100-mm cysts/bubbles within lamina propria
    (b) linear/curvilinear type = streaks of gas oriented parallel to bowel wall
    Location: any part of GI tract; may be discontinuous with spread to distant sites along mesentery
    Site: subserosa > submucosa > muscularis > mesentery; mesenteric side >> antimesenteric side
  • radiolucent clusters of cysts along contour of bowel wall (best demonstrated on CT)
  • segmental mucosal nodularity (DDx: polyposis)
  • ± pneumoperitoneum/pneumoretroperitoneum (asymptomatic large pneumoperitoneum may persist for months/years)
  • ± gas in mesenteric + portal vein
  • Prognosis:
    • wide spectrum from innocuous to fatal; clinical outcome impossible to predict based on x-ray findings
    • Linear gas collections probably have a more severe connotation
    • Pneumatosis of the colon is likely clinically insignificant
    • Extent of pneumatosis is inversely related to severity of disease
Soap-bubble Appearance in Abdomen of Neonate
  • Feces in infant fed by mouth
  • Meconium ileus:
    • gas mixed with meconium, usually RLQ
  • P.758

  • Meconium plug:
    • gas in and around plug, in distribution of colon
  • Necrotizing enterocolitis: submucosal pneumatosis
  • Atresia/severe stenosis: pneumatosis
  • Hirschsprung disease:
    • impacted stool, sometimes pneumatosis
Abdominal Calcifications & Opacities
Opaque Material in Bowel
mnemonic: CHIPS
  • C hloral hydrate
  • H eavy metals (lead)
  • I ron
  • P henothiazines
  • S alicylates
Diffuse Abdominal Calcifications
  • Cystadenoma of ovary
    • granular, sandlike psammomatous calcifications
  • Pseudomyxoma peritonei
    • pseudomucinous adenoma of ovary
    • mucocele of appendix
  • Undifferentiated abdominal malignancy
  • Tuberculous peritonitis
    • mottled calcifications simulating residual barium
  • Meconium peritonitis
  • Oil granuloma
    • annular/plaquelike calcifications
Focal Alimentary Tract Calcifications
  • ENTEROLITHS
    • Appendicolith: in 10–15% of acute appendicitis
    • Stone in Meckel diverticulum
    • Diverticular stone
    • Rectal stone
    • Proximal to partial obstruction (eg, tuberculosis, Crohn disease)
  • MESENTERIC CALCIFICATIONS
    • Dystrophic calcification of omental fat deposits + appendices epiploicae (secondary to infarction/pancreatitis/TB)
    • Cysts: mesenteric cyst, hydatid cyst
    • Calcified mesenteric lipoma
  • INGESTED FOREIGN BODIES
    • trapped in appendix, diverticula, proximal to stricture
    • 1. Calcified seeds + pits (bezoar)
    • 2. Birdshot
    • Location of intraluminal lodgement:
      • esophagus (68%), stomach (11.6%), small bowel (3.3%), colon (11.6%)
  • TUMOR
    • Mucocele of appendix
      • crescent-shaped/circular calcification
    • Mucinous adenocarcinoma of stomach/colon
      • = COLLOID CARCINOMA
      • small mottled/punctate calcifications in primary site ± in regional lymph node metastases, adjacent omentum, metastatic liver foci
    • Gastric/esophageal leiomyoma: calcifies in 4%
    • Lipoma
Abdominal Wall Calcifications
  • IN SOFT TISSUES
    • Hypercalcemic states
    • Idiopathic calcinosis
  • IN MUSCLE
    • parasites:
      • Cysticercosis = Taenia solium
        • round/slightly elongated calcifications
      • Guinea worm = dracunculiasis
        • stringlike calcifications up to 12 cm long
    • injection sites
      • from quinine, bismuth, calcium gluconate, calcium penicillin
    • myositis ossificans
  • IN SKIN
    • Soft-tissue nodules: papilloma, neurofibroma, melanoma, nevi
    • Scar:
      • linear density
    • Colostomy/ileostomy
    • Tattoo markings
Abdominal Vascular Calcifications
  • ARTERIES
    • Atheromatous plaques
    • Arterial calcifications in diabetes mellitus
  • VEINS
    • phleboliths = calcified thrombus, generally seen below interspinous line
    • Normal/varicose veins
    • Hemangioma
  • LYMPH NODES
    • Histoplasmosis/tuberculosis
    • Chronic granulomatous disease
    • Residual lymphographic contrast
    • Silicosis
Abnormal Intraabdominal Fluid
Ascites
Cause:
  • TRANSUDATE
    • Cirrhosis (75%): poor prognostic sign
    • Hypoproteinemia
    • CHF
    • Constrictive pericarditis
    • Chronic renal failure
    • Budd-Chiari syndrome
  • EXUDATE
    • Carcinomatosis
    • Polyserositis
    • TB peritonitis
    • Pancreatitis
    • Meigs syndrome
  • HEMORRHAGIC/CHYLOUS FLUID
  • Early signs (accumulation in pelvis):
    • round central density in pelvis + ill-defined bladder top
    • thickening of peritoneal flank stripe
    • P.759

    • space between properitoneal fat and gut >3 mm
  • Late signs:
    • Hellmer sign = medial displacement of lateral liver margins
    • medial displacement of ascending + descending colon
    • obliteration of hepatic + splenic angles
    • bulging flanks
    • gray abdomen
    • floating centralized loops
    • separation of loops
High-density Ascites
  • Tuberculosis: 20–45 HU; may be lower
  • Ovarian tumor
  • Appendiceal tumor
Neonatal Ascites
  • GASTROINTESTINAL
    • perforation of hollow viscus
      • Meconium peritonitis
    • inflammatory lesions
      • Meckel diverticulum
      • Appendicitis
    • cyst rupture
      • Mesenteric cyst
      • Omental cyst
      • Choledochal cyst
    • bile leakage
      • Biliary obstruction
      • Biliary perforation
  • PORTOHEPATIC
    • extrahepatic portal vein obstruction
      • Atresia of veins
      • Compression by mass
    • intrahepatic portal vein obstruction
      • Portal cirrhosis (neonatal hepatitis)
      • Biliary cirrhosis (biliary atresia)
  • URINARY TRACT
    • Urine ascites (most common cause) from lower urinary tract obstruction + upper urinary tract rupture: posterior/anterior urethral valves, ureterovesical/ureteropelvic junction obstruction, renal/bladder rupture, anterior urethral diverticulum, bladder diverticula, neurogenic bladder, extrinsic bladder mass
  • GENITAL
    • Ruptured ovarian cyst
    • Hydrometrocolpos
  • HYDROPS FETALIS
    • Immune hydrops
    • Nonimmune hydrops (usually cardiac causes)
  • MISCELLANEOUS
    • Chylous ascites
    • Lymphangiectasia
    • Congenital syphilis, trauma
    • Idiopathic
Chylous Ascites
IN ADULTS: 1. Inflammatory process (35%)
2. Tumor (30%)
3. Idiopathic (23%)
4. Trauma (11%)
5. Congenital (1%)
IN CHILDREN: 1. Congenital (39%)
2. Inflammatory process (15%)
3. Trauma (12%)
4. Tumor (3%)
5. Idiopathic (33%)
Fluid Collections
mnemonic: BLUSCHINGS
  • Biloma
  • Lymphocele, Lymphangioma, Lymphoma (almost anechoic by US)
  • Urinoma
  • Seroma
  • Cyst (pseudocyst, peritoneal inclusion cyst)
  • Hematoma (aneurysm, AVM)
  • Infection, Infestation (empyema, abscess, Echinococcus)
  • Neoplasm (necrotic)
  • GI tract (dilated loops, ileus, duplication)
  • Serosa (ascites, pleural fluid, pericardial effusion)
Intraabdominal Cyst in Childhood
  • Omental cyst (greater omentum/lesser sac, multilocular)
  • Mesenteric cyst (between leaves of small bowel mesentery)
  • Choledochal cyst
  • Intestinal duplication
  • Ovarian cyst
  • Pancreatic pseudocyst
  • Cystic renal tumor
  • Abscess
  • Meckel diverticulum (communicates with GI tract)
  • Lymphangioma
  • Mesenteric lymphoma
  • Intramural tumor
Mechanical Intestinal Obstruction
  • = occlusion/constriction of bowel lumen
Prevalence: 20% of acute abdominal admissions
— 80% small bowel obstruction
— 20% large bowel obstruction
Air Progression in Neonates
stomach within minutes after birth
entire small bowel within 3 hours
sigmoid colon after 8–9 hours
Cause of Absent Gas in Neonate
  • GI obstruction
  • Mechanical ventilation in severe respiratory distress
  • Continuous gastric suction
Cause of Delayed Passage of Gas in Neonate
  • Traumatic delivery
  • Septicemia
  • Hypoglycemia
  • Brain damage
Passage of Meconium
  • NORMAL
    • in 94% within 24 hours
    • P.760

    • in 99% within 48 hours
    exceptions: prematurity, severely asphyxiated term infants
  • DELAYED PASSAGE
    • Hirschsprung disease
    • Ileal/jejunal atresia
    • Meconium ileus
    • Meconium plug syndrome
    • Colon atresia
    • Imperforate anus
Common Causes of Obstruction in Children
Time of presentation:
Nursery Intestinal atresia, midgut volvulus, meconium ileus, Hirschsprung disease, small bowel atresia with meconium ileus, meconium plug syndrome, small left colon syndrome, imperforate anus, obstruction from duplication cyst
First 3 months Hypertrophic pyloric stenosis, inguinal hernia, Hirschsprung disease, midgut volvulus
6–24 months Ileocolic intussusception
Childhood Appendicitis
Terminology:
  • High obstruction = proximal to midileum
    • Rarely needs further radiologic evaluation
    • • bilious vomiting (after first feeding)
    • • abdominal distention
    • few dilated bowel loops
  • Low obstruction = distal ileum/colon
    • More difficult to accurately localize
    • Requires contrast enema examination to diagnose microcolon, position of cecum, level of obstruction
    • • abdominal distention + vomiting
    • • failure to pass meconium
    • many dilated intestinal loops
Intestinal Obstruction in Neonate:
  • abdominal distension
  • vomiting
  • failure to pass meconium
  • Duodenal atresia (50%), stenosis (40%), web (10%)
  • Midgut volvulus
  • Jejunal/ileal atresia
  • Meconium ileus
  • Meconium plug syndrome
  • Hirschsprung disease
  • Necrotizing enterocolitis
NEONATAL OBSTRUCTION WITH MICROCOLON
  • Ileal atresia
  • Distal jejunal atresia
  • Meconium ileus
NEONATAL OBSTRUCTION WITH NORMAL COLON
  • Meconium plug
  • Hirschsprung disease
Intestinal Obstruction in Infant & Child
  • Hypertrophic pyloric stenosis
  • Appendicitis
  • Intussusception
Gastric Outlet Obstruction
  • CONGENITAL LESION
    • Antral mucosal diaphragm = antral web
    • Gastric duplication: usually along greater curvature, abdominal mass in infancy
    • Hypertrophic pyloric stenosis
  • INFLAMMATORY NARROWING
    • Peptic ulcer disease: cause in adults in 60–65%
    • Corrosive gastritis
    • Crohn disease, sarcoidosis, syphilis, tuberculosis
  • MALIGNANT NARROWING
    • Antral carcinoma: cause in adults in 30–35%
    • Scirrhous carcinoma of pyloric channel
  • OTHERS
    • Prolapsed antral polyp/mucosa
    • Bezoar
    • Gastric volvulus
    • Postoperative stomal edema
  • Abdominal plain film:
    • large smoothly marginated homogeneous mass displacing transverse colon + small bowel inferiorly
    • one/two air-fluid levels
Duodenal Obstruction
Cause:
  • CONGENITAL
    • Annular pancreas
    • Peritoneal bands = Ladd bands
    • Aberrant vessel
  • INFLAMMATORY NARROWING
    • Chronic duodenal ulcer scar
    • Acute pancreatitis: phlegmon, abscess, pseudocyst
    • Acute cholecystitis: perforated gallstone
  • INTRAMURAL HEMATOMA
    • Blunt trauma (accident, child abuse)
    • Anticoagulant therapy
    • Blood dyscrasia
  • TUMORAL NARROWING
    • Primary duodenal tumors
    • Tumor invasion from pancreas, right kidney, lymph node enlargement
  • EXTRINSIC COMPRESSION
    • Aortic aneurysm
    • Pseudoaneurysm
  • OTHERS
    • Superior mesenteric artery syndrome from extensive burns, body cast, rapid weight loss, prolonged bed rest
    • Bezoar (in gastrectomized patient)
mnemonic: VA BADD TU BADD
child adult
Volvulus Tumor
Atresia Ulcer
Bands Bands
Annular pancreas Annular pancreas
Duplication Duplication
Diverticulum Diverticulum
P.761

  • Abdominal plain film:
    • double-bubble sign = air-fluid levels in stomach + duodenum
    • frequently normal due to absence of gas from vomiting
Jejunal and Ileal Obstruction
  • = SMALL BOWEL OBSTRUCTION (SBO)
Frequency: accounts for 20% of all surgical admissions
Mortality: 5.5% (dictum: “Never let the sun rise or set on small-bowel obstruction”)
Cause:
  • CONGENITAL
    • Jejunal atresia
    • Ileal atresia/stenosis
    • Enteric duplication: located on antimesenteric side, mostly in ileum
    • Midgut volvulus from arrest in rotation + fixation of small bowel during fetal life
    • Mesenteric cyst from meconium peritonitis:located on mesenteric side
    • Meckel diverticulum
  • EXTRINSIC BOWEL LESION
    • Fibrous adhesions (50–75%) from previous surgery (80%), peritonitis (15%), congenital/uncertain cause (5%)
    • Hernia (10%): internal/external
    • Volvulus
    • Masses: extrinsic neoplasm (most commonly advanced peritoneal carcinomatosis), abscess, aneurysm, hematoma, endometriosis
  • LUMINAL OCCLUSION
    • swallowed:
      • Foreign body: in children; mentally disturbed/disabled patients
      • Bezoar
      • Gallstone
      • Inspissated milk
      • Bolus of Ascaris lumbricoides
    • after birth:
      • Meconium ileus:
        • microcolon in cystic fibrosis
      • Meconium ileus equivalent
    • other:
      • Intussusception
      • Tumor (rare): eg, lipoma
  • INTRINSIC BOWEL WALL LESION
    • neoplasm
      • Adenocarcinoma
      • Carcinoid tumor
      • Lymphoma
      • Gastrointestinal stromal tumor
    • inflammatory lesion
      • Crohn disease
      • Tuberculous enteritis
      • Eosinophilic gastroenteritis
      • Parasitic disease
    • vascular insufficiency
      • Ischemia (arterial/venous occlusion)
      • Radiation enteropathy
    • intramural hemorrhage
      • Blunt trauma
      • Henoch-Schönlein purpura
      • Anticoagulants
    • strictures
      • Surgical anastomosis
      • Irradiation
      • Potassium chloride tablets
      • Massive deposition of amyloid
Plain abdominal radiograph (50–66% sensitive):
  • “candy cane” appearance in erect position = >3 distended small bowel loops >3 cm with gas-fluid levels (>3–5 hours after onset of obstruction)
  • disparity in size between obstructed loops and contiguous small bowel loops of normal caliber beyond site of obstruction
  • small bowel positioned in center of abdomen
  • little/no gas + stool in colon with complete mechanical obstruction after 12–24 hours
  • “stretch sign” = erectile valvulae conniventes completely encircle bowel lumen
  • “stepladder appearance” in low obstruction (the greater the number of dilated bowel loops, the more distal the site of obstruction)
  • “string-of-beads” indicate peristaltic hyperactivity to overcome mechanical obstruction
  • hyperactive peristalsis/aperistalsis = fatigued small bowel
  • “snake head” appearance = active peristalsis forms bulbous head of barium column in an attempt to overcome obstruction
  • barium appears in colon >12 hours
CAVE: little/no gas in small bowel from fluid-distended loops may lead one to overlook obstruction
Location of obstruction:
  • valvulae conniventes high + frequent = jejunum
  • valvulae conniventes sparse/absent = ileum
Plain abdominal radiographic categories:
  • Normal
    • = absence of small intestinal gas/gas within 3–4 variably shaped loops <2.5 cm in diameter
  • Mild small bowel stasis
    • = single/multiple loops of 2.5–3 cm in diameter with ≥3 air-fluid levels
  • Probable SBO pattern
    • = dilated multiple gas-/fluid-filled loops with air-fluid levels + moderate amount of colonic gas
  • Definite SBO pattern
    • = clearly disproportionate gaseous/fluid distension of small bowel relative to colon
UGI:
  • snake head appearance = active peristalsis forms bulbous head of barium column in an attempt to overcome obstruction
  • barium appears in colon >12 hours
Enteroclysis for adhesive obstruction:
  • abrupt change in caliber of bowel with normal caliber/collapsed bowel distal to obstruction
  • stretched folds of normal pattern
  • P.762

  • angulated + fixed bowel segment
Enteroclysis categories of SBO (Shrake):
  • low-grade partial SBO
    • = sufficient flow of contrast material through point of obstruction so that fold pattern beyond obstruction is readily defined
  • high-grade partial SBO
    • = stasis + delay in arrival of contrast so that contrast material is diluted in distended prestenotic loop with minimal contrast in postobstructive loop leading to difficulty in defining fold pattern after transition point
  • complete SBO
    • = no passage of contrast material 3–24 hours after start of examination
CT (66% accurate, 78% specific, 63% sensitive, [81% sensitive for high-grade obstruction, 48% sensitive for low-grade partial obstruction]):
  • small bowel dilatation >2.5 cm (not reliable to distinguish from adynamic ileus):
    • “small bowel feces” sign = gas bubbles mixed with particulate matter immediately proximal to obstruction (DDx: cystic fibrosis)
  • discrepant caliber at transition zone from dilated to nondilated bowel:
    • level of obstruction best determined by relative lengths of dilated versus collapsed bowel
    • passage of contrast material through transition zone indicates incomplete obstruction
  • triangular beak immediately beyond dilated segment = point of transition
DDx: adynamic ileus (distension of entire small bowel)
US:
  • small bowel loops dilated >3 cm
  • length of dilated segment >10 cm
  • increased peristalsis of dilated segment (may become paralytic in prolonged obstruction)
  • colon collapsed
Strangulated Obstruction:
  • = impaired circulation/ischemia of obstructed segment
Prevalence: 5–10–42% of patients with SBO
At risk: patients with acute complete/high-grade SBO; risk increases over time
TRIAD:
  • closed-loop obstruction of the involved segment (majority of cases)
  • mechanical obstruction proximal to the involved segment
  • venous congestion of the involved loop
CT (63–100% detection rate):
  • slight circumferential thickening of bowel wall:
    • increased wall attenuation
    • target/halo sign
  • serrated beaklike narrowing at site of obstruction (32–100% specific) = closed loop with regional mesenteric vascular engorgement + bowel wall thickening at the obstructed segment
  • unusual course of mesenteric vasculature
  • vascular compromise of affected bowel:
    • poor/no enhancement of bowel wall (100% SPECIFIC)
    • delayed prolonged enhancement of bowel wall
    • mesenteric haziness due to edema (95% specific)
    • diffuse engorgement of mesenteric vasculature
    • localized mesenteric fluid/hemorrhage
  • large amount of ascites
  • pneumatosis intestinalis
  • gas in portal vein
Prognosis:
  • 20–37% mortality rate (compared with 5–8% for a recently reduced simple obstruction) due to delay in diagnosis: 8% for surgery performed in <36 hours, 25% mortality for surgery performed in >36 hours
CLOSED-LOOP OBSTRUCTION
  • = obstruction at two points along the course of the bowel at a single site usually with involvement of mesentery
Pathophysiology: impaired venous ± arterial flow
  • Most common cause of strangulation!
Cause: adhesion (75%), incarcerated hernia
  • fixation of bowel loop = no change in position:
    • “coffee bean sign” = gas-filled loop
    • “pseudotumor” = fluid-filled loop
    • U- or C-shaped dilated bowel loop on CT
  • increasing intraluminal fluid
  • “beak sign” = point of obstruction on CT/UGI
  • “whirl sign” = twisting of bowel + mesentery on CT:
    • stretched engorged mesenteric vessels converging toward site of obstruction/torsion ± delayed enhancement
Cx: volvulus
Acquired Small Bowel Obstruction in Childhood
mnemonic: AAIMM
  • Adhesions
  • Appendicitis
  • Intussusception
  • Incarcerated hernia
  • Malrotation
  • Meckel diverticulum
Small Bowel Obstruction in Adulthood
mnemonic: SHAVIT
  • Stone (gallstone ileus)
  • Hernia (21%)
  • Adhesion (49%)
  • Volvulus
  • Intussusception
  • Tumor (16%)
SBO IN VIRGIN ABDOMEN OF ADULTHOOD
  • Bowel ischemia including ischemic stricture
  • Primary small bowel neoplasm
  • Metastatic small bowel neoplasm
  • Extrinsic abdominal mass
  • Internal/abdominal wall hernia
  • Crohn disease
Colonic Obstruction
Incidence: 25% of all intestinal obstructions
P.763

Cause:
  • NEONATAL COLONIC OBSTRUCTION
    • Meconium plug syndrome
    • Colonic atresia
    • Anorectal malformation: rectal atresia, imperforate anus
    • Hirschsprung disease
    • functional colonic immaturity (especially in premies + infants of mothers treated with magnesium or high doses of sedatives/opiates, children with septicemia, hypothyroidism, hypoglycemia, diabetic mothers)
      • small left colon syndrome
      • meconium plug syndrome
  • LUMINAL OBTURATION
    • Fecal impaction
      • bubbly pattern of large mass of stool
    • Fecaloma
    • Gallstone (in sigmoid narrowed by diverticulitis)
    • Intussusception
  • BOWEL WALL LESION
    • malignant (60–70% of obstructions) predominantly in sigmoid
    • inflammatory
      • Crohn disease
      • Ulcerative colitis
      • Mesenteric ischemia
      • Sigmoid diverticulitis (15%)
        • stenotic segment >6 cm
      • Acute pancreatitis
    • infectious:
      • infectious granulomatous process
        • Actinomycosis
        • Tuberculosis
        • Lymphogranuloma venereum
      • parasitic disease
        • Amebiasis
        • Schistosomiasis
    • wall hematoma:
      • blunt trauma, coagulopathy
  • EXTRINSIC
    • mass impression
      • Endometriosis
      • Large tumor mass: prostate, bladder, uterus, tubes, ovaries
      • Pelvic abscess
      • Hugely distended bladder
      • Mesenteritis
      • Poorly formed colostomy
    • severe constriction
      • Volvulus (3rd most common cause): sigmoid colon, cecum, transverse colon, compound volvulus (= ileosigmoid knot)
      • Hernia: transverse colon in diaphragmatic hernia, sigmoid colon in left inguinal hernia
      • Adhesion
Abdominal plain-film patterns:
  • dilated colon only = competent ileocecal valve
  • dilated small bowel (25%) = incompetent ileocecal valve
  • dilated colon + dilated small bowel = ileocecal valve obstruction secondary to cecal overdistension
  • gas-fluid levels distal to hepatic flexure (fluid is normal in cecum + ascending colon); sign not valid with diarrhea/saline catharsis/enema
  • cecum most dilated portion (in 75% of cases); critical at 10 cm diameter (high probability for impending perforation)
  • The lower the obstruction, the more proximal the distension!
BE: Emergency barium enema of unprepared colon in suspected obstruction!
Contraindicated in toxic megacolon, pneumatosis intestinalis, portal vein gas, extraluminal gas
Ileus
  • [ileus = stasis/inability to push fluid along (term does not distinguish between mechanical and nonmechanical causes)]
  • = ADYNAMIC/PARALYTIC/NONOBSTRUCTIVE ILEUS
  • = derangement impairing proper distal propulsion of intestinal contents
Cause:
  • in neonate:
    • Hyperbilirubinemia
    • Intracranial hemorrhage
    • Aspiration pneumonia
    • Necrotizing enterocolitis
    • Aganglionosis
  • in child/adult:
    • Postoperative ileus
      • usually resolves by 4th postoperative day
    • Visceral pain: obstructing ureteral stone, common bile duct stone, twisted ovarian cyst, blunt abdominal/chest trauma
    • Intraabdominal inflammation/infection: peritonitis, appendicitis, cholecystitis, pancreatitis, salpingitis, abdominal abscess, hemolytic-uremic syndrome, gastroenteritis
    • Ischemic bowel disease
    • Anticholinergic drugs: atropine, propantheline, morphine + derivatives, tricyclic antidepressants, dilantin, phenothiazines, hexamethonium bromide
    • Neuromuscular disorder: diabetes, hypothyroidism, porphyria, lead poisoning, uremia, hypokalemia, amyloidosis, urticaria, sprue, scleroderma, Chagas disease, vagotomy, myotonic dystrophy, CNS trauma, paraplegia, quadriplegia
    • Systemic disease: septic/hypovolemic shock, urticaria
    • Chest disease: lower lobe pneumonia, pleuritis, myocardial infarction, acute pericarditis, congestive heart failure
    • Retroperitoneal disease: hemorrhage (spine trauma), abscess
mnemonic: Remember the P’s
  • Pancreatitis
  • Pendicitis
  • Peptic ulcer
  • Perforation
  • Peritonitis
  • Pneumonia
  • P.764

  • Porphyria
  • Postoperative
  • Potassium paucity
  • Pregnancy
  • Pyelonephritis
  • • intestinal sounds decreased/absent
  • • abdominal distension
  • large + small bowel ± gastric distension
  • decreased small bowel distension on serial films
  • delayed but free passage of contrast material
Rx: not amenable to surgical correction
Localized Ileus
  • = isolated distended loop of small/large bowel
  • = SENTINEL LOOP
Often associated with: adjacent acute inflammatory process
Etiology:
1. Acute pancreatitis: duodenum, jejunum, transverse colon
2. Acute cholecystitis: hepatic flexure of colon
3. Acute appendicitis: terminal ileum, cecum
4. Acute diverticulitis: descending colon
5. Acute ureteral colic: GI tract along course of ureter
Intestinal Pseudoobstruction
  • TRANSIENT PSEUDOOBSTRUCTION
    • Electrolyte imbalance
    • Renal failure
    • Congestive heart failure
  • ACUTE COLONIC PSEUDOOBSTRUCTION (Ogilvie syndrome)
  • CHRONIC PSEUDOOBSTRUCTION
    • Scleroderma
    • Amyloidosis
  • IDIOPATHIC PSEUDOOBSTRUCTION
    • Chronic intestinal pseudoobstruction syndrome
    • Megacystis-microcolon-intestinal-hypoperistalsis syndrome
Esophagus
Esophageal Contractions
  • Esophageal motor activity needs to be evaluated in recumbent position without influence of gravity!
  • PERISTALTIC EVENT = coordinated contractions of esophagus
  • PERISTALTIC SEQUENCE = aboral stripping wave clearing esophagus
Primary Esophageal Peristalsis
  • = orderly peristaltic sequence with progressive aboral stripping traversing entire esophagus with complete clearance of barium; centrally mediated (medulla) swallow reflex via glossopharyngeal + vagal nerve; initiated by swallowing
  • rapid wave of inhibition followed by slower wave of contraction
  • Normal peristaltic sequence will be interrupted by repetitive swallowing before peristaltic sequence is complete!
Secondary Esophageal Peristalsis
  • = local peristaltic wave identical to primary peristalsis but elicited through esophageal distension = sensorimotor stretch reflex
  • Esophageal motility can be evaluated with barium injection through nasoesophageal tube despite patient’s inability to swallow!
Tertiary Esophageal Contractions
  • = nonpropulsive esophageal motor event characterized by disordered up-and-down movement of bolus without clearing of esophagus
Cause:
  • Presbyesophagus
  • Diffuse esophageal spasm
  • Hyperactive achalasia
  • Neuromuscular disease:
    • @ diabetes mellitus, parkinsonism, amyotrophic lateral sclerosis, multiple sclerosis, thyrotoxic myopathy, myotonic dystrophy
  • Obstruction of cardia:
    • neoplasm, distal esophageal stricture, benign lesion, S/P repair of hiatal hernia
    • Tertiary activity does not necessarily imply a significant motility disturbance!
Age: in 5–10% of normal adults during 4th–6th decade
  • nonsegmental = partial luminal indentation
    Location: in lower 2/3 of esophagus
    • spontaneous repetitive nonpropulsive contraction
    • “yo-yo” motion of barium
    • “corkscrew” appearance = scalloped configuration of barium column
    • “rosary bead”/“shish kebab” configuration = compartmentalization of barium column
    • no lumen-obliterating contractions
  • segmental = luminal obliteration (rare)
    • “curling” = erratic segmental contractions
    • “rosary-bead” appearance
Abnormal Esophageal Peristalsis
  • PRIMARY MOTILITY DISORDERS
    • Achalasia
    • Diffuse esophageal spasm
      • • severe intermittent pain while swallowing
      • compartmentalization of esophagus by numerous tertiary contractions
      Dx: extremely high pressures on manometry
    • Presbyesophagus
    • Chalasia
    • Congenital TE fistula
    • Intestinal pseudoobstruction
  • SECONDARY MOTILITY DISORDERS
    • connective tissue disease
      • Scleroderma
      • SLE
      • Rheumatoid arthritis
      • Polymyositis
      • Dermatomyositis
      • Muscular dystrophy
    • P.765

    • chemical/physical injury
      • Reflux/peptic esophagitis
      • S/P vagotomy
      • Caustic esophagitis
      • Radiotherapy
    • infection
      — fungal: candidiasis
      — parasitic: Chagas disease
      — bacterial: TB, diphtheria
      — viral: herpes simplex
    • metabolic disease
      • Diabetes mellitus
      • Amyloidosis
      • Alcoholism
      • Electrolyte disturbances
    • endocrine disease
      • Myxedema
      • Thyrotoxicosis
    • neoplasm
    • drug-related: atropine, propantheline, curare
    • muscle disease
      • Myotonic dystrophy
      • Muscular dystrophy
      • Oculopharyngeal dystrophy
      • Myasthenia gravis (disturbed motility only in striated muscle of upper 1/3 of esophagus)
        • persistent collection of barium in upper third of esophagus
        • findings reversed by cholinesterase inhibitor edrophonium (Tensilon®)
    • neurologic disease
      • Parkinsonism
      • Multiple sclerosis
      • CNS neoplasm
      • Amyotrophic lateral sclerosis
      • Bulbar poliomyelitis
      • Cerebrovascular disease
      • Huntington chorea
      • Ganglioneuromatosis
      • Wilson disease
      • Friedreich ataxia
      • Familial dysautonomia (Riley-Day)
      • Stiff-man syndrome
Diffuse Esophageal Dilatation
  • = ACHALASIA PATTERN = MEGAESOPHAGUS
  • ESOPHAGEAL MOTILITY DISORDER
    • Idiopathic achalasia
    • Chagas disease: patients commonly from South America; often associated with megacolon + cardiomegaly
    • Postvagotomy syndrome
    • Scleroderma
    • Systemic lupus erythematosus
    • Presbyesophagus
    • Ehlers-Danlos syndrome
    • Diabetic/alcoholic neuropathy
    • Anticholinergic drugs
    • Idiopathic intestinal pseudoobstruction
      • = degeneration of innervation
    • Amyloidosis: associated with macroglossia, thickened small bowel folds
    • Esophagitis
  • DISTAL OBSTRUCTION
    • Infiltrating lesion of distal esophagus/gastric cardia (eg, carcinoma) = pseudoachalasia
    • Benign stricture
    • Extrinsic compression
    mnemonic: MA’S TACO in a SHell
    • M uscular disorder (eg, myasthenia gravis)
    • A chalasia
    • S cleroderma
    • T rypanosomiasis (Chagas disease)
    • A myloidosis
    • C arcinoma
    • O bstruction
    • S tricture (lye, potassium, tetracycline)
    • H iatal hernia
Air Esophagogram
  • Normal variant
  • Scleroderma
  • Distal obstruction: tumor, stricture, achalasia
  • Thoracic surgery
  • Mediastinal inflammatory disease
  • S/P total laryngectomy (esophageal speech)
  • Endotracheal intubation + PEEP
Abnormal Esophageal Folds
  • TRANSVERSE FOLDS
    • Feline esophagus
      • frequently seen with gastroesophageal reflux; normally found in cats
        • transient contraction of longitudinally oriented muscularis mucosae
    • Fixed transverse folds
      • due to scarring from reflux esophagitis
      • stepladder appearance in distal esophagus
  • LONGITUDINAL FOLDS
    normal: 1–2 mm wide, best seen in collapsed esophagus
    • >3 mm with submucosal edema/inflammation
    • Gastroesophageal reflux
    • Opportunistic infection
    • Caustic ingestion
    • Irradiation
DDx: (1) Varices
√ tortuous/serpentine folds that can be effaced by esophageal distension
(2) Varicoid carcinoma
√ fixed rigid folds with abrupt demarcation due to submucosal spread
Esophageal Inflammation
  • CONTACT INJURY
    • reflux related
      • Peptic ulcer disease
      • Barrett esophagus
      • Scleroderma (patulous LES)
      • Nasogastric intubation
    • P.766

    • caustic
      • Foreign body
      • Corrosives
    • thermic
      • habitual ingestion of excessively hot meals/liquids
  • RADIATION INJURY
  • INFECTION
    • Candidiasis
    • Herpes simplex virus/CMV
    • Diphtheria
  • SYSTEMIC DISEASE
    • dermatologic disorders
      • blistering of skin + mucous membranes in response to minor trauma
      • Epidermolysis bullosa dystrophica
        Histo: intraepidermal bullae
      • Benign mucous membrane pemphigoid
        • = rare disease of unknown cause
        Histo: subepidermal bullae without acantholysis
        Age: 4th decade; M < F
        • esophageal lesions (in 2–13%) most frequent at sites of relative stasis (aortic knob, carina, GE junction):
          • thin smooth webs arising from anterior aspect
          • stenoses of variable length
      • Pemphigus vulgaris
    • others:
      • Crohn disease
      • Graft-versus-host disease
      • Behçet disease
      • Eosinophilic gastroenteritis
Esophageal Ulcer
  • PEPTIC
    • Reflux esophagitis: scleroderma
    • Barrett esophagus
    • Crohn disease
    • Dermatologic disorders: benign mucous membrane pemphigoid, epidermolysis bullosa dystrophica, Behçet disease
  • INFECTIOUS
    • Herpes
    • Cytomegalovirus
  • CONTACT INJURY/EXTERNAL INJURY
    • Corrosives: alkali, strictures in 50%
    • Alcohol-induced esophagitis
    • Drug-induced esophagitis
    • Radiotherapy: smooth stricture >4,500 rads
      • shallow/deep ulcers conforming to radiation portal
    • Nasogastric tube
      • elongated stricture in middle + distal 1/3
    • Endoscopic sclerotherapy
  • MALIGNANT
    • Esophageal carcinoma
Location:
  • @ Upper esophagus
    • Barrett ulcer in islets of gastric mucosa
  • @ Midesophagus
    • Herpes esophagitis
    • CMV esophagitis
    • Drug-induced esophagitis
  • @ Distal esophagus
    • Reflux esophagitis
    • CMV esophagitis
  • DDx:
    • Sacculation
      • = outpouching in distal esophagus due to asymmetric scarring in reflux esophagitis
    • Esophageal intramural pseudodiverticula
    • Artifact
      • tiny precipitates of barium
      • transient mucosal crinkling in inadequate distension
      • irregular Z-line
Small Esophageal Ulcer (<1 cm)
  • Herpes simplex virus type I
  • Drug-induced
  • Reflux esophagitis
  • Behçet syndrome
  • Benign mucous membrane pemphigoid
  • Acute radiation change
Large Esophageal Ulcer (>1 cm)
  • Cytomegalovirus
  • Human immunodeficiency virus
  • Carcinoma
  • Drug-induced
  • Barrett esophagus
  • Sclerotherapy for varices
Double-barrel esophagus
  • Dissecting intramural hematoma from emetogenic injury
  • Mallory-Weiss tear trauma, esophagoscopy (in 0.25%), bougienage (in 0.5%), ingestion of foreign bodies, spontaneous (bleeding diathesis)
  • Intramural abscess
  • Intraluminal diverticulum
  • Esophageal duplication (if communication with esophageal lumen present)
Esophageal Diverticulum
  • Zenker diverticulum (pharyngoesophageal)
  • Interbronchial diverticulum
    • = traction diverticulum
    • = response to pull from fibrous adhesions following lymph node infection (TB), contains all 3 esophageal layers
      Location: usually on right anterolateral wall of interbronchial segment
    • calcified mediastinal nodes
  • Interaorticobronchial diverticulum
    • = thoracic pulsion diverticulum
    Location: on left anterolateral wall between inferior border of aortic arch + upper margin of left main bronchus
  • Epiphrenic diverticulum (rare)
    Location: usually on lateral esophageal wall, right > left, in distal 10 cm
    • often associated with hiatus hernia
  • P.767

  • Intramural esophageal pseudodiverticulosis
    • outpouching from mucosal glands
Tracheobronchoesophageal Fistula
  • CONGENITAL
    • Congenital tracheoesophageal fistula
  • MALIGNANCY (in 60%)
    • Lung cancer
    • Metastases to mediastinal lymph nodes
    • Esophageal cancer
      • In 5–10% of patients with advanced esophageal cancer
    • Radiation treatment of mediastinal malignancy
  • TRAUMATIC
    • Instrumentation (esophagoscopy, bougienage, pneumatic dilatation)
    • Blunt (“crush injury”)/penetrating chest trauma
    • Surgery
    • Foreign-body perforation
    • Corrosives
    • Postemetic rupture = Boerhaave syndrome
  • INFECTIOUS/INFLAMMATORY
    • TB, syphilis, histoplasmosis, actinomycosis, Crohn disease
    • Perforated diverticulum
    • Pulmonary sequestration/cyst
Long Smooth Esophageal Narrowing
  • Congenital esophageal stenosis
    • at junction between middle + distal third
    • weblike/tubular stenosis of 1 cm in length
  • Surgical repair of esophageal atresia
    • interruption of primary peristaltic wave at anastomosis
    • secondary contractions may produce retrograde flow with aspiration
    • impaction of food
  • Caustic burns = alkaline burns
  • Alendronate (= inhibitor of osteoclastic activity)
  • Gastric acid: reflux, hyperemesis gravidarum
  • Intubation: reflux + compromise of circulation
  • Radiotherapy for esophageal carcinoma; tumor of lung, breast, or thymus; lymphoma; metastases to mediastinal lymph nodes
    Onset of stricture: usually 4–8 months post Rx
    Dose: 3,000–5,000 rad
  • Postinfectious: moniliasis (rare)
Lower Esophageal Narrowing
mnemonic: SPADE
  • S cleroderma
  • P resbyesophagus
  • A chalasia; A nticholinergics
  • D iffuse esophageal spasm
  • E sophagitis
Focal Esophageal Narrowing
  • Esophageal web
    • = 1–2-mm thick (vertical length) area of complete/incomplete circumferential narrowing
  • Esophageal ring
    • = 5–10-mm thick (vertical length) area of complete/incomplete circumferential narrowing
  • Esophageal stricture
    • = >10 mm in vertical length
mnemonic: LETTERS MC
  • Lye ingestion
  • Esophagitis
  • Tumor
  • Tube (prolonged nasogastric intubation)
  • Epidermolysis bullosa
  • Radiation
  • Surgery, S cleroderma
  • Moniliasis
  • Congenital
Midesophageal Stricture
  • Barrett esophagus
  • Radiation injury
  • Caustic esophagitis
  • Primary carcinoma: squamous cell carcinoma
  • Metastatic cancer (from subcarinal nodes/left mainstem bronchus)
  • Drug-induced stricture (esp. potassium chloride)
  • Esophageal intramural pseudodiverticulosis
  • Dermatologic disorder: benign mucous membrane pemphigoid, epidermolysis bullosa
  • Graft-versus-host disease
Long Distal Esophageal Stricture
  • SEVERE ACID EXPOSURE
    • Nasogastric intubation
    • Zollinger-Ellison syndrome
    • Alkaline reflux esophagitis
  • INFLAMMATION
    • Crohn disease
Short Distal Esophageal Stricture
  • Reflux esophagitis
  • Carcinoma (adenocarcinoma)
  • Crohn disease
  • Schatzki ring
Esophageal Filling Defect
  • BENIGN TUMORS
    • <1% of all esophageal tumors
    • Submucosal tumor (75%)
      • = nonepithelial, intramural
      • Leiomyoma (50% of all benign tumors)
        • Most common submucosal mass in esophagus
      • Granular cell myoblastoma
      • Lipoma, fibroma, lipoma, fibrolipoma, myxofibroma, hamartoma, hemangioma, lymphangioma, neurofibroma, schwannoma,
        • primary wave stops at level of tumor
        • proximal esophageal dilatation + hypotonicity
        • rigid esophageal wall at site of tumoral implant
        • disorganized/altered/effaced mucosal folds around defect
        • tumor shadow on tangential view extending beyond esophageal margin
    • P.768

    • Mucosal tumor (25%) = epithelial, intraluminal
      • Squamous papilloma
        • = most common benign mucosal tumor; rarely multiple (esophageal papillomatosis)
        • small sessile slightly lobulated polyp
      • Fibrovascular polyp
        Path: fibrovascular + adipose tissue
        Location: cervical esophagus near cricopharyngeus
        • giant sausage-shaped intraluminal mass
        Cx: regurgitation into larynx causes sudden death
      • Inflammatory esophagogastric polyp
        • = sentinel polyp = bulbous tip of thickened gastric fold
        Cause: sequelae of chronic reflux esophagitis
        Prognosis: no malignant potential
      • Adenoma
        • = originates in Barrett mucosa
        • sessile/pedunculated polyp
        Cx: malignant degeneration
      • Glycogen acanthosis
  • MALIGNANT TUMORS
    • Esophageal cancer
      • squamous/varicoid squamous cell carcinoma
      • adenocarcinoma
      • spindle cell carcinoma: leiomyosarcoma, carcinosarcoma, pseudosarcoma
    • Carcinoma of cardia (gastric cancer)
    • Metastases: malignant melanoma, lymphoma (<1% of gastrointestinal lymphomas), stomach, lung, breast
  • VASCULAR
    • Varices
  • INFECTION/INFLAMMATION
    • Candida/herpes esophagitis
    • Drug-induced inflammatory reaction
  • CONGENITAL/NORMAL VARIANT
    • Prolapsed gastric folds
    • Esophageal duplication cyst (0.5–2.5% of all esophageal tumors)
  • FOREIGN BODIES
    • Retained food particles (chicken bone, fish bone, pins, coins, small toys, meat)
    • Undissolved effervescent crystals
    • Air bubbles
Esophageal Mucosal Nodules/Plaques
plaque = discrete irregular/ovoid elevation barely protruding above mucosal surface
nodule = small more rounded elevation
  • Candida esophagitis
  • Reflux esophagitis (early stage)
  • Barrett esophagus
  • Glycogen acanthosis
  • Superficial spreading carcinoma
  • Artifacts (undissolved effervescent agent, air bubbles, debris)
Extrinsic Esophageal Impression
Cervical Causes of Esophageal Impression
  • OSSEOUS LESIONS
    • Anterior marginal osteophyte/DISH
    • Anterior disk herniation
    • Cervical trauma + hematoma
    • Osteomyelitis
    • Bone neoplasm
  • ESOPHAGEAL WALL LESIONS
    • muscle
      • Cricopharyngeus
      • Esophageal web
    • vessel
      • Pharyngeal venous plexus
      • Lymph node enlargement
  • ENDOCRINE ORGANS
    • Thyroid/parathyroid enlargement (benign/malignant)
    • Fibrotic traction after thyroidectomy
  • Retropharyngeal/mediastinal abscess
Thoracic Causes of Esophageal Impression
  • NORMAL INDENTATIONS
    • aortic arch, left mainstem bronchus, left inferior pulmonary vein, diaphragmatic hiatus
  • ABNORMAL VASCULATURE
    • right-sided aortic arch, cervical aortic arch, aortic unfolding, aortic tortuosity, aortic aneurysm, double aortic arch (“reverse S”), coarctation of aorta (“reverse figure 3”), aberrant right subclavian artery
    • = arteria lusoria (semilunar/bayonet-shaped imprint upon posterior wall of esophagus), aberrant left pulmonary artery (between trachea + esophagus), anomalous pulmonary venous return (anterior), persistent truncus arteriosus (posterior)
  • CARDIAC CAUSES
    • enlargement of chambers
      • left atrial/left ventricular enlargement: mitral disease (esophageal displacement backward + to the right)
    • pericardial masses
      • pericardial tumor/cyst/effusion
  • MEDIASTINAL CAUSES
    • mediastinal tumor, lymphadenopathy (metastatic, tuberculous), inflammation, cyst
  • PULMONARY CAUSES
    • pulmonary tumor, bronchogenic cyst, atypical pulmonary fibrosis (retraction)
  • ESOPHAGEAL ABNORMALITIES
    • Esophageal diverticulum
    • Paraesophageal hernia
    • Esophageal duplication
Stomach
Gastric Tumor
Classification based on Biologic Behavior
  • MALIGNANT (10–15%)
    • Adenocarcinoma (>95%)
    • Lymphoma, mucosa-associated lymphoid tissue (MALT)
    • P.769

    • Sarcoma: leiomyosarcoma, Kaposi sarcoma
    • Carcinoid tumor
    • Metastasis
      • hematogenous: malignant melanoma, breast cancer
        • one/more submucosal masses
        • target/bull’s-eye lesion if centrally ulcerated
        • giant cavitated lesion
        • linitis plastica (usually in breast cancer)
      • direct invasion
        • Barrett cancer: gastric fundus
        • Pancreatic cancer: stomach/duodenal sweep
        • Colonic cancer: greater gastric curvature
        • Omental cake: greater gastric curvature
  • BENIGN (85–90%)
    • epithelial/mucosal tumor (50%)
      • Hyperplastic polyp
      • Adenomatous polyp
      • Brunner gland hyperplasia
    • mesenchymal tumor (50%)
      • Leiomyoma
      • Ectopic pancreatic rest
Mesenchymal Tumors of GI Tract
  • SOMATIC SOFT TISSUE TUMOR
    • smooth muscle tumor
      • True leiomyoma
      • True leiomyosarcoma
    • neural tumor
      • 4% of all benign gastric tumors
      • Schwannoma
      • Neurofibroma
      • Plexosarcoma
    • lipocytic tumor
      • Lipoma (2–3% of all benign gastric tumors)
      • Liposarcoma
    • vascular/perivascular tissue
      • 2% of all benign gastric tumors
      • Glomus tumor (most common)
      • Hemangioma
      • Lymphangioma
  • GASTROINTESTINAL STROMAL TUMOR
Calcified Gastric Tumor
  • Mucinous adenocarcinoma: miliary/punctate
  • Stromal tumors: amorphous calcifications
  • Hemangioma: clusters of phleboliths
Congenital Gastric Obstruction
  • COMPLETE OBSTRUCTION
    • Gastric atresia
      Frequency: <1% of all GI obstructions
      May be associated with: epidermolysis bullosa
      Site: antrum + pylorus
      • • regurgitation of bile-free vomitus within first few hours after birth
      • “single bubble” appearance of air in stomach
      • membranous mucosal diaphragm
    • Congenital peritoneal bands
    • Annular pancreatic tissue
  • PARTIAL GASTRIC OUTLET OBSTRUCTION
    • cyclic transient postprandial vomiting
    • Incomplete prepyloric diaphragm
    • Antral stenosis
    • Aberrant pancreatic tissue in gastric antrum
    • Antral duplication cyst
Widened Retrogastric Space
  • PANCREATIC MASSES (most common cause)
    • Acute + chronic pancreatitis
    • Pancreatic pseudocyst
    • Pancreatic cystadenoma + carcinoma
  • OTHER RETROPERITONEAL MASSES
    • Sarcoma
    • Renal tumor, adrenal tumor
    • Lymph node enlargement
    • Abscess, hematoma
  • GASTRIC MASSES
    • Leiomyoma, leiomyosarcoma
  • OTHERS
    • Aortic aneurysm
    • Choledochal cyst
    • Obesity
    • Postsurgical disruptions + adhesions
    • Ascites
    • Gross hepatomegaly + enlarged caudate lobe
    • Hernia involving omentum
Gas within Stomach Wall
  • NONINFECTIOUS
    • Interstitial gastric emphysema
      • = gas accumulation in submucosa/subserosa/or both
      Cause: air from an extrinsic source
      • obstructive (due to raised intragastric pressure):
        • gastric outlet obstruction, volvulus, overinflation during gastroscopy, profuse severe vomiting
      • pulmonary (due to rupture + dissection of subpleural blebs in bullous emphysema along esophageal wall/mediastinum): pulmonary emphysema
      • traumatic (due to mucosal trauma):
        • instrumentation of stomach, recent gastroduodenal surgery, endoscopy (1.6%)
      • • benign clinical course with spontaneous resolution
      • linear lucency conforming to contour of a thinwalled distended stomach
    • Cystic pneumatosis
      • = PNEUMATOSIS CYSTOIDES INTESTINALIS
      Cause: similar to interstitial gastric emphysema
      • • little/no gastrointestinal symptoms
      • multiple 1–2-mm gas-filled cysts in wall of stomach and intestines
  • INFECTIOUS
    • Emphysematous gastritis
    predisposing: corrosive gastritis, acid ingestion, severe necrotizing gastroenteritis, gastric ulcer disease with intramural perforation, gastric carcinoma, volvulus, gastric infarction
P.770

Gastric Atony
  • = gastric retention in the absence of mechanical obstruction
Pathophysiology: reflex paralysis
  • abdominal distension
  • vascular collapse (decreased venous return)
  • vomiting
  • large stomach filled with air + fluid (up to 7,500 mL)
  • retention of barium
  • absent/diminished peristaltic activity
  • patulous pylorus
  • frequently dilated duodenum
DDx: gastric volvulus, pyloric stenosis
Acute Gastric Atony
  • (may develop within 24–48 hours)
  • Acute gastric dilatation: secondary to decreased arterial perfusion (ischemia, congestive heart failure) in old patients, usually fatal
  • Postsurgical atony, ureteral catheterization
  • Immobilization: body cast, paraplegia, postoperative state
  • Abdominal trauma: especially back injury
  • Severe pain: renal/biliary colic, migraine headaches, severe burns
  • Infection: peritonitis, pancreatitis, appendicitis, subphrenic abscess, septicemia
Chronic Gastric Atony
  • Neurologic abnormalities: brain tumor, bulbar poliomyelitis, vagotomy, tabes
  • Muscular abnormalities: scleroderma, muscular dystrophy
  • Drug-induced atony: atropine, morphine, heroin, ganglionic blocking agents
  • Electrolyte imbalance: diabetic ketoacidosis, hypercalcemia, hypocalcemia, hypokalemia, hepatic coma, uremia, myxedema
  • Diabetes mellitus = gastroparesis diabeticorum (0.08% incidence)
  • Emotional distress
  • Lead poisoning
  • Porphyria
Narrowing of Stomach
  • = linitis plastica type of stenosis
  • MALIGNANCY
    • Scirrhous gastric carcinoma (involving portion/all of stomach)
    • Hodgkin lymphoma, NHL
    • Metastatic involvement (carcinoma of breast, pancreatic carcinoma, colonic carcinoma)
  • INFLAMMATION
    • Chronic gastric ulcer disease with intense spasm
    • Pseudo-Billroth-I pattern of Crohn disease
    • Sarcoidosis
      • polypoid appearance, pyloric hypertrophy
      • gastric ulcers, duodenal deformity
    • Eosinophilic gastritis
    • Polyarteritis nodosa
    • Stenosing antral gastritis/hypertrophic pyloric stenosis
  • INFECTION
    • Tertiary stage of syphilis
      • absent mucosal folds + peristalsis
      • no change over years
    • Tuberculosis (rare)
      • hyperplastic nodules/ulcerative lesion/annular lesion
      • pyloric obstruction, may cross into duodenum
    • Histoplasmosis
    • Actinomycosis
    • Strongyloidiasis
    • Phlegmonous gastritis
    • Toxoplasmosis
  • TRAUMA
    • Corrosive gastritis
    • Radiation injury
    • Gastric freezing
    • Hepatic arterial chemotherapy infusion
  • OTHERS
    • Perigastric adhesions (normal mucosa, no interval change, normal peristalsis)
    • Amyloidosis
    • Pseudolymphoma
    • Exogastric mass (hepatomegaly, pancreatic pseudocyst)
mnemonic: SLIMRAGE
  • Scirrhous carcinoma of stomach
  • Lymphoma
  • Infiltration from adjacent neoplasm
  • Metastasis (breast carcinoma)
  • Radiation therapy
  • Acids (corrosive ingestion)
  • Granulomatous disease (TB, sarcoidosis, Crohn)
  • Eosinophilic gastroenteritis
Antral Narrowing
mnemonic: SPICER
  • Sarcoidosis, Syphilis
  • Peptic ulcer disease
  • Infection (tuberculosis, chronic granulomatous disease of childhood)
  • Cancer (linitis plastica), Crohn disease, Caustic ingestion
  • Eosinophilic gastritis
  • Radiation
Antral Pad Sign
  • = extrinsic impression of the posteroinferior wall of antrum
  • Pancreatic cancer in head/body
  • Pancreatitis
  • Pancreatic pseudocyst
  • Normal/distended gallbladder (patient in RAO position)
Intramural-Extramucosal Lesions of Stomach
  • sharply delineated marginal/contour defect
  • stretched folds over intact mucosa
  • acute angle at margins
  • may ulcerate centrally
  • may become pedunculated and acquire polypoid appearance over years
P.771

  • NEOPLASTIC
    1. Leiomyoma (48%)
    2. Neurogenic tumors (14%)
    3. Heterotopic pancreas (12%)
    4. Fibrous tumor (11%)
    5. Lipoma (7%)
    6. Hemangioma (7%)
    7. Glomus tumor (rare)
    8. Carcinoid
    9. Metastatic tumor
  • INFLAMMATION/INFECTION
    • Granuloma
      • Foreign-body granuloma
      • Sarcoidosis
      • Crohn disease
      • Tuberculosis
      • Histoplasmosis
    • Eosinophilic gastritis
    • Tertiary syphilis: infiltrative/ulcerative/tumorous type
    • Echinococcal cyst
  • PANCREATIC ABNORMALITIES
    • Ectopic pancreas
    • Annular pancreas
    • Pancreatic pseudocyst
  • DEPOSITS
    • Amyloid
    • Endometriosis
    • Localized hematoma
  • OTHERS
    • Varices (ie, fundal)
    • Duplications (4% of all GI tract duplications)
Gastric Filling Defects
  • INTRINSIC WALL LESIONS
    • benign (most common)
      • Polyps: hyperplastic, adenomatous, villous, hamartomatous (Peutz-Jeghers syndrome, Cowden disease)
      • Leiomyoma
      • Granulomatous lesions
        • Eosinophilic granuloma
        • Crohn disease
        • Tuberculosis
        • Sarcoidosis
      • Pseudolymphoma = benign reactive proliferation of lymphoid tissue
      • Extramedullary hematopoiesis
      • Ectopic pancreas
      • Gastric duplication cyst
      • Intramural hematoma
      • Esophagogastric herniation
    • malignant
      • Gastric carcinoma, lymphoma
      • Gastric sarcoma: leiomyosarcoma, liposarcoma, leiomyoblastoma
      • Gastric metastases: melanoma, breast, pancreas, colon
  • EXTRINSIC IMPRESSIONS ON STOMACH
    • in 70% nonneoplastic (extrinsic pseudotumors in 20%)
    • normal organs: organomegaly, tortuous aorta, heart, cardiac aneurysm
    • benign masses:
      • cysts of pancreas, liver, spleen, adrenal, kidney; gastric duplication, postoperative deformity (eg, Nissen fundoplication)
    • malignant masses: enlarged celiac nodes
    • inflammatory lesion:
      • left subphrenic abscess/hematoma
      • — lateral displacement: enlarged liver, aortic aneurysm, enlarged celiac nodes
      • — medial displacement: splenomegaly, mass in colonic splenic flexure, cardiomegaly, subphrenic abscess
  • INTRALUMINAL GASTRIC MASSES
    • Bezoar
    • Foreign bodies: food, pills, blood clot, gallstone
  • TUMORS OF ADJACENT ORGANS
    • Pancreatic carcinoma + cystadenoma
    • Liver carcinoma
    • Carcinoma of gallbladder
    • Colonic carcinoma
    • Renal carcinoma
    • Adrenal carcinoma
    • Lymph node involvement
  • THICKENED GASTRIC FOLDS
Filling Defect of Gastric Remnant
  • IATROGENIC
    • surgical deformity/plication defect, suture granuloma
  • INFLAMMATORY
    • bile reflux gastritis, hyperplastic polyps
  • INTUSSUSCEPTION
    • Jejunogastric intussusception
      • (efferent loop in 75%, afferent loop in 25%)
      • (a) acute form: high intestinal obstruction, left hypochondriac mass, hematemesis
      • (b) chronic/intermittent form: may be self-reducing
      • “coiled spring” appearance of gastric filling defect
    • Gastrojejunal/gastroduodenal mucosal prolapse
      • often asymptomatic
      • bleeding partial obstruction
  • NEOPLASTIC
    • Gastric stump carcinoma: >5 years after resection for benign disease; 15% within 10 years; 20% after 20 years
    • Recurrent carcinoma (10%) secondary to incomplete removal of gastric cancer
    • Malignancy at anastomosis (incomplete resection)
  • INTRALUMINAL MATTER: bezoar
    mnemonic: PUBLICS
    • Polyp (hyperplastic polyp due to bile reflux)
    • Ulcer (anastomotic)
    • Bezoar, Blind loop syndrome
    • Loop (afferent loop syndrome)
    • Intussusception at gastrojejunostomy
    • Cancer (recurrent, residual, de novo)
    • Surgical deformity, Suture granuloma
P.772

Thickened Gastric Folds
  • INFLAMMATION/INFECTION
    • Inflammatory gastritis:
      • alcoholic, hypertrophic, antral, corrosive, postirradiation, gastric cooling
    • Crohn disease
    • Sarcoidosis
    • Infectious gastritis:
      • bacterial invasion, bacterial toxins from botulism, diphtheria, dysentery, typhoid fever, anisakiasis, TB, syphilis
    • Pseudolymphoma
  • MALIGNANCY
    • Lymphoma
    • Gastric carcinoma
  • INFILTRATIVE PROCESS
    • Eosinophilic gastritis
    • Amyloidosis
  • PANCREATIC DISEASE
    • Pancreatitis
    • Direct extension from pancreatic carcinoma
  • OTHERS
    • Zollinger-Ellison syndrome
    • Ménétrier disease
    • Gastric varices
    mnemonic: ZEAL VOLUMES C3MP3
    • Zollinger-Ellison syndrome
    • Amyloidosis
    • Lymphoid hyperplasia
    • Varices
    • Operative defect
    • Lymphoma
    • Ulcer disease (peptic)
    • Ménétrier disease
    • Eosinophilic gastroenteritis
    • Syphilis
    • Crohn disease, Carcinoma, Corrosive gastritis
    • Pancreatitis, Pancreatic carcinoma,
    • Postradiation gastritis
Bull’s-eye Lesions
  • PRIMARY NEOPLASMS
    • Leiomyoma, leiomyosarcoma
    • Lymphoma
    • Carcinoid
    • Primary carcinoma
  • HEMATOGENOUS METASTASES
    • Malignant melanoma
      • usually spares large bowel
    • Breast cancer (15%)
      • scirrhous appearance in stomach
    • Cancer of lung
    • Renal cell carcinoma
    • Kaposi sarcoma
    • Bladder carcinoma
  • ECTOPIC PANCREAS
    • in duodenum/stomach
  • EOSINOPHILIC GRANULOMA
    • most frequently in stomach
Complications of Postoperative Stomach
  • Filling defect of gastric remnant
  • Retained gastric antrum
  • Dumping syndrome
  • Afferent loop syndrome
  • Stomal obstruction
    • temporary reversible: edema of suture line, abscess/hematoma, potassium deficiency, inadequate electrolyte replacement, hypoproteinemia, hypoacidity
    • late mechanical: stomal ulcer (75%)
    mnemonic: LOBULATING
  • Leaks (early)
  • Obstruction (early)
  • Bezoar
  • Ulcer (especially marginal)
  • Loop (afferent loop syndrome)
  • Anemia (macrocytic secondary to decreased intrinsic factor)
  • Tumor (? increased incidence)
  • Intussusception
  • Not feeling well after meals (dumping syndrome)
  • Gastritis (bile reflux)
Lesions Involving Stomach and Duodenum = Transpyloric Disease
  • Lymphoma: in up to 40% of patients with lymphoma
  • Gastric carcinoma: in 5–25%, but 50 × more common than lymphoma
  • Peptic ulcer disease
  • Tuberculosis: in 10% of gastric TB
  • Crohn disease: pseudo-Billroth-I pattern
  • Strongyloidiasis
  • Eosinophilic gastroenteritis
Duodenum
Congenital Duodenal Obstruction
  • • bile-stained vomiting delayed until after first feeding and increasing progressively
  • “double bubble” sign
  • Duodenal atresia/severe stenosis
  • Annular pancreas
  • Midgut volvulus
  • Duodenal web
  • Ladd bands
  • Preduodenal portal vein
  • Duodenal duplication cyst
Extrinsic Pressure Effect on Duodenum
  • BILE DUCTS
    • normal impression, dilated CBD, choledochal cyst
  • GALLBLADDER
    • normal impression, gallbladder hydrops, Courvoisier phenomenon, gallbladder carcinoma, pericholecystic abscess
  • LIVER
    • hepatomegaly, hypertrophied caudate lobe, anomalous hepatic lobe, hepatic cyst, hepatic tumor
  • RIGHT KIDNEY
    • bifid collecting system, hydronephrosis, multiple renal cysts, polycystic kidney disease, hypernephroma
  • RIGHT ADRENAL
    • adrenal carcinoma, enlargement in Addison disease
  • COLON
    • duodenocolic apposition due to anomalous peritoneal fixation, carcinoma of hepatic flexure
  • VESSELS
    • lymphadenopathy, duodenal varices, dilated arterial collaterals, aortic aneurysm, intramural/mesenteric hematoma
P.773

image
Gastric Surgical Procedures
Widened Duodenal Sweep
  • NORMAL VARIANT
  • PANCREATIC LESION
    • Acute pancreatitis
    • Chronic pancreatitis
    • Pancreatic pseudocyst
    • Pancreatic carcinoma
    • Metastasis to pancreas
    • Pancreatic cystadenoma
  • VASCULAR LESION
    • Lymph node enlargement: lymphoma, metastasis, inflammation
    • Cystic lymphangioma of the mesentery
  • RETROPERITONEAL MASS
    • Aortic aneurysm
    • Choledochal cyst
Thickened Duodenal Folds
  • INFLAMMATION
    • within bowel wall:
      • peptic ulcer disease, Zollinger-Ellison syndrome, regional enteritis, lymphoid hyperplasia, uremia
    • surrounding bowel wall:
      • pancreatitis, cholecystitis
  • INFECTION
    • giardiasis, TB, strongyloidiasis, celiac disease
  • P.774

  • NEOPLASIA
    • lymphoma, metastases to peripancreatic nodes
  • DIFFUSE INFILTRATIVE DISORDER
    • Whipple disease, amyloidosis, mastocytosis, eosinophilic enteritis, intestinal lymphangiectasia
  • VASCULAR DISORDER
    • duodenal varices, mesenteric arterial collaterals, intramural hemorrhage (trauma, Schönlein-Henoch purpura), chronic duodenal congestion (congestive heart failure, portal venous hypertension); lymphangiectasia
  • HYPOPROTEINEMIA
    • nephrotic syndrome, Ménétrier disease, protein-losing enteropathy
  • GLANDULAR ENLARGEMENT
    • Brunner gland hyperplasia, cystic fibrosis
mnemonic: BAD HELP
  • Brunner gland hyperplasia
  • Amyloidosis
  • Duodenitis (Z-E syndrome, peptic)
  • Hemorrhage
  • Edema, Ectopic pancreas
  • Lymphoma
  • Pancreatitis, Parasites
Duodenal Filling Defect
  • EXTRINSIC
    • gallbladder impression, CBD impression, gas-filled diverticulum
  • INTRINSIC TO WALL
    • benign neoplastic mass
      • Adenoma
      • Leiomyoma
      • Lipoma
      • Hamartoma (Peutz-Jeghers syndrome)
      • Prolapsed antral polyp
      • Brunner gland adenoma
      • Villous adenoma
      • Islet cell tumor
      • Gangliocytic paraganglioma
    • malignant neoplastic mass
      • Carcinoid tumor
      • Adenocarcinoma
      • Ampullary carcinoma
      • Lymphoma
      • Sarcoma
      • Metastasis (stomach, pancreas, gallbladder, colon, kidney, melanoma)
      • Retroperitoneal lymph node involvement
    • nonneoplastic mass
      • Papilla of Vater
      • Choledochocele
      • Duplication cyst
      • Pancreatic pseudocyst
      • Duodenal varix
      • Mesenteric artery collaterals
      • Intramural hematoma
      • Adjacent abscess, stitch abscess
      • Ectopic pancreas, heterotopic gastric mucosa
      • Prolapsed antral mucosa
      • Brunner gland hyperplasia
      • Benign lymphoid hyperplasia
  • INTRALUMINAL
    • Blood clot
    • Foreign body: fruit pit, gallstone, feeding tube
Duodenal Tumor
Benign Duodenal Tumors
  • Leiomyoma (27%)
  • Adenomatous polyp (21%)
  • Lipoma (21%)
  • Brunner gland adenoma (17%)
  • Angiomatous tumor (6%)
  • Ectopic pancreas (2%)
  • Duodenal cyst (2%)
  • Neurofibroma (2%)
  • Hamartoma (2%)
Malignant Duodenal Tumors
  • Adenocarcinoma (73%)
    Location: 40% in duodenum, most often in 2nd + 3rd portion = periampullary neoplasm
    (a) suprapapillary: apt to cause obstruction + bleeding
    (b) peripapillary: extrahepatic jaundice
    (c) intrapapillary: GI bleeding
    Predisposed: Gardner syndrome, celiac disease
    May be associated with: Peutz-Jeghers syndrome
    √ annular/polypoid/ulcerative
    Metastases: regional lymph nodes (2/3)
    DDx: (1) Primary bile duct carcinoma
    (2) Ampullary carcinoma
  • Leiomyosarcoma (14%)
    • most often beyond 1st portion of duodenum
      • up to 20 cm in size
      • frequently ulcerated exophytic mass
  • Carcinoid (11%)
  • Lymphoma (2%)
    • marked wall thickening
    • bulky periduodenal lymphadenopathy
Enlargement of Papilla of Vater
[Abraham Vater (1684–1751), anatomist in Wittenberg, Germany]
  • Normal variant
    • identified in 60% of UGI series; atypical location in 3rd portion of duodenum in 8%; 1.5 cm in diameter in 1% of normals
  • Papillary edema
    • Impacted stone
    • Pancreatitis (Poppel sign)
    • Acute duodenal ulcer disease
    • Papillitis
  • Perivaterian neoplasms
    • = tumor mass + lymphatic obstruction
    • 1. Adenocarcinoma
    • 2. Adenomatous polyp (premalignant lesion)
      • irregular surface + erosions
  • Lesions simulating enlarged papilla
    • Benign spindle cell tumor
    • Ectopic pancreatic tissue
P.775

Duodenal Narrowing
  • DEVELOPMENTAL ANOMALIES
    • Duodenal atresia
    • Congenital web/duodenal diaphragm
    • Intraluminal diverticulum
    • Duodenal duplication cyst
    • Annular pancreas
    • Midgut volvulus, peritoneal bands (Ladd bands)
  • INTRINSIC DISORDERS
    • inflammation/infection
      • Postbulbar ulcer
      • Crohn disease
      • Sprue
      • Tuberculosis
      • Strongyloidiasis
    • tumor
      • duodenal/ampullary malignancy
  • DISEASE IN ADJACENT STRUCTURES
    • Pancreatitis, pseudocyst, pancreatic carcinoma
    • Cholecystitis
    • Contiguous abscess
    • Metastases to pancreaticoduodenal nodes (lymphoma, lung cancer, breast cancer)
  • TRAUMA
    • Duodenal rupture
    • Intramural hematoma
  • VASCULAR
    • Superior mesenteric artery syndrome
    • Aorticoduodenal fistula
    • Preduodenal portal vein (anterior to descending duodenum)
Dilated Duodenum
Megaduodenum = marked dilatation of entire C-loop
Megabulbus = dilatation of duodenal bulb only
  • VASCULAR COMPRESSION
    • superior mesenteric artery syndrome, abdominal aortic aneurysm, aorticoduodenal fistula
  • PRIMARY DUODENAL ATONY
    • scleroderma, dermatomyositis, SLE
    • Chagas disease, aganglionosis, neuropathy, surgical/chemical vagotomy
    • focal ileus: pancreatitis, cholecystitis, peptic ulcer disease, trauma
    • altered emotional status, chronic idiopathic intestinal pseudoobstruction
  • INFLAMMATORY/NEOPLASTIC INDURATION OF MESENTERIC ROOT
    • Crohn disease, tuberculous enteritis, pancreatitis, peptic ulcer disease, strongyloidiasis, metastatic disease
  • FLUID DISTENSION
    • celiac disease, Zollinger-Ellison syndrome
Postbulbar Ulceration
  • Benign postbulbar peptic ulcer
    • medial aspect of upper 2nd portion
    • incisura pointing to ulcer
    • occasionally barium reflux into common bile duct
    • ring stricture
    • stress- and drug-induced ulcers heal without deformity
  • Zollinger-Ellison syndrome
    • multiple ulcers distal to duodenal bulb
    • thickening of folds + hypersecretion
  • Leiomyoma
  • Malignant tumors:
    • primaries
      • adenocarcinoma, lymphoma, sarcoma
    • contiguous spread
      • pancreas, colon, kidney, gallbladder
    • hematogenous spread
      • melanoma, Kaposi sarcoma
    • lymphogenic spread
      • metastases to periduodenal lymph nodes
  • Granulomatous disease: Crohn disease, TB
  • Aorticoduodenal fistula
  • Mimickers: ectopic pancreas, diverticulum
Small Bowel
Anatomic Predilection for Intestinal Involvement
@ proximal jejunum diverticulosis, giardiasis, adenocarcinoma, Whipple disease, Z-E syndrome, celiac disease
@ distal ileum Crohn disease, TB, infectious enteritis, lymphoma, carcinoid, metastases
@ mesenteric border diverticulosis, Crohn disease, mesenteric hematoma, intraperitoneal spread of tumor
@ antimesenteric border Meckel diverticulum, sacculations in scleroderma, hematogenous metastases
Increased Fluid within Small Bowel
  • Ingestion
  • Resection/removal of stomach
  • Small-bowel obstruction
  • Enteritis
  • Malabsorption: celiac disease, Whipple disease
  • Peritoneal carcinomatosis
Small Bowel Diverticula
  • TRUE DIVERTICULA
    • Duodenal diverticula
      • Racemose diverticula: bizarre, lobulated
      • Giant diverticula
      • Intraluminal diverticula: result of congenital web/diaphragm
    • Jejunal diverticulosis
    • Meckel diverticulum
  • PSEUDODIVERTICULA
    • Scleroderma
    • Crohn disease
    • Lymphoma
    • Mesenteric ischemia
    • Communicating ileal duplication
    • Giant duodenal ulcer
P.776

Small Bowel Ulcer
Aphthous Ulcers of Small Bowel
  • INFECTION
    • Yersinia enterocolitis (25%)
    • Salmonellosis
    • Tuberculosis
    • Rickettsiosis
  • INFLAMMATION
    • Crohn disease (22%)
    • Behçet syndrome
    • Reiter syndrome
    • Ankylosing spondylitis
Large Nonstenotic Ulcers of Small Bowel
  • Primary nonspecific ulcer 47% incidence
  • Yersiniosis 33%
  • Crohn disease 30%
  • Tuberculosis 18%
  • Salmonellosis/shigellosis 7%
  • Meckel diverticulum 5%
Multiple Small Bowel Ulcers
  • DRUGS
    • Potassium tablets
    • Steroids
    • Nonsteroidal antiinflammatory drugs
  • INFECTION/INFLAMMATION
    • Bacillary dysentery
    • Ischemic enteritis
    • Ulcerative jejunoileitis as complication of celiac disease
  • TUMOR
    • Neoplasms
    • Intestinal lymphoma
Cavitary Small Bowel Lesion
  • PRIMARY TUMOR
    • Lymphoma (exoenteric form)
    • Leiomyosarcoma (exoenteric form)
    • Primary adenocarcinoma
  • METASTASIS
    • Malignant melanoma
    • Lung cancer
  • INFLAMMATION
    • Diverticulitis with abscess (Meckel, jejunal)
    • Communicating duplication cyst
Separation of Bowel Loops
  • INFILTRATION OF BOWEL WALL/MESENTERY
    • inflammation/infection
      • Crohn disease
      • TB
      • Radiation injury
      • Retractile mesenteritis
      • Intraperitoneal abscess
    • deposits
      • Intestinal hemorrhage/mesenteric vascular occlusion
      • Whipple disease
      • Amyloidosis
    • tumor
      • Carcinoid tumor: local release of serotonin responsible for muscular thickening + fibroplastic proliferation = desmoplastic reaction
      • Primary carcinoma of small bowel (unusual presentation)
      • Lymphoma
      • Neurofibromatosis
  • ASCITES/INTRAPERITONEAL BLEEDING
    • hepatic cirrhosis (75%), peritonitis, peritoneal carcinomatosis, congestive heart failure, constrictive pericarditis, primary/metastatic lymphatic disease
  • EXTRINSIC MASS
    • Intraperitoneal spread of tumor: peritoneal mesothelioma, mesenteric tumors (fibroma, lipoma, fibrosarcoma, leiomyosarcoma, malignant mesenteric lymphoid tumor, metastases)
    • Interloop abscesses/loculated fluid collection
    • Endometriosis
    • Retractile mesenteritis (fibrosis, fatty infiltration, panniculitis)
    • Mesenteric fat deposits
    • Fibrofatty proliferation: Crohn disease, mesenteric panniculitis
Normal Small Bowel Folds & Diarrhea
  • Pancreatic insufficiency
  • Lactase deficiency
  • Lymphoma/pseudolymphoma
Dilated Small Bowel & Normal Folds
mnemonic: SOS
  • Sprue
  • Obstruction
  • Scleroderma
  • EXCESSIVE FLUID
    • mechanical obstruction
      • due to adhesion, hernia, neoplasm
      • “string-of-beads sign” = air bubbles between mucosal folds in a fluid-filled small bowel
      • “pseudotumor sign” = closed-loop obstruction
    • malabsorption syndromes
      • Celiac disease, tropical + nontropical sprue
      • Lactase deficiency
  • BOWEL WALL PARALYSIS
    • = functional ileus = adynamic ileus
    • 1. Surgical vagotomy
    • 2. Chemical vagotomy from drug effects: atropine-like substances, morphine, L-dopa, glucagon
    • 3. Chagas disease
    • 4. Metabolic: hypokalemia, diabetes
    • 5. Intrinsic + extrinsic intraabdominal inflammation
    • 6. Chronic idiopathic pseudoobstruction
  • VASCULAR COMPROMISE
    • Mesenteric ischemia (atherosclerosis)
    • Acute radiation enteritis
    • Amyloidosis
    • SLE
  • BOWEL WALL DESTRUCTION
    • Lymphoma
    • P.777

    • Scleroderma (smooth muscle atrophy)
    • Dermatomyositis
Abnormal Small Bowel Folds
Abnormal Folds + Increased Intraluminal Fluid
  • Malabsorption syndrome
  • Crohn disease, infectious enteritis
  • Parasitic infestation/giardiasis
  • Ischemia proximal to an obstruction
  • Zollinger-Ellison syndrome
  • Lymphangiectasia, mesenteric lymphadenopathy
Thickened Folds of Stomach & Small Bowel
  • Lymphoma
  • Crohn disease
  • Eosinophilic gastroenteritis
  • Zollinger-Ellison syndrome
  • Ménétrier disease
  • Cirrhosis = gastric varices + hypoproteinemia
  • Amyloidosis
  • Whipple disease
  • Systemic sclerosis
Thickened Smooth Folds ± Dilatation
  • EDEMA
    • hypoproteinemia
      • Cirrhosis
      • Nephrotic syndrome
      • Protein-losing enteropathy (celiac disease, Whipple disease)
    • increased capillary permeability
      • Angioneurotic edema
      • Gastroenteritis
    • increased hydrostatic pressure
      • Portal venous hypertension
    • Zollinger-Ellison syndrome
  • HEMORRHAGE
    • vessel injury
      • Ischemia
      • Infarction
      • Trauma
    • vasculitis
      • Connective tissue disease
      • Henoch-Schönlein purpura
      • Thrombangitis obliterans, irradiation
    • hypocoagulability
      • Hemophilia
      • Anticoagulant therapy
      • Hypofibrinogemia
      • Circulating anticoagulants
      • Fibrinolytic system activation
      • Idiopathic thrombocytopenic purpura
      • Coagulation defects (leukemia, lymphoma, multiple myeloma, metastatic carcinoma)
      • Hypoprothrombinembinema
  • LYMPHATIC BLOCKAGE
    • Tumor infiltration: lymphoma, pseudolymphoma
    • Irradiation
    • Mesenteric fibrosis
    • Intestinal lymphangiectasia
    • Whipple disease
  • DEPOSITS
    • Eosinophilic enteritis
    • Pneumatosis intestinalis
    • Amyloidosis
    • Abetalipoproteinemia
    • Crohn disease
    • Graft-versus-host disease
    • Immunologic deficiency: hypo-/dysgammaglobulinemia
Thickened Irregular Folds ± Dilatation
  • INFLAMMATION
    • Crohn disease
  • NEOPLASTIC
    • Lymphoma, pseudolymphoma
  • INFECTION
    • protozoan
      • giardiasis, strongyloidiasis, hookworm
    • bacterial
      • Yersinia enterocolitica, typhoid fever, tuberculosis
    • fungal: histoplasmosis
    • AIDS-related infection
  • IDIOPATHIC
    • lymphatic dilatation
      • Lymphangiectasia
      • Inflammatory process, tumor growth, irradiation fibrosis
      • Whipple disease
    • cellular infiltration
      • Eosinophilic enteritis
      • Mastocytosis
    • deposits
      • Zollinger-Ellison syndrome
      • Amyloidosis
      • Alpha chain disease: defective secretory IgA system
      • A-β-lipoproteinemia: recessive, retinitis pigmentosa, neurologic disease
      • A-α-lipoproteinemia
      • Fibrocystic disease of the pancreas
      • Polyposis syndrome
mnemonic: G. WILLIAMS
  • Giardiasis
  • Whipple disease, Waldenström macroglobulinemia
  • Ischemia
  • Lymphangiectasia
  • Lymphoma
  • Inflammation
  • Amyloidosis, Agammaglobulinemia
  • Mastocytosis, Malabsorption
  • Soft-tissue neoplasm (carcinoid, lipoma)
Tethered Folds
  • = indicative of desmoplastic reaction
  • kinking, angulation, tethering, separation of bowel loops
  • 1. Carcinoid
  • 2. Postoperative in Gardner syndrome
  • 3. Retractile mesenteritis
  • 4. Hodgkin disease
  • 5. Peritoneal implants
  • P.778

  • 6. Endometriosis
  • 7. Tuberculous peritonitis
  • 8. Mesothelioma
  • 9. Postoperative adhesions
Atrophy of Small Bowel Folds
  • Chronic malabsorption: celiac disease
  • Chronic ischemic changes: radiation injury, amyloidosis
  • Crohn disease in burned-out stage
  • Parasitic infestation: strongyloidiasis
  • Graft-versus-host disease
Ribbonlike Small Bowel
  • = featureless/tubular nature of small bowel with effacement of folds
  • 1. Graft-versus-host disease
  • 2. Celiac disease
  • 3. Small bowel infection (eg, viral enteritis)
  • 4. Injury from radiation/corrosive medication
  • 5. Allergy (eg, soybeans)
  • 6. Ischemia
  • 7. Amyloid, mastocytosis
  • 8. Lymphoma, pseudolymphoma
  • 9. Crohn disease
Delayed Small Bowel Transit
  • = transit time >6 hours
mnemonic: SPATS DID
  • Scleroderma
  • Potassium (hypokalemia)
  • Anxiety
  • Thyroid (hypothyroidism)
  • Sprue
  • Diabetes (poorly controlled)
  • Idiopathic
  • Drugs (opiates, atropine, phenothiazine)
Constricting Lesion of Small Bowel
  • Primary adenocarcinoma (proximal jejunum)
  • Carcinoid (distal ileum)
  • Lymphoma, metastasis
  • Endometriosis
  • Adhesion, mucosal diaphragm
  • Strictures: Crohn disease, radiation enteritis, ischemia, potassium chloride tablets
Multiple Stenotic Lesions of Small Bowel
  • Crohn disease
  • End-stage radiation enteritis
  • Metastatic carcinoma
  • Endometriosis
  • Eosinophilic gastroenteritis
  • Tuberculosis
  • Drug-induced (eg, potassium chloride tablets, NSAIDs)
Small Bowel Filling Defects
Solitary Filling Defect of Small Bowel
  • INTRINSIC TO BOWEL WALL
    • benign neoplasm: leiomyoma (97%), adenoma, lipoma, hemangioma, neurofibroma
    • malignant primary: adenocarcinoma, lymphoma (desmoplastic response), sarcoma, carcinoid
    • metastases: from melanoma, lung, kidney, breast
    • inflammation: inflammatory pseudotumor
    • infection: parasites
  • EXTRINSIC TO BOWEL WALL
    • Duplication cyst
    • Endometrioma
  • INTRALUMINAL
    • Gallstone ileus
    • Parasites (ascariasis, strongyloidiasis)
    • Inverted Meckel diverticulum
    • Blood clot
    • Foreign body, bezoar, pills, seeds
Multiple Filling Defects of Small Bowel
  • POLYPOSIS SYNDROMES
    • Peutz-Jeghers syndrome
    • Gardner syndrome
    • Disseminated gastrointestinal polyposis
    • Generalized gastrointestinal juvenile polyposis
    • Cronkhite-Canada syndrome
  • BENIGN TUMORS
    • Multiple simple adenomatous polyps
    • Hemangioma, blue rubber bleb nevus syndrome
    • Leiomyoma, neurofibroma, lipoma
    • Nodular lymphoid hyperplasia
      • = normal terminal ileum in children + adolescents; may be associated with dysgammaglobulinemia
      • symmetric fairly sharply demarcated filling defects
    • Varices (= multiple phlebectasia in jejunum, oral mucosa, tongue, scrotum)
  • MALIGNANT TUMORS
    • Carcinoid tumor
    • Lymphoma
      • primary lymphoma (rarely multiple)
      • secondary lymphoma: gastrointestinal involvement in 63% of disseminated disease; 19% in small intestine
    • Kaposi sarcoma
    • Submucosal metastases: melanoma > lung > breast > choriocarcinoma > kidney > stomach, uterus, ovary, pancreas
  • INTRALUMINAL
    • Gallstones
    • Foreign bodies, food particles, seeds, pills
    • Parasites: ascariasis, strongyloidiasis, hookworm, tapeworm
Sandlike Lucencies of Small Bowel
  • Waldenström macroglobulinemia
  • Mastocytosis
  • Histoplasmosis
  • Nodular lymphoid hyperplasia
  • Intestinal lymphangiectasia
  • Eosinophilic gastroenteritis
  • Lymphoma
  • Crohn disease
  • Whipple disease
  • Yersinia enterocolitis
  • P.779

    P.780

  • Cronkhite-Canada syndrome
  • Cystic fibrosis
  • Food particles/gas bubbles
  • Strongyloides stercoralis
image
ABNORMAL SMALL BOWEL CALIBER & CONTOUR
Small Bowel Tumors
Incidence: 1:100,000; 1.5–6% of all GI neoplasms
  • Malignant:benign = 1:1
  • Symptomatic malignant:symptomatic benign = 3:1
  • Location of small bowel primaries:
    • ileum (41%), jejunum (36%), duodenum (18%)
ROENTGENOGRAPHIC APPEARANCE:
  • pedunculated intraluminal tumor, usually originating from mucosa
    • smooth/irregular surface without visible mucosal pattern
    • moves within intestinal lumen twice the length of the stalk
  • sessile intraluminal tumor without stalk, usually from tissues outside mucosa
    • smooth/irregular surface without visible mucosal pattern
  • intra-/extramural tumor
    • base of tumor greater than any part projecting into the lumen
    • mucosal pattern visible, may be stretched
  • serosal tumor
    • displacement of adjacent loops
    • small bowel obstruction (rare)
    • coil-spring pattern of intussusceptum
CT:
  • small bowel wall >1.5 cm thick
Cx: small-bowel obstruction (in up to 10%)
Benign Small Bowel Tumors
  • asymptomatic (80%)
  • melena, intermittent abdominal pain, weakness
  • palpable abdominal mass (20%)
Types:
  • Leiomyoma (36–49%)
    Location: any segment
  • Adenoma (15–20%)
  • Lipoma (14–16%)
    Location: duodenum (32%), jejunum (17%), ileum (51%)
    √ fat-density on CT
  • Hemangioma (13–16%)
  • Lymphangioma (5%)
    Location: duodenum > jejunum > ileum
  • Neurogenic tumor (1%)
Malignant Small Bowel Tumors
At risk: Crohn disease, celiac disease, polyposis syndromes, history of small-bowel diverting surgery
  • asymptomatic (10–30%)
  • pain due to intermittent obstruction (80%)
  • weight loss (66%)
  • gastrointestinal blood loss (50%)
  • palpable abdominal mass (50%)
PRIMARY MALIGNANT SMALL BOWEL TUMOR
  • Carcinoid (25–41%)
    • Most common primary small bowel tumor!
      Location: predominantly distal ileum
    • calcified mesenteric mass on CT
  • Adenocarcinoma (25–26%)
    Location: duodenum (48%), jejunum (44%), ileum (8%)
  • Non-Hodgkin lymphoma (16–17%)
    • 2nd most common location after stomach
    • aneurysmal dilatation
  • Gastrointestinal stromal tumor (GIST)
  • = leiomyosarcoma (9–10%)
    Location: ileum (50%)
  • Vascular malignancy (1%)
  • Fibrosarcoma (0.3%)
Secondary Malignant Small Bowel Tumor
  • Most common neoplasm of small intestines!
Cecum
Primary Neoplasm of the Appendix
  • Mucinous adenoma (44%)/adenocarcinoma (23%)
  • Colonic-type adenocarcinoma (13%)
  • NHL
  • Carcinoid tumor
Incidence: 0.5–1.0% of appendectomy specimens
  • • appendicitis symptomatology (30–50%)
  • appendiceal diameter increased >15 mm (86%)
  • cystic dilatation of appendix (mucocele)
  • soft-tissue mass
  • appendiceal wall thickening
  • periappendiceal fat stranding
Ileocecal Valve Abnormalities
  • Lipomatosis: >40 years of age, female
    • stellate/rosette pattern
  • NEOPLASM
    • Lipoma, adenomatous polyp, villous adenoma
    • Carcinoid tumor
    • Adenocarcinoma: 2% of all colonic cancers
    • Lymphoma: often involving terminal ileum
  • INFLAMMATION
    • Crohn disease
    • Ulcerative colitis
      • patulous valve, fixed in open position
    • Tuberculosis
    • Amebiasis
      • terminal ileum not involved (in USA)
    • Typhoid fever, anisakiasis, schistosomiasis, actinomycosis
    • Cathartic abuse
  • PROLAPSE
    • antegrade: indistinguishable from lipomatosis/prolapsing mucosa/neoplasm
    • retrograde
  • INTUSSUSCEPTION
  • LYMPHOID HYPERPLASIA
P.781

Coned Cecum
  • INFLAMMATION
    • Crohn disease
      • involvement of ascending colon + terminal ileum
    • Ulcerative colitis
      • backwash ileitis (in 10%)
      • gaping ileocecal valve
    • Appendicitis
    • Typhlitis
    • Perforated cecal diverticulum
  • INFECTION
    • Tuberculosis
      • colonic involvement more prominent than that of terminal ileum
    • Amebiasis
      • involvement of cecum in 90% of amebiasis
      • thickened ileocecal valve fixed in open position
      • reflux into normal terminal ileum
      • skip lesions in colon
    • Actinomycosis
      • palpable abdominal mass
      • indolent sinus tracts in abdominal wall
    • Blastomycosis
    • Anisakiasis
    • Typhoid, Yersinia
  • TUMOR
    • Carcinoma of the cecum
    • Metastasis to cecum
Cecal Filling Defect
  • ABNORMALITIES OF THE APPENDIX
    • Acute appendicitis/appendiceal abscess
    • Crohn disease
    • Inverted appendiceal stump/appendiceal intussusception
    • Mucocele
    • Myxoglobulosis
    • Appendiceal neoplasm: carcinoid tumor (90%), leiomyoma, neuroma, lipoma, adenocarcinoma, metastasis
  • COLONIC LESION
    • Ameboma
    • Primary cecal neoplasm
    • Ileocolic intussusception
    • Lipomatosis of ileocecal valve
  • UNUSUAL ABNORMALITIES
    • Ileocecal diverticulitis (in 50% < age 30 years)
    • Solitary benign ulcer of the cecum
    • Adherent fecolith (eg, in cystic fibrosis)
    • Endometriosis
    • Burkitt lymphoma
mnemonic: CECUM TIP SALE
  • Carcinoma
  • Enteritis
  • Carcinoid
  • Ulcerative colitis
  • Mucocele of appendix
  • Tuberculosis
  • Intussusception
  • Periappendiceal abscess
  • Stump of the appendix
  • Ameboma
  • Lymphoma
  • Endometriosis
Appendiceal Intussusception
  • Mucocele
  • Endometrioma
  • Fecolith
  • Foreign body
  • Polyp (juvenile, inflammatory)
  • Papilloma
  • Adenoma/adenocarcinoma
  • Carcinoid tumor
  • Postappendectomy stump
Pericecal Fat-Stranding on CT
  • Appendicitis
  • Crohn disease
  • Tuboovarian abscess
  • Cecal diverticulitis
  • Perforated cecal carcinoma
Colon
Colon Transit Time
Sitzmarks diagnostic test:
Indication: adults with severe constipation but otherwise normal GI examination
  • 1. Withhold laxatives/enemas/suppositories for 5 days
  • 2. Patient takes 1 capsule (contains 24 radiopaque polyvinyl chloride markers of 1 × 4.5 mm)
  • 3. Take KUB on day 3 and 5 to determine location + extent of marker elimination
    • ≥19 markers (80%) expelled = grossly normal colonic transit time
    • markers scattered about the colon = colonic hypomotility/inertia
    • markers in rectum/rectosigmoid = functional outlet obstruction (eg, internal rectal prolapse/anismus)
    • ≥5 markers (20%) retained need follow-up KUB on day 7
  • All markers are usually in colon by 12 hours
Colon Cutoff Sign
  • = abrupt termination of colonic gas column at splenic flexure with decompression of the distal colon due to spasm + obstruction at the splenic flexure impinging on a paralytic transverse colon
  • IMPINGEMENT VIA PHRENICOCOLIC LIGAMENT
    • Acute pancreatitis/postpancreatitic stricture
    • Pancreatic/gastric carcinoma
    • Hemorrhage from rupture of splenic artery/abdominal aortic aneurysm
  • COLONIC DISEASE
    • Colon cancer
    • Mesenteric thrombosis
    • Ischemic colitis
    • P.782

    • Perforated appendicitis (in 20%)
      N.B.: amputation of gas at the hepatic flexure due to spastic ascending colon
Colonic Thumbprinting
  • = sharply defined fingerlike marginal indentations at contours of wall
  • 1. ISCHEMIA = Ischemic colitis
    • occlusive vascular disease, hypercoagulability state, hemorrhage into bowel wall (bleeding diathesis, anticoagulants), traumatic intramural hematoma
  • 2. INFLAMMATION
    • ulcerative colitis, Crohn colitis
  • 3. INFECTION
    • acute amebiasis, schistosomiasis, strongyloidiasis, cytomegalovirus (in renal transplant recipients), pseudomembranous colitis
  • 4. MALIGNANT LESIONS
    • localized primary lymphoma, hematogenous metastases
  • 5. MISCELLANEOUS
    • endometriosis, amyloidosis, pneumatosis intestinalis, diverticulosis, diverticulitis, hereditary angioneurotic edema
mnemonic: PSALM II
  • Pseudomembranous colitis
  • Schistosomiasis
  • Amebic colitis
  • Lymphoma
  • Metastases (to colon)
  • Ischemic colitis
  • Inflammatory bowel disease
Colonic Urticaria Pattern
  • OBSTRUCTION
    • Obstructing carcinoma
    • Cecal volvulus
    • Colonic ileus
  • ISCHEMIA
  • INFECTION/INFLAMMATION
    • Yersinia enterocolitis
    • Herpes
    • Crohn disease
  • URTICARIA
Colonic Ulcers
  • IDIOPATHIC
    • Ulcerative colitis
    • Crohn colitis
  • ISCHEMIC
    • Ischemic colitis
  • TRAUMATIC
    • Radiation injury
    • Caustic colitis
  • NEOPLASTIC
    • Primary colonic carcinoma
    • Metastases (prostate, stomach, lymphoma, leukemia)
  • INFLAMMATORY
    • Pseudomembranous colitis
    • Pancreatitis
    • Diverticulitis
    • Behçet syndrome
    • Solitary rectal ulcer syndrome
    • Nonspecific benign ulceration
  • INFECTION
    • protozoan
      • Amebiasis
      • Schistosomiasis
      • Strongyloidiasis
    • bacterial
      • Shigellosis, salmonellosis
      • Staphylococcal colitis
      • Tuberculosis
      • Gonorrheal proctitis
      • Yersinia colitis
      • Campylobacter fetus colitis
    • fungal
      • histoplasmosis, mucormycosis, actinomycosis, candidiasis
    • viral
      • Lymphogranuloma venereum
      • Herpes proctocolitis
      • Cytomegalovirus (transplants)
Aphthous Ulcers of Colon
  • Crohn disease
  • Amebic colitis
  • Yersinia enterocolitis
    Organism: gram-negative
    • fever, diarrhea, RLQ pain
    Location: terminal ileum
    √ thickened folds + ulceration
    √ lymphoid nodular hyperplasia
  • Salmonella, shigella infection
  • Herpes virus infection
  • Behçet syndrome
  • Lymphoma
  • Ischemia
Multiple Bull’s-eye Lesions of Colonic Wall
mnemonic: MaCK CLaN
  • Melanoma and
  • Carcinoma
  • Kaposi sarcoma
  • Carcinoid
  • Lymphoma and
  • Neurofibromatosis
Double-Tracking of Colon
  • = longitudinal extraluminal tracks paralleling the colon
  • 1. Diverticulitis: generally 3–6 cm in length
  • 2. Crohn disease: generally >10 cm
  • 3. Ulcerative colitis
  • 4. Primary carcinoma: wider + more irregular
Colonic Narrowing
  • CHRONIC STAGE OF ANY ULCERATING COLITIS
    • inflammatory:
      • Ulcerative colitis
      • P.783

      • Crohn colitis
      • Solitary rectal ulcer syndrome
      • Nonspecific benign ulcer
    • infectious:
      • Amebiasis
      • Schistosomiasis
      • Bacillary dysentery
      • Tuberculosis
      • Fungal disease
      • Lymphogranuloma venereum
      • Herpes zoster
      • Cytomegalovirus
      • Strongyloides
    • ischemic
      • Ischemic colitis
    • traumatic
      • Radiation injury
      • Cathartic colon
      • Caustic colitis
  • MALIGNANT LESION
    • primary
      • Colonic carcinoma (annular/scirrhous)
      • Complication of ulcerative colitis + Crohn colitis
    • metastatic:
      • from prostate, cervix, uterus, kidney, stomach, pancreas, primary intraperitoneal sarcoma
      • — hematogenous (eg, breast)
      • — lymphangitic spread
      • — peritoneal seeding
  • EXTRINSIC PROCESS
    • inflammation
      • Retractile mesenteritis
      • Diverticulitis
      • Pancreatitis
    • deposits
      • Amyloidosis
      • Endometriosis
      • Pelvic lipomatosis
  • POSTSURGICAL
    • Adhesive bands
    • Surgical anastomosis
  • NORMAL
    • Cannon point
Localized Colonic Narrowing
mnemonic: SCARED CELL-MATE
  • Schistosomiasis
  • Carcinoid
  • Actinomycosis
  • Radiation
  • Endometriosis
  • Diverticulitis
  • Colitis
  • Extrinsic lesion
  • Lymphoma
  • Lymphogranuloma venereum
  • Metastasis
  • Adenocarcinoma
  • Tuberculosis
  • Entamoeba histolytica
Microcolon
mnemonic: MI MCA
  • Meconium ileus, Meconium peritonitis (cystic fibrosis)
  • Ileal/jejunal atresia
  • Megacystis-microcolon-hypoperistalsis syndrome
  • Colonic atresia (distal to atretic segment)
  • Aganglionosis (Hirschsprung disease)
Colonic Filling defects
Submucosal Tumor of Colon
  • Lipoma
  • Carcinoid
  • Leiomyoma
  • Lymphangioma, hemangioma
Single Colonic Filling Defect
  • BENIGN TUMOR
    • Polyp
      • (hyperplastic, adenomatous, villous adenoma, villoglandular); most common benign tumor
    • Lipoma
      • Most common intramural tumor; 2nd most common benign tumor; M < F
      Location: ascending colon + cecum > left side of colon
    • Carcinoid: 10% metastasize
    • Spindle cell tumor
      • (leiomyoma, fibroma, neurofibroma); 4th most common benign tumor; rectum > cecum
    • Lymphangioma, hemangioma
  • MALIGNANT TUMOR
    • primary tumor:
      • carcinoma, sarcoma
    • secondary tumor:
      • metastases (breast, stomach, lung, pancreas, kidney, female genital tract), lymphoma, invasion by adjacent tumors
  • INFECTION
    • Ameboma
    • Polypoid granuloma: schistosomiasis, TB
  • INFLAMMATION
    • Inflammatory pseudopolyp: ulcerative colitis, Crohn disease
    • Periappendiceal abscess
    • Diverticulitis
    • Foreign-body perforation
  • NONSESSILE INTRALUMINAL BODY
    • Fecal impaction
    • Foreign body
    • Gallstone
    • Bolus of Ascaris worms
  • MISCELLANEOUS
    • Endometriosis
      • 3rd most common benign tumor
      Location: sigmoid colon, rectosigmoid junction (at level of cul-de-sac)
      • may cause bleeding (after invasion of mucosa)
    • Localized amyloid deposition
    • Suture granuloma
    • P.784

    • Intussusception
    • Pseudotumor (adhesions, fibrous bands)
    • Colitis cystica profunda
Multiple Colonic Filling Defects
  • NEOPLASMS
    • polyposis syndrome:
      • familial polyposis, Gardner syndrome, Peutz-Jeghers syndrome, Turcot syndrome, juvenile polyposis syndrome, disseminated gastrointestinal polyps, multiple adenomatous polyps
    • hematogenous metastases:
      • from breast, lung, stomach, ovary, pancreas, uterus
    • multiple tumors
      • benign:
        • neurofibromatosis, colonic lipomatosis, multiple hamartoma syndrome (Cowden disease)
      • malignant:
        • lymphoma, leukemia, adenocarcinoma
  • INFLAMMATORY PSEUDOPOLYPS
    • ulcerative colitis, Crohn colitis, ischemic colitis, amebiasis, schistosomiasis, strongyloidiasis, trichuriasis
  • ARTIFACTS
    • feces, air bubbles, oil bubbles, mucous strands, ingested foreign body (eg, corn kernels)
  • MISCELLANEOUS
    • nodular lymphoid hyperplasia, lymphoid follicular pattern, hemorrhoids, diverticula, pneumatosis intestinalis, colitis cystica profunda, colonic urticaria, submucosal colonic edema secondary to obstruction, cystic fibrosis, amyloidosis, ulcerative pseudopolyps, proximal to obstruction
mnemonic: MILL P3
  • Metastases (to colon)
  • Ischemia (thumbprinting)
  • Lymphoma
  • Lymphoid hyperplasia
  • Polyposis
  • Pseudopolyposis (with inflammatory bowel disease)
  • Pneumatosis cystoides
Carpet Lesions of Colon
  • = flat lobulated lesions with alteration of surface texture + little/no protrusion into lumen
Location: rectum > cecum > ascending colon
Cause:
  • NEOPLASM
    • Tubular/tubulovillous/villous adenoma
    • Familial polyposis
    • Adenocarcinoma
    • Submucosal tumor spread (from adjacent carcinoma)
  • MISCELLANEOUS
    • Nonspecific follicular proctitis
    • Biopsy site
    • Endometriosis
    • Rectal varices
    • Colonic urticaria
Colonic Polyp
Terminology:
  • Polyp
    • = mass projecting into the lumen of a hollow viscus above the level of the mucosa; usually arises from mucosa, may derive from submucosa/muscularis propria
    • (a) neoplastic: adenoma/carcinoma
    • (b) nonneoplastic: hamartoma/inflammatory polyp
  • Pseudopolyp
    • = scattered island of inflamed edematous mucosa on a background of denuded mucosa
    • (a) pseudopolyposis of ulcerative colitis
    • (b) “cobblestoning” of Crohn disease
  • Postinflammatory (filiform) polyp
    • = fingerlike projection of submucosa covered by mucosa on all sides following healing + regeneration of inflammatory (most common in ulcerative colitis)/ischemic/infectious bowel disease
Histologic classification:
  • ADENOMATOUS POLYPS
    • = Familial adenomatous polyposis syndrome
      Cause: abnormality on chromosome 5
      Cx: adenomatous polyps are premalignant eventually leading to colorectal carcinoma
    • 1. Familial (multiple) polyposis
    • 2. Gardner syndrome
    • 3. Turcot syndrome
  • HAMARTOMATOUS POLYPS
    • = Hamartomatous polyposis syndromes
    • 1. Peutz-Jeghers syndrome (most in small bowel)*
    • 2. Cowden disease*
    • 3. Juvenile polyposis*
    • 4. Cronkhite-Canada syndrome
    • 5. Bannayan-Riley-Ruvalcaba syndrome
  • POLYPOSIS LOOK-ALIKES
    • Inflammatory polyposis
    • Lymphoid hyperplasia
    • Lymphoma
    • Metastases
    • Pneumatosis coli
Polyposis Syndromes
  • = more than 100 polyps in number
Mode of transmission:
  • HEREDITARY
    • autosomal dominant
      • Familial (multiple) polyposis
      • Gardner syndrome
      • Peutz-Jeghers syndrome
      • Juvenile polyposis coli
    • autosomal recessive
      • Turcot syndrome
  • NONHEREDITARY
    • Cronkhite-Canada syndrome
    • Juvenile polyposis
P.785

Differential Diagnosis of Colonic polyps
Single Polyp Multiple Polyps
Neoplastic (10%)
— epithelial (adenomatous)
  1. Tubular adenoma
  2. Tubulovillous adenoma
  3. Villous adenoma
  1. Familial multiple polyposis
  2. Adenomatosis of GI tract
  3. Gardner syndrome
  4. Turcot syndrome
— nonepithelial
  1. Carcinoid
  2. Leiomyoma
  3. Lipoma
  4. Hemangioma, lymphangioma
  5. Fibroma, neurofibroma
Nonneoplastic (90%)
— unclassified
  1. Hyperplastic polyp
  1. Hyperplastic polyposis
— hamartomatous
  1. Juvenile polyps
  1. Juvenile polyposis
  2. Peutz-Jeghers syndrome
  3. Cronkhite-Canada syndrome
— inflammatory
  1. Benign lymphoid polyp
  2. Fibroid granulation polyp
  1. Ulcerative colitis
Mural Stratification of Intestinal Tract
  • = bowel wall thickening with abnormal separation of bowel layers on cross-sectional imaging
  • CECT:
    • “double halo/target” sign during arterial phase:
      • contrast enhancement of inner layer:
        • (1) mucosa + (2) muscularis propria
      • interposed edema (water)/hemorrhage (blood)/inflammatory cell infiltrate (pus, cells)/fatty proliferation:
        • (3) submucosa
      • contrast enhancement of outer layer:
        • (4) muscularis propria + (5) serosa
  • Cause:
    • Tumor has not been reported to cause stratification!
    • EDEMA
      • low-density/water-density separation
      • 1. Ulcerative colitis (50%): rectum
      • 2. Proximal to obstructing tumor/intussusception
    • INFLAMMATORY CELL INFILTRATE
      • Crohn disease (in up to 50%)
      • Mycobacterium tuberculosis
      • Eosinophilic enteritis
      • Cytomegalovirus
      • Clostridium difficile
      • Entamoeba histolytica
      • Vibrio cholerae
      • Shigella
      • Escherichia coli
    • ISCHEMIA/INFARCTION
      • Arterial obstruction: thromboembolism, plaque thrombus
      • Peripheral vasculopathy
      • Venous obstruction: thrombosis, bowel torsion, closed-loop obstruction
      • Hypoperfusion: proximal arterial stenosis potentiated by myocardial infarction, bradycardia, dehydration
        N.B.: closed-loop obstruction with signs of bowel infarction is a surgical condition!
        • signs of bowel infarction:
          • free peritoneal fluid
          • asymmetric bowel wall enhancement
          • persistent enhancement of bowel wall/segmental arteries
          • arterial/venous filling defects
          • increased density of mesentery
          • bowel obstruction
    • INTESTINAL WALL HEMORRHAGE
      • Anticoagulation
      • Blood dyscrasia: thrombocytopenic purpura
      • Blunt trauma
        • “snow-cone” appearance of duodenum
Pseudomembranous Colitis
  • Clostridium difficile
  • Ischemic colitis: acute/subacute
  • Staphylococcus
  • Shigella
  • Pseudomonas aeruginosa
6. Drugs: chlorpropamide, mercuric compounds, gold, NSAIDs
Accordion Sign
  • = gross irregular polypoid thickening of colonic wall with wide separation of inner + outer walls
  • Radiation-induced colitis
  • Ischemic colitis
  • Infectious colitis: Clostridium difficile, tuberculosis
  • Typhlitis, neutropenic colitis
  • Inflammation: Crohn disease, ulcerative colitis
    • The only 2 conditions with wall thickening >10 mm
  • P.786

  • Lymphangiectasia
  • Intramural hemorrhage
Rectum & Anus
Rectal Narrowing
  • Pelvic lipomatosis + fibrolipomatosis
  • Lymphogranuloma venereum
  • Radiation injury of rectum
  • Chronic ulcerative colitis
Enlarged Presacral Space
  • Normal width <5 mm in 95%; abnormal width >10 mm
  • RECTAL INFLAMMATION/INFECTION
    • ulcerative colitis, Crohn colitis, idiopathic proctosigmoiditis, radiation therapy
  • RECTAL INFECTION
    • Proctitis (TB, amebiasis, lymphogranuloma venereum, radiation, ischemia)
    • Diverticulitis
  • BENIGN RECTAL TUMOR
    • Developmental cyst (dermoid, enteric cyst, tailgut cyst)
    • Lipoma, neurofibroma, hemangioendothelioma
    • Epidermal cyst
    • Rectal duplication
  • MALIGNANT RECTAL TUMOR
    • Adenocarcinoma, cloacogenic carcinoma
    • Lymphoma, sarcoma, lymph node metastases
    • Prostatic carcinoma, bladder tumors, cervical cancer, ovarian cancer
  • BODY FLUIDS/DEPOSITS
    • Hematoma: surgery, sacral fracture
    • Pus: perforated appendix, presacral abscess
    • Serum: edema, venous thrombosis
    • Deposit of fat: pelvic lipomatosis, Cushing disease
    • Deposit of amyloid: amyloidosis
  • SACRAL TUMOR
    • Sacrococcygeal teratoma, anterior sacral meningocele
    • Chordoma, metastasis to sacrum
  • MISCELLANEOUS
    • Inguinal hernia containing segment of colon
    • Colitis cystica profunda
    • Pelvic lipomatosis
Lesions of Ischiorectal Fossa
  • Congenital and developmental anomalies
    • Gartner duct cyst
    • Klippel-Trenaunay syndrome
    • Tailgut cyst
  • Inflammatory and hemorrhagic lesions
    • Fistula in ano
    • Ischiorectal/perirectal abscess
    • Extraperitoneal pelvic hematoma
    • Rectal perforation
  • Secondary neoplasm
    • per direct extension/hematogenous spread:
      • anorectal/prostatic/pelvic/sacral tumor; lung cancer; melanoma; lymphoma
  • Primary neoplasm
    • Aggressive angiomyxoma
    • Lipoma
    • Plexiform neurofibroma
    • Anal adenocarcinoma
    • Squamous cell carcinoma
Peritoneum
Peritoneal Mass
  • SOLID MASS
    • Peritoneal mesothelioma
    • Peritoneal carcinomatosis
  • INFILTRATIVE PATTERN
    • Peritoneal mesothelioma
  • CYSTIC MASS
    • Cystic mesothelioma
    • Pseudomyxoma peritonei
    • Bacterial/mycobacterial infection
Multiple Peritoneal Masses
  • Metastases: RCC
  • Endometriosis
  • Abdominal lymphoma
Mesentery & Omentum
Short Mesentery
  • = shortened line of fixation
  • 1. Malrotation + midgut volvulus
  • 2. Omphalocele
  • 3. Gastroschisis
  • 4. Congenital diaphragmatic hernia
  • 5. Asplenia + polysplenia
“Apple peel” Small Bowel
  • = distal small intestines spirals around its vascular supply resembling an apple peel resulting in a very short intestine
  • 1. Proximal jejunal atresia
  • 2. Absence of distal superior mesenteric artery
  • 3. Shortening of small bowel distal to atresia
  • 4. Absence of dorsal mesentery
Cx: propensity toward necrotizing enterocolitis
Prognosis: high mortality
Omental Mass
  • 33% of primary omental tumors are malignant!
  • Secondary neoplasms are more frequent than primary!
  • SOLID MASS
    • benign
      • Leiomyoma
      • Lipoma
      • Neurofibroma
    • malignant
      • Leiomyosarcoma
      • Liposarcoma
      • Fibrosarcoma
      • Lymphoma
      • Peritoneal mesothelioma
      • Hemangiopericytoma
      • Metastases
    • Infection: tuberculosis
  • P.787

  • CYSTIC MASS
    • Hematoma
    • Cystic mesothelioma
Omental Cake
  • = replacement of normal fat of the greater omentum by a soft-tissue density
  • Peritoneal metastases
    mnemonic: COPS
    • Colon
    • Ovary
    • Pancreas
    • Stomach
  • Lymphoma
  • Mesothelioma
  • Tuberculosis
Mesenteric Mass
  • ROUND SOLID MASSES
    • Benign primary tumors are more common than malignant primary tumors!
    • Secondary neoplasms more frequent than primary
    • Cystic tumors more common than solid tumors!
    • Malignant solid tumors have a tendency to be located near root of mesentery, benign solid tumors in periphery near bowel!
    • 1. Metastases especially from colon, ovary (most frequent neoplasm of mesentery)
    • 2. Lymphoma
    • 3. Leiomyosarcoma (more frequent than leiomyoma)
    • 4. Neural tumor (neurofibroma, ganglioneuroma)
    • 5. Lipoma (uncommon), lipomatosis, liposarcoma
    • 6. Fibrous histiocytoma
    • 7. Hemangioma
    • 8. Desmoid tumor (most common primary)
    • 9. Desmoplastic small round cell tumor of peritoneum
  • ILL-DEFINED MASSES
    • Metastases (ovary)
    • Lymphoma
    • Fibromatosis, fibrosing mesenteritis (associated with Gardner syndrome)
    • Lipodystrophy
    • Mesenteric panniculitis
  • STELLATE MASSES
    • 1. Peritoneal mesothelioma
    • 2. Retractile mesenteritis
    • 3. Fibrotic reaction of carcinoid
    • 4. Radiation therapy
    • 5. Desmoid tumor
    • 6. Hodgkin disease
    • 7. Tuberculous peritonitis
    • 8. Ovarian metastases
    • 9. Diverticulitis
    • 10. Pancreatitis
    • A calcified mesenteric mass suggests carcinoid tumor!
  • LOCULATED CYSTIC MASSES (2/3)
    • Cystic lymphangioma (most common)
    • Pseudomyxoma peritonei
    • Cystic mesothelioma
    • Mesenteric cyst
    • Mesenteric hematoma
    • Benign cystic teratoma
    • Cystic spindle cell tumor (= centrally necrotic leiomyoma/leiomyosarcoma)
Mesenteric/Omental Cysts
  • = “BUBBLES OF THE BELLY”
  • The first step is to determine the organ of origin!
  • 1. Lymphangioma
  • 2. Nonpancreatic pseudocyst
    • = sequelae of mesenteric/omental hematoma/abscess
    Path: thick-walled, usually septated cystic mass with hemorrhagic/purulent contents
  • 3. Duplication cyst
  • 4. Mesothelial cyst
  • 5. Enteric cyst
  • 6. Cystic metastasis
  • 7. Cystic mesothelioma
Mesenteric Edema/Congestion
  • increase of mesenteric fat attenuation to–40 to–60 HU
  • loss of sharp interfaces between mesenteric vessels + fat
  • SYSTEMIC FLUID OVERLOAD
    • Hypoalbuminemia
    • Liver cirrhosis
    • Nephrosis
    • Heart failure
  • LOCAL VESSEL DISEASE
    • Portal vein thrombosis
    • Mesenteric vein/artery thrombosis
    • Vasculitis
    • SMA dissection
  • CELL INFILTRATE
    • Malignant neoplasm
    • Inflammation
    • Trauma (small hemorrhage)
Comb Sign
  • = vascular dilatation of vasa recta + interconnected arterial arcades aligned as the teeth of a comb
  • multiple tubular tortuous opacities on mesenteric side of ileum
  • 1. Crohn disease
  • 2. Ulcerative colitis
  • 3. Vasculitis: Lupus, polyarteritis nodosa, Henoch-Schönlein syndrome, microscopic polyangiitis, Behçet syndrome
  • 4. Mesenteric thromboembolism
  • 5. Strangulated bowel obstruction
Fat Ring Sign
  • = fat-stranding of the fat plane surrounding the root of mesenteric vessels
  • benign
    • Mesenteric panniculitis
    • Mesenteric lipodystrophy
    • Retractile mesenteritis
  • malignant
    • Carcinoid
    • Desmoid tumor
    • Lymphoma
P.788

Umbilical Tumor
  • PRIMARY (38%)
    • benign/malignant neoplasm, skin tumor
  • METASTASES (30%)
    • = “Sister Joseph nodule”
    • • firm painful nodule
    • • ± ulceration with serosanguinous/purulent discharge
    Cause: gastrointestinal cancer (50%), undetermined (25%), ovarian cancer, pancreatic cancer, small cell carcinoma of lung (very rare)
    • Spread:
      • direct extension from anterior peritoneal surface
      • extension along embryonic remnants: falciform, median umbilical, omphalomesenteric ligaments
      • hematogenous
      • retrograde lymphatic flow from inguinal, axillary, paraaortic nodes
      • iatrogenic: laparoscopic tract, tract of percutaneous needle biopsy
  • NONNEOPLASTIC
    • Endometriosis (32%)
    • Granuloma
    • Incarcerated hernia
Abdominal Lymphadenopathy
Regional Patterns of Lymphadenopathy
  • @ Retrocrural nodes
    Abnormal size: >6 mm
    Common cause: lung carcinoma, mesothelioma, lymphoma
  • @ Gastrohepatic ligament nodes
    • = superior portion of lesser omentum suspending stomach from liver
    Abnormal size: >8 mm
    Common cause: carcinoma of lesser curvature of stomach, distal esophagus, lymphoma, pancreatic cancer, melanoma, colon + breast cancer
    DDx: coronary varices
  • @ Porta hepatis nodes
    • = in porta hepatis extending down hepatoduodenal ligament, anterior + posterior to portal vein
    Abnormal size: >6 mm
    Common cause: carcinoma of gallbladder + biliary tree, liver, stomach, pancreas, colon, lung, breast
    Cx: high extrahepatic biliary obstruction
  • @ Pancreaticoduodenal nodes
    • = between duodenal sweep + pancreatic head anterior to IVC
    Abnormal size: >10 mm
    Common cause: lymphoma, pancreatic head, colon, stomach, lung, breast cancer
  • @ Perisplenic nodes
    • = in splenic hilum
    Abnormal size: >10 mm
    Common cause: NHL, leukemia, small bowel neoplasm, ovarian cancer, carcinoma of right/transverse colon
  • @ Retroperitoneal nodes
    • = periaortic, pericaval, interaortocaval
    Abnormal size: >10 mm
    Common cause: lymphoma, renal cell, testicular, cervical, prostatic carcinomas
  • @ Celiac and superior mesenteric artery nodes
    • = preaortic nodes
    Abnormal size: >10 mm
    Common cause: any intraabdominal neoplasm
  • @ Pelvic nodes
    • = along common, external + internal iliac vessels
    Abnormal size: >15 mm
    Common cause: carcinoma of bladder, prostate, cervix, uterus, rectum
Low-Attenuation Abdominal Adenopathy
  • = ENLARGED LYMPH NODE WITH LOW-DENSITY CENTER
  • 1. Mycobacterial infection (TB, M. avium-intracellulare)
  • 2. Pyogenic infection
  • 3. Whipple disease
  • 4. Lymphoma
  • 5. Metastatic disease after radiation + chemotherapy
  • 6. Lymphangioleiomyomatosis
  • 7. Neurofibromatosis type I
  • 8. Cavitating mesenteric lymph node syndrome
P.789

Anatomy and Function of Gastrointestinal Tract
Gastrointestinal hormones
Cholecystokinin
  • = CCK = 33 amino acid residues (former name: Pancreozymin); the 5 C-terminal amino acids are identical to those of gastrin, causing similar effects as gastrin; 2.5-minute serum half-life
Produced in: duodenal + upper intestinal mucosa
Released by: fatty acids, some amino acids (phenylalanine, methionine), hydrogen ions
  • Effects:
    • @ Stomach
      • weakly stimulates HCl secretion
      • given alone: inhibits gastrin, which leads to decrease in HCl production
      • stimulates pepsin secretion
      • stimulates gastric motility
    • @ Pancreas
      • stimulates secretion of pancreatic enzymes (= Pancreozymin)
      • stimulates bicarbonate secretion (weakly by direct effect; strongly through potentiating effect on secretin)
      • stimulates insulin release
    • @ Liver
      • stimulates water + bicarbonate secretion
    • @ Intestine
      • stimulates secretion of Brunner glands
      • increases motility
    • @ Biliary tract
      • strong stimulator of gallbladder contraction with maximum effect within 5–15 minutes + return to basal size in 1 hour
      • relaxation of sphincter of Oddi
  • Medication:
    • sincalide (Kinevac®) = synthetic C-terminal octapeptide of the hormone cholecystokinin
    Use: may be used to empty gallbladder about 30 minutes (to 4 hours) before tracer injection in patients on prolonged fasting (gallbladder atony + retained bile and sludge secondary to absence of endogenously produced CCK)
    • Dose for hepatobiliary scintigraphy:
      • preferred: IV infusion of 0.01 μg/kg Kinevac® over 30–60 minutes;
      • package insert: with slow IV injection of 0.01 μg/kg Kinevac® over 3 minutes (concentration of 1 μg/mL) the response is too variable
    Useful in:
    1. (a) patient fasting >24 hours/on total parenteral nutrition
    2. (b) acalculous cholecystitis
    3. (c) chronic GB dysfunction
    4. (d) GB ejection fraction
    Side effect: increase in biliary-to-bowel transit time, dizziness, flushing, nausea, abdominal cramps, urge to defecate
    • Contraindications:
      • acute pancreatitis, acute cholecystitis, obstruction of cystic duct/CBD, appendicitis, peritonitis, pyloric stenosis, peptic ulcer
Gastrin
  • = 17 amino acid peptide amide;
  • PENTAGASTRIN
    • = acyl derivative of the biologic active C-terminal tetrapeptide amide
Produced in: antral cells + G cells of pancreas
Released by:
  1. vagal stimulation, gastric distension
  2. short-chain alcohol (ethanol, propanol)
  3. amino acids (glycine, β-alanine)
  4. caffeine
  5. hypercalcemia

mediated by neuroendocrine cholinergic reflexes
Inhibited by: drop in pH of antral mucosa to <3.5
  • Effects:
    • @ Stomach:
      • stimulation of gastric HCl secretion from parietal cells, which in turn:
      • increases pepsinogen production by chief cells through local reflex
      • increase in antral motility
      • trophic effect on gastric mucosa (parietal cell hyperplasia)
    • @ Pancreas
      • strong increase in enzyme output
      • weakly stimulates fluid + bicarbonate output
      • stimulates insulin release
    • @ Liver
      • water + bicarbonate secretion
    • @ Intestine
      • stimulates secretion of Brunner glands
      • increases motility
    • @ Gallbladder
      • stimulates contraction
    • @ Esophagus
      • increases resting pressure of LES
Glucagon
Produced in: α cells (and β cells) of pancreas
Released by: low blood glucose levels
  • Effects:
    • @ Intestines
      • lowers pressure of GE sphincter
      • hypotonic effect on duodenum > jejunum > stomach > colon
    • @ Hormones
      • releases catecholamines from the adrenal gland that paralyze intestinal smooth muscle
      • increases serum insulin + glucose levels (mobilization of hepatic glycogen)
    • @ Biliary tract
      • increases bile flow
      • P.790

      • relaxes gallbladder + sphincter of Oddi
Dose for radiologic imaging: 1 mg maximum
  • IV administration causes a quick response + rapid dissipation of action!
  • IM administration prolongs onset + increases length of action!
Half-life: 3–6 minutes
Side effects: nausea + vomiting, weakness, dizziness (delayed onset of 1.5–4 hours after IM administration)
  • Contraindication:
    • hypersensitivity/allergy to glucagon: urticaria, periorbital edema, respiratory distress, hypotension, coronary artery spasm (?), circulatory arrest
    • known hypertensive response to glucagon
    • pheochromocytoma: glucagon stimulates release of catecholamines
    • insulinoma: insulin-releasing effect may result in hypoglycemia
    • glucagonoma
    • poorly controlled diabetes mellitus
Secretin
Produced in: duodenal mucosa
Released by: hydrogen ions providing a pH <4.5
  • Effects:
    • @ Stomach
      • inhibits gastrin activity, which leads to decrease in HCl secretion
      • stimulates pepsinogen secretion by chief cells (potent pepsigogue)
      • decreases gastric and duodenal motility + contraction of pyloric sphincter
    • @ Pancreas
      • increases alkaline pancreatic secretions (NaHCO3)
      • weakly stimulates enzyme secretion
      • stimulates insulin release
    • @ Liver
      • stimulates water + bicarbonate secretion (most potent choleretic)
    • @ Intestine
      • stimulates secretion of Brunner glands
      • inhibits motility
    • @ Esophagus
      • opens LES
Embryology of alimentary tract
Origin: as a pouchlike extension of the yolk sac
Development of GI tube:
  • continuous tubular structure by 6 weeks GA; divided into:
    • foregut (supplied by celiac artery)
    • midgut (supplied by superior mesenteric artery)
    • hindgut (supplied by inferior mesenteric artery)
Rotation about omphalomesenteric vessels by 270°:
  • <6 weeks GA
    • 90° counterclockwise rotation of duodenojejunal segment toward the right of SMA
    • 90° counterclockwise rotation of ileocolic segment toward the left of SMA
  • during 6th week GA
    • additional 90° counterclockwise rotation of duodenum posterior to SMA
    • remainder of midgut within umbilical cord
  • 10–12 weeks GA
    • intestines slides back into peritoneal cavity
    • final 90° counterclockwise rotation of duodenum
    • final 180° counterclockwise rotation of cecum
Peritoneal fixation of small bowel:
  • broad-based mesentery extending from ligament of Treitz to ileocecal valve
image
Stages of Intestinal Rotation
P.791

image
Blood Supply of Stomach, Duodenum, and Pancreas
image
Blood Supply of Large Intestine
P.792

Vascular Supply of Bowel
  • bowel receives 20% of resting cardiac output (2/3 for intestinal mucosa) which increases up to 35% in postprandial phase
    • earliest + fast rise after intake of carbohydrates
    • slower + large rise after intake of fat + proteins
Celiac Trunk
Supply for: from distal esophagus to descending duodenum
Anastomosis: to SMA via gastroduodenal artery as the 1st branch off the celiac trunk
Superior Mesenteric Artery (SMA)
Supply for: transverse + descending duodenum, jejunum, ileum, large bowel to splenic flexure
Anastomosis: to IMA via marginal artery of Drummond, arcade of Riolan
Inferior Mesenteric Artery (IMA)
Supply for: colon from splenic flexure to rectum
Anastomoses: to lumbar branches of abdominal aorta, sacral artery, internal iliac aa.
Arcades
  • up to four arcades are formed by these arteries which continue toward the periphery as
    • Primary parallel circuits for
      • muscularis propria
      • submucosa
      • mucosa
    • Serial circuits of
      • resistance arterioles
      • precapillary sphincters
      • capillaries
      • postcapillary sphincters
      • venous capacitance vessels
Esophagus
Lower Esophageal Anatomy
  • Esophageal Vestibule
    • = saccular termination of lower esophagus with upper boundary at tubulovestibular junction + lower boundary at esophagogastric junction
    • collapsed during resting state
    • assumes bulbous configuration with swallowing
    • (a) tubulovestibular junction = A level = junction between tubular and saccular esophagus
    • (b) phrenic ampulla = bell-shaped part above diaphragm (term should be discarded because of dynamic changes of configuration)
    • (c) submerged segment = infrahiatal part of esophagus
      • widening/disappearance is indicative of gastroesophageal reflux disease (GERD)
  • Gastroesophageal Junction
    Site: at upper level of gastric sling fibers, straddles cardiac incisura demarcating the left lateral margin of GE junction
  • Z-line = B level = zigzag-shaped squamocolumnar junction line
    • Not acceptable criterion for locating GE junction
    Site: 1–2 cm above gastric sling fibers
  • Lower Esophageal Sphincter
    • = physiologic 2–4-cm high pressure zone corresponding to esophageal vestibule
    • tightly closed during resting state
    • assumes bulbous configuration with swallowing
Muscular Rings of Esophagus
A Ring
  • = contracted/hypertrophied muscles in response to incompetent GE sphincter
  • • rarely symptomatic/dysphagia
Location: at tubulovestibular junction = superior aspect of vestibule
  • usually 2 cm proximal to GE junction at upper end of vestibule
  • varies in caliber during the same examination, may disappear on maximum distension
  • broad smooth narrowing with thick rounded margins
  • visible only if tubular esophagus above + vestibule below are distended
B Ring
  • = sling fibers representing a U-shaped thickening of inner muscle layers with open arm of U toward lesser curvature = inferior aspect of vestibule
Location: < 2 cm from hiatal margins
  • only visible when esophagogastric junction is above hiatus
  • thin ledge-like ring just below the mucosal junction (Z-line)
Swallowing function
Technique: videofluoroscopy of a modified barium swallow study to assess handling of bolus (with consistency of nectar liquid, honey liquid, pureed food, soft solid food, hard solid food); preferably together with speech pathologist
Document patient behavior + reaction: episode of refusal, cough, silent aspiration, apnea, bradycardia
CNS involved: cranial nerves V, VII, IX, X, XII; 5 cervical nerves; cortical + subcortical pathways; midbrain; brainstem
Muscles involved: 32 groups of muscles
Developmental: swallowing as early as 11 weeks GA; suckling at 18–24 weeks GA; nonnutritive sucking at 27–28 weeks GA; single breath sucking at 35–36 weeks GA
Phases:
  • Oral preparatory phase
    • food chewed + mixed with saliva
  • Oral phase
    • bolus propelled posteriorly to tongue
    • Path:
      • spillage from mouth
      • small bolus formation
      • tongue tremor
      • incomplete tongue elevation
      • early spillage into valleculae prior to initiation of swallow
  • P.793

  • Pharyngeal phase
    • elevation of soft palate + valleculae (to seal nasopharynx)
    • elevation of larynx (to close vestibule)
    • relaxation of cricopharyngeal muscle
    • contraction of lateral pharyngeal wall
    • Path:
      • nasopharyngeal reflux
      • laryngeal penetration (= contrast material enters laryngeal vestibule
        Cause: delayed elevation of larynx
      • tracheal aspiration (= contrast material enters airway below vocal cord level)
        Cause: delayed elevation of larynx, delayed pharyngeal transit time, decreased clearance of bolus with residual in vallecula + pyriform sinus spilling into larynx + trachea
  • Esophageal phase
    • contraction of cricopharyngeal muscle
    • bolus transfer into esophagus
    Path: cricopharyngeal achalasia (with reflux of bolus into oropharynx/pooling in pyriform sinus)
Stomach
Gastric cells
  • Chief cells
    • = peptic/zymogenic cells
    Location: body + fundus
    produce: pepsinogen
  • Parietal cells
    • = oxyntic cells
    Location: body + fundus
    produce: H+, Cl-, intrinsic factor, prostaglandins
  • Mucous neck cells
    produce: mucoprotein, mucopolysaccharide, aminopolysaccharide sulfate
  • Argentaffine cells
    • = enteroendocrine cells
    Location: body + fundus
    produce: glucagon-like substance (A-cells), somatostatin (D-cells), vasoactive intestinal polypeptide (D1-cells), 5-hydroxytryptamine (EC-cells)
  • G-cells
    Location: pylorus
    produce: gastrin
Effect of Bilateral Vagotomy
  • = cholinergic denervation
  • (1) decreased MOTILITY of stomach + intestines
  • (2) decreased GASTRIC SECRETION
  • (3) decreased TONE OF GALLBLADDER + bile ducts
  • (4) increased TONE OF SPHINCTERS (Oddi + lower esophageal sphincter)
Pylorus
  • = fan-shaped specialized circular muscle fibers with:
    • distal sphincteric loop = right canalis loop
      • corresponds to radiologic pyloric sphincter
    • proximal sphincteric loop = left canalis loop
      • 2 cm proximal to distal sphincteric loop on greater curvature (seen during complete relaxation)
    • torus
      • = fibers of both sphincters converge on the lesser curvature side to form a muscular prominence; prolapse of mucosa between sphincteric loops produces a niche simulating ulcer
  • pyloric channel 5–10 mm long, wall thickness of 4–8 mm
  • concentric indentation of the base of the duodenal bulb
image
Pyloric Muscular Anatomy
Small Bowel
  • Longest tubular organ in body measuring 550–600 cm (18–22 feet) in length
Segments: –duodenum of 25–30 cm in length
–jejunum of 10–12 feet in length (= proximal 60%)
–ileum of 6–8 feet in length (= distal 40%)
Mesentery: 15 cm long between ligament of Treitz + ileocecal junction
Duodenal Segments
  • duodenal bulb + short postbulbar segment:
    • intraperitoneal + freely movable
  • descending duodenum:
    • retroperitoneal attached to head of pancreas
  • horizontal = transverse segment:
    • retroperitoneal crossing the spine
  • ascending portion
    • retroperitoneal ascending to level of duodenojejunal junction
  • VARIATIONS:
    • “mobile duodenum”/“water-trap duodenum”
      • = long postbulbar segment with undulation/redundancy
    • duodenum inversum/duodenum reflexum
      • = distal duodenum ascends to the right of spine to the level of duodenal bulb + then crosses spine horizontally + fixated in normal location
Small Bowel Folds
  • Circular small bowel folds = folds of Kerckring
    • = valvulae conniventes = two mucosal layers around a core of submucosa
  • NORMAL FOLD THICKNESS
    @ jejunum 1.7–2.0 mm >2.5 mm pathologic
    @ ileum 1.4–1.7 mm >2.0 mm pathologic
  • P.794

  • NORMAL NUMBER OF FOLDS
    @ jejunum 4–7/inch
    @ ileum 2–4/inch
  • NORMAL FOLD HEIGHT
    @ jejunum 3.5–7.0 mm
    @ ileum 2.0–3.5 mm
  • NORMAL LUMEN DIAMETER
    @ upper jejunum 3.0–4.0 cm >4.5 cm pathologic
    @ lower jejunum 2.5–3.5 cm >4.0 cm pathologic
    @ ileum 2.0–2.8 cm >3.0 cm pathologic
  • RULE OF 3’s:
    • Wall thickness <3 mm
    • Valvulae conniventes <3 mm
    • Diameter <3 cm
    • Air-fluid levels <3
Normal Bowel Caliber
mnemonic: 3-6-9-12
3 cm maximal size of small bowel
<25 mm on CT
6 cm maximal size of transverse colon
9 cm maximal size of cecum
12 cm maximal caliber of cecum before it may burst
Small Bowel Peristalsis
  • INCREASED
    • Vagal stimulation
    • Acetylcholine
    • Anticholinesterase (eg, neostigmine)
    • Cholecystokinin
  • DECREASED
    • Atropine (eg, Pro-Banthine®)
    • Bilateral vagotomy
Intestinal function
Intestinal Gas
  • INFLUX
    1. Aerophagia
    2. Liberation from intestinal tract
      1. neutralization of bicarbonate insecretions (CO2)
      2. bacterial fermentation (CO2, H2, CH4, H2S)
    3. Diffusion from blood (N2, O2, CO2)
    2 L

    8 L
    15 L
  • EFFLUX
    1. Diffusion from intestines into bloodand expulsion from lung
    2. Expulsion from anus
    50 L
    2 L
Intestinal Fluid
  • INFLUX
    1. Oral ingestion
    2. Intestinal secretions
      saliva
      bile
      gastric secretions
      pancreatic secretions
      intestinal secretions
    2.5 L
    8.2 L
    1.5 L
    0.5 L
    2.5 L
    0.7 L
    3.0 L
  • EFFLUX
    1. Peranal
    2. Intestinal resorption (primarily in ileum+ ascending colon)
    10.6 L
    0.1 L
Intestinal Transit Time
(measured by pH telemetry); affected by type of diet
Small bowel transit time: 3–11 hours
Colonic transit time: 20–71 hours
Defecography/Evacuation Proctography
evacuation time = 15 (range 5–40) seconds
anorectal angle = angle formed between central axis of anal canal + line parallel to posterior wall of rectum
√ 90° at rest and during voluntary contraction (squeeze maneuver)
√ more obtuse during defecation straining (void)
anorectal junction = point of taper of distal rectal ampulla as it merges with the anal canal; position of anorectal junction referenced to plane of ischial tuberosities = 0–3.5 cm; elevation during squeeze of 0–4.5 cm; elevation during void of–3.0–0 cm
rectovaginal space = space between vagina and rectum
perineum = area between external genital organs and anal verge
rectocele = measurement of anteroposterior depth of convex wall protrusion extending beyond expected margin of normal rectal wall
  small <2 cm;
  moderate = 2–4 cm;
  large >4 cm
peritoneocele = extension of rectouterine excavation to below upper third of vagina; containing liquid/bowel/omentum
enterocele = bowel present in peritoneocele
rectal prolapse = descent of entire thickness of rectal wall through anal verge
rectal intussusception = descent of the entire thickness of the rectal wall possibly extending into anal canal; starting 6–11 cm above anus; accompanied by formation of a circular indentation forming a ring pocket
√ infolding of <3 mm in width/> 3 mm in width/intraluminal narrowing/descent into anal canal/external prolapse
image
Defecographic Measurements
P.795

Peritoneum
image
Ligaments and Peritoneal Spaces in Upper Abdomen
Peritoneal Spaces
  • Definitions:
    Ligament = formed by two folds of peritoneum supporting a structure within the peritoneal cavity
    Omentum = specialized structure connecting stomach to an additional structure
    Mesentery = two peritoneal folds connecting a portion of bowel to the retroperitoneum
  • Embryology:
    • above transverse mesocolon:
      • RIGHT PERITONEAL SPACE
        • forms perihepatic space + lesser sac:
          • Right subphrenic space:
            • located between right hepatic lobe + diaphragm
            • limited posteriorly by right superior reflection of coronary lig. + right triangular ligament
          • Right subhepatic space:
            • divided into
              • anterior right subhepatic space: located just posterior to porta hepatis, communicating with lesser sac via epiploic foramen (= foramen of Winslow)
              • posterior right subhepatic space
                • = Morison pouch = hepatorenal fossa
                • Most dependent portion of the abdomen in supine patient!
          • Bare area of liver
            • situated between reflections of right + left coronary ligaments
            • continuous with right anterior pararenal space
          • Lesser sac:
            • superior recess:
              • surrounds medial aspect of caudate lobe
              • separated from splenic recess by gastropancreatic fold
            • splenic recess:
              • extends across midline to splenic hilum
            • inferior recess:
              • separates stomach from pancreas + transverse mesocolon
              • anteriorly covered by lesser omentum
          • Lesser omentum = combination of gastrohepatic ligament + hepatoduodenal ligament
          • Right triangular ligament:
            • forms from coalescence of superior and inferior reflections of right coronary ligament
            • divides posterior aspect of right perihepatic space into right subphrenic space + posterior right subhepatic space
      • LEFT PERITONEAL SPACE
        • forms left subphrenic space
          • Left subphrenic space:
            • artificially divided into
              • immediate subphrenic space:
                • between diaphragm + gastric fundus
              • perisplenic space:
                • bounded inferiorly by phrenicocolic lig.
              • P.796

              • subhepatic space = gastrohepatic recess:
                • located between lateral segment of left hepatic lobe + stomach
            • separated from right subphrenic space by falciform ligament
          • Left triangular ligament:
            • forms from coalescence of superior and inferior reflections of left coronary ligament
            • located along superior aspect of left hepatic lobe
      • DORSAL MESENTERY gives rise to:
        • Gastrophrenic ligament
          • courses through immediate subphrenic space
          • suspends stomach from dome of diaphragm
        • Gastropancreatic ligament
          • formed by proximal left gastric artery
          • attaches posterior aspect of gastric fundus to retroperitoneum
          • partially separates superior recess of lesser sac from splenic recess
        • Phrenicocolic ligament
          • major suspensory ligament of spleen
          • attaches proximal descending colon to left hemidiaphragm
          • separates left subphrenic space from left paracolic gutter
        • Gastrosplenic ligament
          • remnant of dorsal mesentery
          • connects greater curvature of stomach with splenic hilum
          • contains short gastric vessels
        • Splenorenal ligament
          • connects posterior aspect of spleen to anterior pararenal space
          • contributes to left lateral + posterior border of lesser sac
          • encloses tail of pancreas + distal splenic artery + proximal splenic vein
        • Gastrocolic ligament
          • forms portion of anterior border of lesser sac
          • forms superior aspect of greater omentum
          • connects greater curvature of stomach with superior aspect of transverse colon
          • contains gastroepiploic vessels
      • VENTRAL MESENTERY gives rise to:
        • Falciform ligament
          • = sickle-shaped fold composed of two layers of peritoneum
          • — attaches ventral surface of liver to anterior abdominal wall
          • — its right layer continues into the superior layer of the coronary ligament, its left layer continues into the anterior layer of the left triangular ligament
          • — contains ligamentum teres (= obliterated umbilical vein) in its free inferoposterior margin
          • — continuous with fissure for ligamentum venosum
        • Gastrohepatic ligament:
          • arises in fissure of ligamentum venosum
          • connects medial aspect of liver to lesser curvature of stomach as part of lesser omentum
          • contains left gastric artery, coronary vein, lymph nodes
        • Hepatoduodenal ligament:
          • forms inferior edge of gastrohepatic ligament
          • forms anterior margin of epiploic foramen
          • extends from proximal duodenum to porta hepatis
          • contains common hepatic duct, common bile duct, hepatic artery, portal vein
    • below transverse mesocolon:
      • VENTRAL MESENTERY regresses
      • DORSAL MESENTERY forms:
        • Transverse mesocolon:
          • suspends transverse colon from retroperitoneum along anteroinferior edge of pancreas
          • forms posteroinferior border of lesser sac
          • contains middle colic vessels
        • Small bowel mesentery:
          • suspends small bowel from retroperitoneum
          • extends from ligament of Treitz to ileocecal valve
          • contains superior mesenteric vessels + lymph nodes
        • Sigmoid mesocolon:
          • attaches sigmoid colon to posterior pelvic wall
          • contains sigmoid + hemorrhoidal vessels
        • Greater omentum:
          • inferior continuation of gastrocolic ligament
          • formed by double reflection of dorsal mesogastrium thus composed of 4 layers of peritoneum
        • Superior + inferior ileocecal recesses:
          • located above + below terminal ileum
        • Retrocecal space:
          • present only if peritoneum reflects posterior to cecum
        • Right + left paracolic gutters:
          • located lateral to ascending + descending colon
        • Intersigmoid recess:
          • located along undersurface of sigmoid mesocolon
P.797

Gastrointestinal Disorders
Achalasia
  • = failure of organized peristalsis + relaxation at level of lower esophageal sphincter
Etiology: (a) idiopathic: abnormality of Auerbach plexus/medullary dorsal nucleus; ¿ neurotropic virus, ¿ gastrin hypersensitivity
(b) Chagas disease
  • megaesophagus = dilatation of esophagus beginning in upper 1/3, ultimately entire length
  • absence of primary peristalsis below level of cricopharyngeus
  • nonperistaltic contractions
  • “bird-beak”/“rat tail” deformity = V-shaped conical + symmetric tapering of stenotic segment with most marked narrowing at GE junction
  • Hurst phenomenon = temporary transit through cardia when hydrostatic pressure of barium column is above tonic LES pressure
  • sudden esophageal emptying after ingestion of carbonated beverage (eg, Coke)
  • “vigorous achalasia” = numerous tertiary contractions in nondilated distal esophagus of early achalasia
  • prompt relaxation of LES upon amyl nitrate inhalation (smooth-muscle relaxant)
CXR:
  • right convex opacity behind right heart border; occasionally left convex opacity if thoracic aorta tortuous
  • right convex opacity may be tethered by azygos arch allowing for greater dilatation above + below
  • air-fluid level (stasis in thoracic esophagus filled with retained secretions + alimentary residue)
  • small/absent gastric air bubble
  • anterior displacement + bowing of trachea (LAT view)
  • patchy bilateral alveolar opacities resembling acute/chronic aspiration pneumonia (M. fortuitum-chelonei infection)
Cx: esophageal carcinoma in 2–7% (usually midesophagus)
Rx: pneumatic dilatation/surgical myotomy
DDx: (1) Neoplasm (separation of gastric fundus from diaphragm; normal peristalsis; asymmetric tapering)
(2) Peptic stricture of esophagus
Secondary Achalasia
  • = carcinoma of cardia/gastric fundus invading esophagus
    Age: >50 years
  • • duration of symptoms for <6 months
  • irregular/asymmetric narrowing
  • abrupt transition
  • associated fundal lesion
Adenoma of Small Bowel
Location: duodenum (21%), jejunum (36%), ileum (43%) esp. ileocecal valve
Histo:
  • Hamartomatous polyp (77%), multiple in 47%, 1/3 of multiple lesions associated with Peutz-Jeghers syndrome
  • adenomatous polyp (13%), may have malignant potential
  • polypoid gastric heterotopic tumor (10%)
Adenomatous Colonic Polyp
  • = EPITHELIAL POLYP
  • Most common benign colonic tumor (68–79%)
Predisposed: previously detected polyp/cancer; family history of polyps/cancer; idiopathic inflammatory bowel disease; Peutz-Jeghers syndrome; Gardner syndrome; familial polyposis
Prevalence: 3% in 3rd decade; 10% in 7th decade;
26% in 9th decade
Location: rectum (21–34%); sigmoid (26–38%); descending colon (6–18%); transverse colon (12–13%); ascending colon (9–12%); multiple in 35–50% (usually <5–10 in number)
Histo:
  • Tubular adenoma (75%)
    • = cylindrical glandular formation lined by stratified columnar epithelium + containing nests of epithelium within lamina propria
    • usually <10 mm in diameter
    • often pedunculated if >10 mm
    malignant potential: <10 mm in 1%; 10–20 mm in 10%; >20 mm in 35%
  • Tubulovillous adenoma (15%)
    • = mixture between tubular + villous adenoma
    malignant potential: <10 mm in 4%; 10–20 mm in 7%; >20 mm in 46%
  • Villous adenoma (10%)
    • = thin frondlike surface projections (“villous fronds”)
    • • potassium depletion
    • often >20 mm in diameter with papillary surface
    • often broad-based sessile lesion
    malignant potential: <10 mm in 10%; 10–20 mm in 10%; >20 mm in 53%
Adenoma size & incidence of malignancy:
  • <5 mm in 0.5%; 5–9 mm in 1%; 10–20 mm in 5–10% >20 mm in 10–50% malignant
  • Invasive carcinoma (= penetration of muscularis mucosa):
    • rare in a pedunculated adenoma of <15 mm
    • in 30% of villous adenomas of >50 mm
  • All polyps >10 mm should be removed!
  • Time for adenoma-carcinoma sequence probably averages 10–15 years!
Probability of coexistent colonic growth:
  • synchronous adenoma in 50%
  • metachronous adenoma in 30–40%
  • synchronous adenocarcinoma in 1.5–5%
  • metachronous adenocarcinoma in 5–10%
  • • asymptomatic (75%)
  • • diarrhea, abdominal pain
  • • peranal hemorrhage (67%)
  • Colonoscopy (incomplete in 16–43%)
BE:
Sensitivity of DCBE in detecting polyps:
  • <10 mm 80–83%; >10 mm 96–97%; all 84–88%; rate of detection of polyps <10 mm higher with DCBE than SCBE
    P.798

    • sessile flat/round polyp
    • pedunculated polyp: stalk >2 cm in length almost always indicative of a benign polyp
    • suggestive of malignancy: irregular lobulated surface, broad base = width of the base greater than height, retraction of colonic wall = dimpling/indentation/puckering at base of tumor, interval growth
    • lacelike/reticular surface pattern CHARACTERISTIC for villous adenoma (occasionally in tubular adenoma)
DDx: (1) Nonneoplastic: hyperplastic polyp, inflammatory pseudopolyp, lymphoid tissue, ameboma, tuberculoma, foreign-body granuloma, malacoplakia, heterotopia, hamartoma
(2) Neoplastic subepithelial: lipoma, leiomyoma, neurofibroma, hemangioma, lymphangioma, endothelioma, myeloblastoma, sarcoma, lymphoma, enteric cyst, duplication, varix, pneumatosis, hematoma, endometriosis
Adenocarcinoma of Small Bowel
Frequency: 35% of primary malignant neoplasms of small bowel; about 50 × less common than colonic carcinoma
⋄ Most common primary malignancy of small bowel
Risk factors: familial adenomatous polyposis (FAP), Crohn disease, sprue, Peutz-Jeghers syndrome, hereditary nonpolyposis colon cancer syndrome (Lynch syndrome), congenital bowel duplication, ileostomy, duodenal/jejunal bypass surgery
Histo: mostly moderately to well differentiated; may arise in villous tumors/de novo; no correlation between size and invasiveness
  • vague mild abdominal pain
  • anemia, weight loss
  • nausea, vomiting, anorexia
Location: duodenum (54%, especially near ampulla), jejunum (28%) > ileum (18%)
–in FAP: duodenum
–in celiac disease: jejunum
–in Crohn disease: ileum
  • annular stricture with “overhanging edges” (60%)
  • lobulated/ovoid polypoid sessile mass (41%)
  • Duodenal tumors tend to be papillary/polypoid!
  • ulcerated mass (27%)
CT:
  • soft-tissue mass with heterogeneous attenuation
  • moderate contrast enhancement
Cx: intussusception
Prognosis: poor (often disseminated at time of presentation); 30% 5-year survival rate
DDx: lymphoma (lymphadenopathy more bulky)
Afferent Loop Syndrome
  • = PROXIMAL LOOP/BLIND LOOP SYNDROME
  • = partial intermittent obstruction of afferent loop leading to overdistension of loop by gastric juices after Billroth-II gastrojejunostomy
Cause: gastrojejunostomy with left-to-right anastomosis (= proximal jejunal loop attached to greater curvature instead of lesser curvature), mechanical factors (intussusception, adhesion, kinking), inflammatory disease, neoplastic infiltration of local mesentery or anastomosis, idiopathic motor dysfunction
  • postprandial epigastric fullness relieved by bilious vomiting
  • vitamin B12 deficiency with megaloblastic anemia
  • afferent loop with abnormal bacterial flora (Gram negative, resembling colon in quality + quantity)
Abdominal plain film:
  • normal in 85% (no air in lumen of afferent loop)
UGI:
  • preferential emptying of stomach into proximal loop
  • proximal loop stasis
  • regurgitation
CT:
  • rounded water-density masses adjacent to head + tail of pancreas forming a U-shaped loop
  • oral contrast material may not enter loop
  • may result in biliary obstruction (increased pressure at ampulla)
Rx: antibiotic therapy
Aids
  • Gastrointestinal involvement due to opportunistic infections + AIDS-associated neoplasms!
  • Pathologic abnormalities at multiple sites with single/several opportunistic organisms are frequent!
  • A. VIRAL PATHOGENS
    • Cytomegalovirus infection
      • Most common cause of life-threatening opportunistic viral infection in AIDS patients!
        Organism: double-stranded DNA virus of the herpes family
        Infection: ubiquitous among humans occurring at an early age in populations with poor sanitation + crowded living conditions
      • Result of reactivation of latent virus in previously infected host!
        Prevalence: 13% of all gastrointestinal diseases in AIDS patients
        Path: infection of endothelial cells leads to small vessel vasculitis resulting in hemorrhage, ischemic necrosis, ulceration
        Histo: large mononuclear epithelial/endothelial cells that contain intranuclear/cytoplasmatic inclusions with surrounding inflammation
        Location: colon > small bowel (terminal ileum) > esophagus > stomach
      • @ Esophagus
        • single/multiple large superficial ulcers
      • @ Small bowel
        • luminal narrowing secondary to marked bowel wall thickening
        • thickened irregular folds (vasculitis leading to thrombosis + ischemia)
        • penetrating ulcer ± perforation
        • CMV pseudotumor (uncommon)
      • P.799

      • @ Colon (CMV colitis)
        • • hematochezia, crampy abdominal pain, fever
        • findings of toxic megacolon
        • discrete small well-defined nodules (similar to lymphoid nodular hyperplasia) throughout entire colon
        • aphthous ulcers on background of normal mucosa
        • marked bowel wall thickening
        • double-ring/target sign on CT (due to increased submucosal edema)
        • ascites
        • inflammation of pericolonic fat + fascia
        Rx: ganciclovir (effective in 75%)
    • Herpes simplex virus infection
      • Result of reactivation of latent virus in previously infected host
        Organism: neurotropic DNA virus of herpes family
        Prevalence: 70% for type 1, 16% for type 2 (endemic in United States); type 2 much more common in AIDS
        Infection: direct inoculation through mucous membrane contact; from dormant state in root ganglia reactivated + transported via efferent nerves to mucocutaneous surface
        Location: oral cavity, esophagus, rectum, anus
      • multiple small discrete ulcers
    • HIV infection
      • Not an AIDS-defining illness!
        Infection: acute HIV-infection with transient immunosuppression/during AIDS
      • >2-cm large solitary ulcer in the mid- or distal esophagus (HIV-infected cells cause alterations in cytokines resulting in infiltration of inflammatory cells into submucosa + destruction of mucosa)
      Rx: corticosteroids
  • B. FUNGAL PATHOGENS
    • Candidiasis
      • The absence of thrush does not exclude the diagnosis of candida esophagitis!
        Organism: commensal fungus Candida albicans
        Prevalence: 10–20% (in United States); up to 80% in developing countries
        Location: oral cavity, esophagus
      • discrete linear/irregular longitudinally oriented filling defects in esophagus
      Cx: disseminated systemic candidiasis (rare + indicative of granulocytopenia from chemotherapy/direct inoculation via catheter)
    • Histoplasmosis
      Organism: dimorphic opportunistic fungus
      Prevalence: 10% GI involvement with disseminated histoplasmosis in AIDS patients
      Location: colon > terminal ileum
      • segmental inflammation/apple core lesion/bowel stricture
      • hepatosplenomegaly
      • mesenteric lymphadenopathy
      • diffuse hypoattenuation of spleen
  • C. PROTOZOAN PATHOGENS
    • Cryptosporidiosis
      • One of the most common causes of enteric + biliary disease in AIDS patients!
        Organism: intracellular parasite Cryptosporidium
        Prevalence: isolated in 6% of all patients with AIDS; in 16% (in United States) + in up to 48% (in developing countries) in patients with diarrhea
      • • severe choleralike debilitating diarrhea with fluid loss of 10-17 L/day
        Location: jejunum > other small bowel > stomach > colon
      • Cryptosporidium antritis (= area of focal gastric thickening + ulceration)
      • small bowel dilatation (increased secretions)
      • regular fold thickening + effacement (atrophy, blunting, fusion, loss of villi)
      • “toothpaste” appearance of small bowel (mimicking sprue)
      • dilution of barium (hypersecretion)
      • marked antral narrowing (extensive inflammation)
      • AIDS-related cholangitis
      Dx: microscopic identification in stool/biopsy
    • Pneumocystosis
      • Likely to occur in patients treated with aerosolized pentamidine!
        Organism: eukaryotic microbe Pneumocystis carinii
        Prevalence: pulmonary infection in 75% of AIDS
        patients; in <1% dissemination
        Location: liver, spleen, lymph nodes
      • hepatic + splenic + nodal punctate calcifications
      • multiple tiny echogenic foci in spleen
      • multiple low-attenuation lesions of varying size in spleen (foamy eosinophilic material) with subsequently progressive rimlike/punctate calcifications
  • D. BACTERIAL PATHOGENS
  • 1. tuberculosis
    • Most common cause of serious HIV-related infection worldwide with tendency to occur earlier than other AIDS-defining opportunistic infections!
      Prevalence: 4% (in United States) + 43% (in developing countries) of HIV-infected persons
      Infection: swallowing of infected sputum; hematogenous spread from pulmonary focus; direct extension from lymph node
      Location: lymph nodes, liver, spleen, peritoneum, GI tract (especially ileum, colon, ileocecal valve)
    • low-attenuation mesenteric lymphadenopathy (suggestive of necrosis)
    • segmental ulceration
    • inflammatory stricture
    • hypertrophic lesion resembling polyp or mass
  • 2.Mycobacterium avium complex infection
    • = PSEUDO-WHIPPLE DISEASE in AIDS
    • Most common opportunistic infection of bacterial origin in AIDS patients!
    • P.800

    • Most common nontuberculous mycobacterial infection in AIDS patients!
      Organism: facultative intracellular acid-fast bacillus M. avium/M. intracellulare
      Infection: invasion of Peyer patches + adjacent mesenteric lymph nodes
      Histo: true granulomas with Langhans giant cells and caseous necrosis are rare because infection occurs in patients with advanced disease and a CD4 cell count of <100/μL
    • • diarrhea, malabsorption (similar clinical picture as in Whipple disease caused by Mycobacterium avium-intracellulare)
      Location: jejunum (most common)
    • mild dilatation of middle + distal small bowel
    • wall thickening of small bowel loops
    • diffuse irregular mucosal fold thickening and nodularity without ulceration
    • mesenteric + retroperitoneal lymphadenopathy (1.0–1.5 cm in size) with homogeneous soft-tissue attenuation causing segmental separation of small bowel loops
    • hepatosplenomegaly
    • multiple tiny echogenic foci in liver + spleen (occasionally large hypoechoic/low-attenuation lesions)
    Dx: (1) Visualization of large numbers of intracellular acid-fast bacilli in foamy histiocytes of tissue specimens
    (2) Tissue culture
    DDx: Whipple disease (positive with periodic acid-Schiff stain just like M. avium, but not with acid-fast stain, responsive to tetracyclines)
  • E. OTHER INFECTIONS
    • Bacillary angiomatosis
      Organism: Rickettsiales Bartonella henselae
      Histo: characteristic pattern of vascular proliferation with bacilli
      Location: cutis (mimicking Kaposi sarcoma), liver, spleen, lymph nodes
      • peliosis (blood-filled cystic spaces) of liver/spleen
      • abdominal lymphadenopathy with contrast enhancement
    • Isospora belli
      • Infection resembles cryptosporidiosis
        Organism: protozoan pathogen
        Histo: oval oocysts within bowel lumen/epithelial cells; localized inflammation; fold atrophy
        Location: small intestine
      • • severe watery diarrhea
      • fold thickening
  • F. AIDS-ASSOCIATED NEOPLASMS
    • Kaposi sarcoma
    • Non-Hodgkin lymphoma
      • 2nd most common AIDS-associated neoplasm
        Prevalence: in 4–10% of AIDS patients (60 times higher risk compared with general population); occurs in all AIDS risk groups
        Histo: multiclonal B-cell lymphoma of high or intermediate grade
      • • at initial presentation widely disseminated disease often with extranodal involvement
        Location: CNS, bone marrow, GI tract (stomach, small bowel)
    • @ Stomach
      • circumferential/focal wall thickening
      • mural mass ± ulceration
    • @ Small bowel
      • diffuse/focal wall thickening
      • excavated mass
      • solitary/multiple liver lesions
Differential diagnostic considerations:
  • Splenomegaly (31–45%)
    Cause: nonspecific (most), lymphoma, infection (M. avium-intracellulare, P. carinii)
  • Lymphadenopathy (21–60%)
    Cause: reactive hyperplasia (most), Kaposi sarcoma, lymphoma, infections
    Size: <3 cm in diameter (in 95%)
  • Hepatomegaly (20%)
    Cause: nonspecific, hepatitis, fatty infiltration, lymphoma, Kaposi sarcoma
  • AIDS-related cholangiopathy:
    Organism: CMV, Cryptosporidium
    • papillary stenosis of CBD
    • dilatation of extra- and intrahepatic bile ducts
    • periductal fibrosis
    • strictures + irregularities of bile ducts resembling primary sclerosing cholangitis
    • intraluminal polypoid filling defects
  • AIDS-related esophagitis:
    Organism: Candida, herpes simplex, CMV
    • giant esophageal ulcer: HIV (76%), CMV (14%)
    • esophageal fistula/perforation: tuberculosis, actinomycosis
  • Gastritis
    Organism: CMV (GE junction + prepyloric antrum), Cryptosporidium (antrum)
  • AIDS enteritis
    Organism: Cryptosporidium, M. avium complex
  • AIDS colitis
    • ischemic bowel
    • acute appendicitis
    • neutropenic colitis
    • pseudomembranous colitis
    • infectious colitis/ileitis
  • Bowel obstruction
    • infection
    • intussusception: Kaposi sarcoma, lymphoma
Amebiasis
  • = primary infection of the colon by protozoan Entamoeba histolytica
Countries: worldwide distribution, most common in warm climates; South Africa, Egypt, India, Asia, Central + South America (20%); United States (5%)
Route: contaminated food/water (human cyst carriers); cyst dissolves in small bowel; trophozoites settle in colon; proteolytic enzymes + hyaluronidase lyse intestinal epithelium; may embolize into portal venous + systemic blood system
Histo: amebic invasion of mucosa + submucosa causing tiny ulcers, which spread beneath mucosa + merge into larger areas of necrosis; mucosal sloughing; secondary bacterial infection
P.801

  • • asymptomatic for months/years
  • • acute attacks of diarrhea (loose mucoid bloodstained stools)
  • • fever, headache, nausea
    Location: (areas of relative stasis) right colon + cecum (90%) > hepatic + splenic flexures > rectosigmoid
  • loss of normal haustral pattern with granular appearance (edema, punctate ulcers)
  • “collarbutton” ulcers
  • cone-shaped cecum
  • several cm long stenosis of bowel lumen in transverse colon, sigmoid colon, flexures (result of healing + fibrosis); in multiple segments
  • ameboma = hyperplastic granuloma with bacterial invasion of amebic abscess; usually annular + constricting/intramural mass/cavity continuous with bowel lumen; shrinkage under therapy in 3–4 weeks
  • ileocecal valve thickened + fixed in open position with reflux
  • involvement of distal ileum (10%)
Dx: stool examination/rectal biopsy
Cx: (1) Toxic megacolon with perforation
(2) Amebic abscess in liver (2%), brain, lung (transdiaphragmatic spread of infection), pericolic, ischiorectal, subphrenic space
(3) Intussusception in children (due to ameboma)
(4) Fistula formation (colovesical, rectovesical, rectovaginal, enterocolic)
Amyloidosis
  • = group of heterogeneous disorders caused by interstitial deposits of a protein-polysaccharide in various organs leading to hypoxia, mucosal edema, hemorrhage, ulceration, mucosal atrophy, muscle atrophy
Cause: (a) prolonged antigenic stimulation of RES by chronic infection
(b) disorder of immunoincompetence
(c) aging
(d) idiopathic
Histo: amorphous eosinophilic hyaline material deposited around terminal blood vessels, stains with Congo red + crystal violet; green birefringence under polarizing light; amyloid fibrils have β-pleated sheet structure (= β fibrilloses)
Biochemical classification (1979):
  • AL amyloidosis
    • (A = amyloidosis, L = light chain immunoglobulin)
    • • monoclonal protein in serum + urine
    • • occurs in primary amyloidosis + myeloma-associated amyloidosis
      Histo: massive deposits in muscularis mucosae + submucosa
    • thickening of folds with polyps/large nodules
  • SAA amyloidosis (S = serum, AA = amyloid A)
    • • occurs in secondary = reactive amyloidosis
      Histo: expansion of lamina propria
    • coarse mucosal pattern + innumerable fine granular elevations
  • AF amyloidosis (A = amyloid, F = familial)
    • AF prealbumin as precursor of fibrils
    • occurs in familial amyloidosis
  • AS amyloidosis (A = amyloid, S = senile)
    • • AS prealbumin as precursor of fibrils
    • • occurs in senile amyloidosis
    • massive amyloid deposition
  • AH amyloidosis (A = amyloid, H = hemodialysis)
    • β2 microglobulin as precursor of fibrils
  • AE amyloidosis (A = amyloid, E = endocrine)
    • calcitonin produced by medullary thyroid carcinoma is precursor of fibrils
Reimann classification (1935):
  • Primary = idiopathic amyloidosis
    • = probably autosomal dominant inheritance with immunologically determined dysfunction of plasma cells
    • • absence of discernible preceding/concurrent disease
    Location: (predominant involvement of connective tissues + mesenchymal organs) heart (90%), lung (30–70%), liver (35%), spleen (40%), kidneys (35%), adrenals, tongue (40%), GI tract (70%), skin + subcutis (25%)
    • tendency to nodular deposition
  • 2.Secondary amyloidosis (most common form)
    • • following/coexistent with prolonged infectious/inflammatory processes
      Cause: rheumatoid arthritis (in 20%), Still disease, tuberculosis, osteomyelitis, leprosy, chronic pyelonephritis, bronchiectasis, ulcerative colitis, Waldenström macro-globulinemia, familial Mediterranean fever, lymphoreticular malignancy, paraplegia
      Location: spleen, liver, kidneys (>80%), breast, tongue, GI tract, connective tissue
    • small amyloid deposits
  • 3.Amyloidosis associated with multiple myeloma
    • • may precede development of multiple myeloma
      Incidence: 10–15%
    • primary amyloidosis with osteolytic lesions in myelomatous disease
  • 4.Tumor-forming/organ-limited amyloidosis
    • • related to primary type
    • (a) hereditary = familial amyloidosis
    • (b) senile amyloidosis (limited to heart/brain/pancreas/spleen)
    • large localized masses
  • GI involvement in primary more common than in secondary amyloidosis!
  • • malabsorption (diarrhea, protein loss)
  • • occult GI bleeding
  • • obstruction
  • • macroglossia
  • @ Esophagus (11%)
    • loss of peristalsis
    • P.802

    • megaesophagus
  • @ Stomach (37%)
    • • postprandial epigastric pain + heartburn
    • • acute erosive hemorrhagic gastritis
    • (a) diffuse infiltrative form
      • small-sized stomach with rigidity + loss of distensibility simulating linitis plastica (from thickening of gastric wall)
      • effaced rugal pattern
      • diminished/absent peristalsis
      • marked retention of food
    • (b) localized infiltration (often located in antrum)
      • irregularly narrowed + rigid antrum
      • thickened rugae
      • superficial erosions/ulcerations
    • (c) amyloidoma = well-defined submucosal mass
  • @ Small bowel (74%)
    • diffuse form (more common)
      • diffuse uniform thickening of valvulae conniventes in entire small bowel
      • broadened flat undulated mucosal folds (mucosal atrophy)
      • “jejunalization” of ileum
      • impaired intestinal motility
      • small bowel dilatation
    • localized form (less common)
      • multiple pea-/marble-sized deposits
      • pseudoobstruction = physical + plain-film findings suggesting mechanical obstruction with patent large + small bowel on barium examination (involvement of myenteric plexus)
    Cx: small bowel infarction
  • @ Colon (27%):
    • pseudopolyps in colon
  • @ Bone:
    • bone cysts
  • @ Liver:
    Path: extracellular deposition of amyloid in the spaces of Disse (= narrow gaps between endothelial linings of sinusoids and hepatocytes of hepatic lamina) with progressive encroachment on hepatic parenchymal cells + sinusoids
    • hepatic function usually preserved
    CT:
    • hepatomegaly
    • regions of low attenuation with decreased contrast enhancement
  • @ Spleen:
    Histo: (a) nodular form involving lymph follicles
    (b) diffuse form infiltrating red pulp
    • discrete masses
    • splenomegaly (4–13%)
    MR:
    • T2 values significantly lower than normal
Cx: spontaneous splenic rupture (from vascular fragility + acquired coagulopathy)
Dx: by rectal/gingival biopsy
DDx: Whipple disease, intestinal lymphangiectasia, lymphosarcoma
Angiodysplasia of Colon
  • = VASCULAR ECTASIA = ARTERIOVENOUS MALFORMATION (not a true AVM)
    Cause: age-related degenerative dilatation of normal vessels in submucosa of bowel wall
    Theory: colonic contractions result in dilatation of colonic veins, venules and capillaries forging multiple small arteriovenous communications
    Associated with: aortic stenosis (20%); NOT related to extraintestinal angiomatous lesions
    Prevalence: most common vascular lesion of GI tract!
    at autopsy: 2%
    at colonoscopy: 0.8% (age >50 years)
    Age: majority > 55 years; M = F
    Location: (a) cecum + ascending colon (74%)
    (b) jejunum, ileum (15%)
    (c) descending + sigmoid colon (¿ 25%)
    Site: usually at antimesenteric border
  • • chronic intermittent low-grade bleeding
  • • occasionally massive bleeding
NUC (Tc-99m labeled RBCs):
  • focus of tracer accumulation at site of bowel hemorrhage migrating with peristalsis
BE:
  • no abnormality (due to soft submucosal lesion)
NUC:
  • increased tracer accumulation of Tc-99m labeled RBC
Angio:
  • “arterial tuft” = cluster/tangle of vessels during arterial phase along antimesenteric border
  • early opacification of draining ileocolic vein
  • densely opacified dilated tortuous ileocolic vein into late venous phase
  • contrast extravasation into bowel lumen (unusual)
Rx: surgical excision
Anisakiasis
  • = parasitic disease of GI tract
    Cause: ingestion of Anisakis larvae present in raw/undercooked fish (mackerel, cod, pollack, herring, whiting, bonito, squid) consumed as sashimi, sushi, ceviche, lomi-lomi
    Organism: worm with straight/serpentine/circular threadlike appearance
  • Site of penetration by larvae determines clinical form!
  • @ Gastric anisakiasis
    • • acute gastric pain, nausea, vomiting a few hours after ingestion (DDx: acute gastritis, peptic ulcer, food poisoning, neoplasia)
    • • eosinophilia
    • mucosal edema
    • about 3-cm-long threadlike filling defects (= larvae)
  • @ Intestinal anisakiasis
    • • diffuse abdominal tenderness/colicky abdominal pain, nausea, vomiting (DDx: acute appendicitis, regional enteritis, intussusception, ileus, diverticulitis, neoplasia)
    • • leukocytosis without eosinophilia (frequent)
      Histo: marked edema, eosinophilic infiltrates, granuloma formation
    • thickened folds
    • P.803

    • disappearance of Kerckring folds
    • thumbprinting/saw-tooth appearance
    • irregular luminal narrowing
    • eosinophilic ascites (DDx: eosinophilic gastroenteritis, hypereosinophilic syndrome)
      Cx: ileus
  • @ Colonic anisakiasis (rare)
    DDx: colonic tumor
Anorectal Malformation
  • Rectal atresia
    • = open anus + atretic rectal segment superior to anus + no fistula
  • Ectopic anus
    • = fistulous opening of bowel due to failure of terminal bowel to descend normally
      Site of arrest: high/low colon arrest = above/below puborectal sling
    • • most common anomaly of anorectal segment
    • • anal dimple + external sphincter in normal position
      Location of fistula: perineum, vestibule, vagina, urethra, bladder, cloaca
    • low small bowel/colonic obstruction
    • “M” line accurately represents level of puborectal muscle = line drawn horizontally through junction of lower 1/3 + upper 2/3 of ischium on lateral radiograph
  • Imperforate anus
    • = blind ending of terminal bowel + no fistula
  • Cloacal malformation
  • Cloacal exstrophy
Embryology:
  • during weeks 3 and 4 the dorsal part of the yolk sac folds are incorporated into embryo forming the primitive hindgut consisting of distal part of transverse + descending + sigmoid colon, rectum, superior portion of anal canal, epithelium of urinary bladder, and most of the urethra; at 4 weeks the transverse rectovesical septum descends caudally between allantois and hindgut dividing the cloaca into urogenital sinus ventrally + anorectal canal dorsally; by 7th week the rectovaginal septum fuses with cloacal membrane creating a urogenital membrane ventrally + anal membrane dorsally; perineum is formed by fusion of rectovesical septum + cloacal membrane; anal membrane ruptures by 9th week
In 48% associated with: (part of VACTERL syndrome)
  • GU anomalies (20%):
    • renal agenesis/ectopia, vesicoureteral reflux, obstruction, hypospadia (3.1%); M > F
  • Lumbosacral segmentation anomalies (30%):
    • dysplasia, agenesis, hemivertebrae
  • GI anomalies (11%):
    • esophageal atresia ± tracheoesophageal fistula (4%), duodenal atresia/stenosis
  • Cardiovascular anomalies (8%)
  • Abdominal wall (2%)
  • Cleft lip–cleft palate (1.6%)
  • Down syndrome (1.5%)
  • Meningomyelocele (0.5%) + occult myelodysplasia
  • Others (8%)
Antral Mucosal Diaphragm
  • = ANTRAL WEB
    Age range: 3 months to 80 years
    Associated with: gastric ulcer (30–50%)
  • • symptomatic if opening <1 cm
    Location: usually 1.5 cm from pylorus (range 0–7 cm)
  • constant symmetric band of 2–3 mm thickness traversing the antrum perpendicular to long axis of stomach
  • “double bulb” appearance (in profile)
  • concentric/eccentric orifice
  • normal peristaltic activity
Appendicitis
Prevalence: 1–4% in children with acute abdominal pain
Lifetime risk: 7–9% in Western world population
Etiology: obstruction of appendiceal lumen by lymphoid hyperplasia (60%), fecolith (33%), foreign bodies (4%), stricture, tumor, parasite; Crohn disease (in 25%)
Cause: luminal obstruction from
  • fecolith (11–52%) = hard crushable concretions from inspissation of fecal material + inorganic salts
  • appendiceal calculus = hard noncrushable calcified stone (7–15%)
  • lymphoid hyperplasia
  • foreign body
  • parasite
  • primary tumor: carcinoid, adenocarcinoma, Kaposi sarcoma, lymphoma
  • metastatic tumor: colon cancer, breast cancer
Pathogenesis:
  • continued secretion of mucus in appendiceal obstruction elevates intraluminal pressure + distends lumen; venous engorgement + arterial compromise + tissue ischemia ensues after intraluminal pressure exceeds capillary perfusion pressure
Peak age: 2nd decade; thereafter declining incidence; M:F = 3:2 (in teens/young adults, thereafter 1:1)
⋄ Rare under the age of 2 years!
  • 80% clinical accuracy (78–92% in males, 58–85% in females):
    Diagnostic dilemma (20–35%):
    • in elderly, ovulating women, infants/young children
    • 32–45% rate of misdiagnosis in women between ages 20–40!
    • 5–25% false-negative appendectomy rate for pediatric population!
  • pain
    • mild poorly localized visceral pain of 4–6 hours duration referred to epigastrium + periumbilical region
    • crampy pain migrates into RLQ pain over appendix = McBurney sign (72%) and becomes continuous + more severe (somatic pain)
  • anorexia, nausea, vomiting (40%)
  • afebrile/low-grade fever (56%)
    • Suspect perforation with temperature >38.3°
  • • leukocytosis with left shift (88%)
Clinical scoring system: “MANTRELS” score of 10
Migration of pain to RLQ 1
Anorexia 1
Nausea and vomiting 1
Tenderness in RLQ 2
Rebound pain 1
Elevated temperature 1
Leukocytosis 2
Shift of WBC count to left 1
P.804

Location:
  • base of appendix: posteromedial wall of cecum + 3 cm below ileocecal valve
    • The appendix is on the same side of the cecum as the ileocecal valve!
  • tip of appendix: retrocecal, subcecal, retroileal, preileal, within pelvis (30%), extraperitoneal (5%)
Abdominal plain film (abnormalities seen in <50%):
  • Plain-film findings become more distinctive after perforation, while clinical findings subside/simulate other diseases!
  • usually laminated calcified appendicolith in RLQ (in 7–15%):
    • Appendicolith + abdominal pain = 90% probability of acute appendicitis!
    • Appendicolith in acute appendicitis means a high probability for gangrene/perforation!
  • cecal changes:
    • thickening of cecal wall
    • water-density mass + paucity/absence of intestinal gas in RLQ (in 24% of perforations)
    • “cecal ileus” = gas-fluid level in cecum in gangrene (= local paralysis)
    • colon cutoff sign = amputation of gas at the hepatic flexure (in 20% of perforations) due to spastic ascending colon
  • small bowel obstruction pattern = small bowel dilatation with air-fluid levels (in 43% of perforations)
  • extraluminal gas (in 33% of perforations):
    • gas loculation
    • mottled bacteriogenic gas
    • pneumoperitoneum (rare)
  • loss of fat planes:
    • focal increase in thickness of lateral abdominal wall in 32% (= edema between properitoneal fat line + cecum)
    • loss of properitoneal fat line
    • loss of pelvic fat planes around the bladder/right obturator (= fluid/pus in cul-de-sac)
    • loss of definition of right inferior hepatic outline (= free peritoneal fluid)
    • distortion of psoas margin + flank stripes
  • scoliosis (due to muscle irritation)
BE/UGI (accuracy 50–84%):
  • failure to fill appendix with barium (normal finding in up to 35%)
  • indentation along medial wall of cecum (= edema at base of appendix/matted omentum/periappendiceal abscess)
Graded-compression US (85% sensitive, 92% specific, 78–96% accurate, 91–94% PPV, 89–97% NPV):
  • Nondiagnostic study in 4% due to inadequate compression of RLQ
  • Useful in ovulating women (false-negative appendectomy rate in males 15%, in females 35%) + infants/children
  • visualization of noncompressible appendix as a blind-ending tubular aperistaltic structure (seen only in 2% of normal adults, but in 50% of normal children)
  • laminated wall with target appearance of ≥6 mm in total diameter on cross section (81% SPECIFIC)/mural wall thickness ≥2 mm
  • lumen may be distended with anechoic/hyperechoic material
  • pericecal/periappendiceal fluid
  • increased periappendiceal echogenicity (= infiltration of mesoappendix/pericecal fat)
  • enlarged mesenteric lymph nodes
  • loss of wall layers = gangrenous appendix
  • perforated appendix (23–73%):
    • loss of echogenic submucosal layer
    • appendix no longer visualized (40–60%)
    • loculated periappendiceal/pelvic fluid collection ± gas bubbles (= abscess)
    • prominent hyperechoic mesoappendix/pericecal fat
    • visualization of appendicolith (6%) = bright echogenic focus with clean distal acoustic shadowing
    • gas bubbles localized to perforation site
  • hypoechoic zones with poor margination within inflamed fat (= phlegmonous appendicitis)
  • sympathetic thickening of adjacent terminal ileum + ascending colon
False-negative US:
  • failure to visualize appendix
    • inability of adequate compression
    • aberrant location of appendix (eg, retrocecal)
    • appendiceal perforation
  • early inflammation limited to appendiceal tip
False-positive US:
  • normal appendix mistaken for appendicitis
  • alternate diagnosis: Crohn disease, pelvic inflammatory disease, inflamed Meckel diverticulum
  • spontaneous resolution of acute appendicitis
Color Doppler US:
  • increased conspicuity (= increase in size + number) of circumferential vessels in and around the wall of the appendix (= hyperemia)
  • decreased resistance of arterial waveforms
  • continuous/pulsatile venous flow
  • decreased/no perfusion = gangrenous appendicitis
CT (87–100% sensitive, 89–98% specific, 93–98% accurate, 92–98% PPV, 95–100% NPV):
  • normal appendix visualized in 67–100%:
    • 1–2 cm below ileocecal junction from posteromedial aspect of cecum with a diameter of up to 10 mm
  • abnormal appendix:
    • distended lumen (appendix >7 mm in diameter)
    • circumferential wall thickening
    • homogeneously enhancing wall ± mural stratification (“target sign”)
    • appendicolith = homogeneous/ringlike calcification (25%)
    • distal appendicitis = abnormal tip of appendix + normal proximal appendix and normal cecal apex
  • periappendicular inflammation (98%):
    • linear streaky densities in periappendicular/pericecal/mesenteric/pelvic fat
    • subtle clouding of mesentery
    • local fascial thickening
    • P.805

    • free peritoneal fluid
    • mesenteric lymphadenopathy
    • marked terminal ileal wall thickening
    • localized lymphadenopathy
    • peritonitis
    • small-bowel obstruction
  • circumferential/focal cecal apical thickening (80%):
    • “arrowhead sign” = funnel of contrast medium in cecum symmetrically centering about occluded orifice of appendix (30% sensitive, 100% specific)
  • perforated appendix:
    • defect in the enhancing appendiceal wall
    • nonvisualization of appendix (due to fragmentation)
    • phlegmon = diffuse substantial inflammation of periappendiceal fat with ill-defined fluid collections(DDx: ileocolitis with secondary inflammation of appendix)
    • pericecal/mesenteric/interloop/pelvic abscess = poorly encapsulated single/multiple fluid collection with air/extravasated contrast material
    • extraluminal appendicolith
    • extraluminal air
False-negative CT:
  • overlapping range in maximal appendiceal diameter between inflamed + uninflamed appendix
  • appendix mistaken for unopacified bowel
  • inflammation limited to appendiceal tip
Prognosis:
  • mild acute appendicitis may resolve spontaneously (after relief of inciting obstruction)
  • recurrent appendicitis (10%) = repeated similar episodic attacks of RLQ pain leading to appendectomy + showing acute inflammation
  • chronic appendicitis (1%) = RLQ pain of >3 weeks + no alternative diagnosis + chronic active inflammation on histology + relief of symptoms after appendectomy
  • Mortality rate of 1% (associated with perforation)
Cx: perforation (13–30–73%), abscess formation, peritonitis, wound infection, sepsis, infertility, adhesions, bowel obstruction, death
Rx: finding of appendicolith is sufficient evidence to perform prophylactic appendectomy in asymptomatic patients (50% have perforation/abscess formation at surgery)
DDx: colitis, diverticulitis, epiploic appendagitis, small bowel obstruction, infectious enteritis, duodenal ulcer, pancreatitis, intussusception, Crohn disease, mesenteric lymphadenitis, ovarian torsion, pelvic inflammatory disease; primary neoplasm of appendix
⋄ Only 22–38% of children referred for suspected appendicitis actually have appendicitis
Ascariasis
  • = most common parasitic infection in world; cosmopolitan occurrence; endemic along Gulf Coast, Ozark Mountains, Nigeria, Southeast Asia
Organism: Ascaris lumbricoides = roundworm parasite, 15–35 cm in length; production of 200,000 eggs daily
Cycle: infection by contaminated soil, eggs hatch in duodenum, larvae penetrate into venules/lymphatics, carried to lungs, migrate to alveoli and up the bronchial tree, swallowed, maturation in jejunum within 2.5 months
Age: children age 1–10 years
  • colic
  • eosinophilia
  • appendicitis
  • hematemesis/pneumonitis
  • jaundice (if bile ducts infested)
    Location: jejunum > ileum (99%), duodenum, stomach, CBD, pancreatic duct
  • 15-35-cm-long tubular filling defects
  • barium-filled enteric canal outlined within Ascaris
  • whirled appearance, occasionally in coiled clusters (“bolus of worms”)
Cx: (1) Perforation of bowel
(2) Mechanical obstruction
Bannayan-Riley-Ruvalcaba Syndrome
  • = RUVALCABA-MYHRE-SMITH SYNDROME
    Cause: autosomal dominant transmission
  • • pigmented genital lesions
  • hamartomatous intestinal polyps (in 45%): usually in distal ileum + colon
  • macrocephaly
  • subcutaneous and visceral lipomas + hemangiomas
Barrett Esophagus
  • = BARRETT SYNDROME
  • = replacement of stratified squamous epithelium by metaplastic columnar epithelium (Barrett epithelium) containing goblet cells but no parietal cells
Cause: chronic gastroesophageal reflux with epithelial injury from esophagitis
Contributing factors:
  • genetic influence, reduced LES pressure, transient LES relaxation, hiatal hernia, delayed acid clearance, reduced acid sensitivity, duodenogastroesophageal reflux, alcohol, tobacco, chemotherapy, scleroderma (37%), S/P repair of esophageal atresia/esophagogastric resection/Heller esophagomyotomy
Histo: (1) specialized columnar epithelium (proximal)
(2) junctional-type epithelium (distal to above)
(3) fundic-type epithelium (most distally)
Prevalence: in general 0.3-4%; 7-10% of patients with advanced chronic reflux esophagitis
Associated with: moderate + severe esophagitis (94%), no/mild esophagitis (6%)
Age: 0-15 years and 40-88 years (mean of 55 years); M > F; mainly among Whites
  • dysphagia (due to esophageal stricture)
  • signs of reflux esophagitis: heartburn, substernal chest pain, regurgitation
  • low-grade upper intestinal bleeding
  • asymptomatic
Location: middle to lower esophagus
N.B.: the squamocolumnar junction does not coincide with the GE junction, is irregular and lies > 2-3 cm orad from the gastroesophageal junction
Distribution: circumferential/focal
P.806

  • several-cm-long stricture (71%) in midesophagus (40%) or lower esophagus (60%) [DDx: peptic stricture without Barrett esophagus]
  • large deep wide-mouthed peptic ulcer (= Barrett ulcer) at upwardly displaced squamocolumnar junction/within columnar epithelium
  • fine reticular mucosal pattern (3-30%) resembling areae gastricae of the stomach = netlike web of barium-filled grooves surrounding small tufts of mucosa; located distally from stricture (DDx: gastroesophageal reflux, monilial + viral esophagitis, superficial spreading carcinoma)
  • thickened irregular mucosal folds (28–86%)
  • fine granular mucosal pattern (DDx: reflux esophagitis, acanthosis, leukoplakia, superficial spreading carcinoma, moniliasis/herpes simplex/CMV esophagitis)
  • gastroesophageal reflux (45–63%)
  • distal esophageal widening (34–66%; due to abnormal motility)
  • hiatal hernia (75–94%)
  • uptake of Tc-99m pertechnetate by columnar epithelium
Dx: velvety pinkish red appearance of gastric-type mucosa extending from gastric mucosa into distal esophagus (endoscopy with biopsy)
Cx: (1) Ulceration ± penetration into mediastinum
(2) Stricture
3. Adenocarcinoma (0–10–46%;) 40-fold higher risk than general population
√ plaquelike/focal irregularity/nodularity/sessile polyps
Rx: (1) stop smoking, avoid bedtime snacks + foods that lower LES pressure, lose excess weight
(2) suppress gastric acidity: antacids, H2-receptor antagonists (cimetidine, ranitidine, famotidine), H+K+-adenosintriphosphatase inhibitor (omeprazole)
(3) improve LES pressure: metoclopramide, bethanechol
(4) esophageal resection in high-grade dysplasia
Behçet Syndrome
[Hulusi Behçet (1889–1948), dermatologist in Istanbul, Turkey]
  • = uncommon chronic multisystem inflammatory disorder of unknown etiology with relapsing course characterized by mucocutaneous-ocular symptoms as a triad of aphthous stomatitis, genital ulcers, ocular inflammation
    Countries: worldwide, most common in eastern Mediterranean countries, eastern rim of Asia
    Histo: nonspecific necrotizing vasculitis with deposition of immune complexes in walls of small blood vessels
    Age at onset: 3rd decade; M:F = 2:1
    Major criteria: buccal + genital ulceration, ocular inflammation, skin lesions
    Minor criteria: thrombophlebitis, GI + CNS lesions, arthritis, family history
  • • abdominal pain + diarrhea (50%)
@ Mucocutaneous: aphthous stomatitis, papules, pustules, vesicles, folliculitis, erythema nodosum-like lesions
@ Genital: ulcers on penis + scrotum/vulva + vagina
@ Ocular: relapsing iridocyclitis, hypopyon, choroiditis, papillitis, retinal vasculitis
@Articular: mild nondestructive arthritis
@ Vascular: migratory thrombophlebitis
@CNS: chronic meningoencephalitis
DDx: Reiter syndrome, Stevens-Johnson syndrome, SLE, ulcerative colitis, ankylosing spondylitis
Intestinal Behçet Disease
  • = large deeply penetrating intestinal ulcers (HALLMARK)
    Incidence: 10–40%
    Location: terminal ileum, cecum, ascending colon, transverse colon
  • deep round ulcers similar in appearance to peptic ulcers of stomach/duodenum
  • multiple shallow/longitudinal/aphthoid ulcers
CT:
  • polypoid lesion/thickened bowel wall (mural edema associated with deep ulcer penetration)
  • contrast enhancement (71%)
  • minimal lymphadenopathy, mostly <10 mm
Cx (56%): panperitonitis with high mortality due to tendency for perforation at multiple sites; fistula; hemorrhage
Prognosis: recurrence in 40–45% adjacent to surgical anastomosis
DDx: ulcerative colitis, Crohn disease
Bezoar
[padzahr, Persian = antidote, counterpoison]
  • = persistent concretions of foreign matter composed of accumulated ingested material in intestines
Incidence: 0.4% (large endoscopic series)
Etiology: material unable to exit stomach because of large size, indigestibility, gastric outlet obstruction, poor gastric motility (diabetes, mixed connective tissue disease, myotonic dystrophy, hypothyroidism)
Predisposition:
  • previous gastric surgery (vagotomy, pyloroplasty, antrectomy, partial gastrectomy), inadequate chewing, missing teeth, dentures, massive overindulgence of food with high fiber contents
  • • anorexia, bloating, early satiety/may be asymptomatic
Phytobezoar
  • = poorly digested fibers, skin + seeds of fruits and vegetables usually forming in stomach, may become impacted in small bowel
    Incidence: 55% of all bezoars
  • • history of recent ingestion of pulpy foods
Food: oranges, persimmons (most common, unripe persimmons contain the tannin shibuol that forms a gluelike coagulum after contact with dilute acid)
Site of impaction: stomach, jejunum, ileum
  • intraluminal filling defect without constant site of attachment to bowel wall
  • interstices filled with barium
  • coiled-spring appearance (rare)
  • partial/complete obstruction
Cx: decubitus ulceration + pressure necrosis of bowel wall, perforation, peritonitis
DDx: lobulated/villous adenoma, leiomyosarcoma, metastatic melanoma, intussusception
P.807

Trichobezoar
[trikho-, thrix, Greek = hair]
  • 80% are < age 30, almost exclusively in females;
Associated with: gastric ulcer in 24–70%
Blue Rubber Bleb Nevus Syndrome
  • = rare disorder characterized by vascular hamartomas of skin + visceral hemangiomas predominantly afflicting the GI tract (but also liver, spleen, heart, skeletal muscle, lung, kidney, thyroid, eyes, CNS)
    Etiology: sporadic/autosomal dominant
    Path: thin layer of connective tissue + single layer of endothelial cells surrounding blood-filled ectatic vessels
  • • red to deep blue soft painless cutaneous lesions evacuating under pressure + slow refilling (commonly present at birth ± increase in size and number with age)
  • • iron deficiency anemia (due to spontaneous hemorrhage)
  • nodular filling defects throughout small bowel
MR:
  • hyperintense lesions on T2WI (due to slow flow/thrombosis)
Cx: intussusception, volvulus; pressure erosion of bone, osseous + soft-tissue hypertrophy (secondary to hypervascularity)
DDx:
  • Maffucci syndrome (dyschondroplasia + osteochondromas + vascular malformations)
  • Klippel-Trenaunay-Weber syndrome (port wine stain, vascular malformations, limb hypertrophy)
  • Kasabach-Merritt syndrome (large vascular malformations + consumptive coagulopathy)
  • Kaposi sarcoma
  • Peutz-Jeghers syndrome (congenital polyposis + melanotic cutaneous lesions)
  • Gardner syndrome (soft-tissue tumors + sebaceous cysts)
Blunt Abdominal Trauma
  • CT is imaging method of choice for evaluation of stable patients
  • US imaging in the detection of intraabdominal injury:
    • 86% sensitive, 99% specific, 98% accurate
Hemoperitoneum
Frequency: 29–34% of patients with abdominal visceral injury have no hemoperitoneum
Location: paracolic gutters, pelvis
CT (negative predictive value of 99.6%):
Attenuation values of blood:
  • during IV contrast administration and assuming an initially normal hematocrit without significant dilution from intraperitoneal fluid (ascites, urine, succus, lavage fluid)
    — serum (after hematocrit effect) 0–20 HU
    — fresh unclotted blood 30–45 HU
    clotted blood 60–100 HU
    — active arterial extravasation >180 HU
  • “sentinel clot” sign = the highest attenuation value of blood clot marks the anatomic site of visceral injury
  • high-density active arterial extravasation always surrounded by lower-density hematoma (DDx: extravasated oral contrast is not surrounded by lower-density material)
US:
  • usually anechoic fluid accumulation in subhepatic space (= Morison pouch) > pouch of Douglas/paravesical space > between bowel loops
    DDx: bowel contents, urine, bile, ascites
  • hemoperitoneum score = depth of largest fluid collection in cm + 1 point for each additional site with fluid (score of ≤2 managed conservatively)
  • hyperechoic/occasionally isoechoic masses (= intraperitoneal clot)
Prognosis: 17% of patients without hemoperitoneum require surgical/angiographic intervention
  • Peritoneal lavage cannot quantify amount of hemoperitoneum + results in a 19–39% rate of nontherapeutic surgeries
Hypovolemia = Hypoperfusion complex
  • “collapsed cava” sign = persistent flattening of IVC (due to decreased venous return)
    N.B.: abort CT examination as shock is imminent!
  • small hypodense spleen (decreased enhancement)
  • small aorta + mesenteric arteries (due to intense vasoconstriction)
  • shock nephrogram = lack of renal contrast excretion
  • “shock bowel” = dilatation of fluid-filled intestines + generalized thickening of small bowel folds + increased enhancement (due to vasoconstriction of mesenteric vessels)
  • marked enhancement of adrenal gland
  • intense pancreatic enhancement
Categories of Splenic Injury
Grade Injury Description
I hematoma subcapsular <25% of surface area
laceration capsular tear <1 cm of parenchymal depth
II hematoma subcapsular 25-50% of surface area; intraparenchymal <5 cm in diameter
laceration 1-3 cm deep without involvement of trabecular vessel
III hematoma subcapsular >50% of surface area; ruptured subcapsular/parenchymal;
intraparenchymal >10 cm/expanding
laceration >3 cm parenchymal depth/involvement of trabecular vessels
IV laceration involving segmental/hilar vessels with devascularization of >25%
V laceration completely shattered spleen
vascular total splenic devascularization
Blunt Trauma To Spleen
  • Most frequently injured intraperitoneal organ in blunt abdominal trauma
Associated with: other solid visceral/bowel injuries (29%); lower rib fractures in 44%, injury to left kidney in 10%, injury to left diaphragm in 2%
P.808

  • 20% of left rib fractures have splenic injury!
  • 25% of left renal injury have splenic injury!
Technique: scanning delay of 60–70 seconds to avoid heterogeneous splenic enhancement
CECT (95% accurate):
  • CT not reliable to determine need for surgical intervention!
  • hemoperitoneum (indicates disruption of splenic capsule)
  • “sentinel clot” (= area of >60 HU adjacent to spleen) sensitive predictor of splenic injury =perisplenic hematoma
  • high-attenuation area (80–370 HU) =active extravasation/pseudoaneurysm:
    N.B.: active extravasation of contrast material usually requires surgery
  • mottled parenchymal enhancement =contusion
  • hypoattenuating line connecting opposing visceral surfaces = linear parenchymal defect =splenic laceration:
    • almost always associated with hemoperitoneum
  • crescentic region of low attenuation along splenic margin flattening/indenting/compressing the normal parenchyma =subcapsular hematoma
  • round hypodense inhomogeneous region ± hyperdense clot =intrasplenic hematoma
  • hypoattenuating hematoma with complete separation of splenic fragments = laceration traversing two capsular surfaces =splenic fracture
  • multiple lacerations = “shattered spleen
US:
  • hyperechoic intraparenchymal region (= acute hematoma/laceration)
  • anechoic intralesional collection (= brisk hemorrhage)
  • diffusely heterogeneous parenchymal pattern containing hyper- and hypo-echoic areas (= extensive splenic injury)
  • loss of normal organ contour (= perisplenic clot)
Sequelae:
  • scar/fibrosis
  • splenic pseudocyst (20–30 HU)
  • pseudoaneurysm formation
  • delayed splenic rupture
    • = hemorrhage >48 hours after trauma
    Cause: subcapsular hematoma
    Prevalence: 0.3–20% of blunt splenic injuries
    Time of onset: in 70% within 2 weeks of injury, in 90% within 4 weeks of injury
    Prognosis: 52% surgery (splenectomy [8%], splenorrhaphy), 48% nonsurgical management
    Rx: up to 91% of stable patients can be treated conservatively with observation; transcatheter embolization
    DDx: (1) Normal lobulation/splenic cleft (smoothly contoured, medially located)
    (2) Adjacent unopacified jejunum simulating splenic tissue
    (3) Early differential enhancement of red and white pulp (scan obtained within 20–50 seconds)
    (4) Perisplenic fluid from ascites/urine/succus/bile/lavage
image
Distribution of Traumatic Hepatic Lesions
Blunt Trauma To Liver (20%)
  • Second most frequently injured intraabdominal viscus
    Associated with: splenic injury in 45%
  • • clinical manifestation often delayed by days/weeks
Location: R > L lobe
Site: perivascular, paralleling right + middle hepatic arteries + posterior branches of right portal vein, avulsion of right hepatic vein from IVC (13%)
⋄ Left lobe injury more often associated with damage to duodenum, pancreas, transverse colon
Categories of Splenic Injury
Grade Injury Description
I hematoma subcapsular <10% of surface area
laceration capsular tear <1 cm of parenchymal depth
II hematoma subcapsular 10-50% of surface area; intraparenchymal <10 cm in diameter
laceration 1-3 cm deep and <10 cm long
III hematoma subcapsular >50% of surface area; ruptured subcapsular/parenchymal;
intraparenchymal >10 cm/expanding
laceration >3 cm parenchymal depth
IV laceration parenchymal disruption 25-75% of
lobe; 1-3 Couinaud segments in single lobe
V laceration disruption >75% of single lobe; >3 Couinaud segments in single lobe
vascular juxtahepatic venous injury (HV, IVC)
VI vascular hepatic avulsion
CECT:
  • hypoattenuating hematoma:
    • lenticular configuration (= subcapsular hematoma) usually resolving within 6-8 weeks
    • irregular linear branching/round regions of low attenuation = laceration
    • focal/diffuse periportal tracking (in up to 22%) due to dissecting hemorrhage/bile/dilated periportal lymphatics (secondary to elevated central venous pressure/injury to lymphatics)
    • P.809

    • alteration in distribution of vessels + ducts
  • hypodense wedge extending to liver surface = focal hepatic devascularization
  • focal hyperdense (80-350 HU) area = active hemorrhage/pseudoaneurysm
  • hemoperitoneum (inability of liver veins to contract)
  • intrahepatic/subcapsular gas (usually due to necrosis)
US:
  • localized area of increased intraparenchymal echogenicity (= acute hematoma/laceration)
  • widespread heterogeneous liver echogenicity + absence of normal vascular pattern (= global parenchymal injury)
Cx: in up to 20%
(1) delayed rupture (rare)
(2) hemobilia
(3) arteriovenous fistula/pseudoaneurysm
(4) biloma ± infection
(5) superinfection of hematoma/devascularized hepatic parenchyma
Rx: conservative treatment in up to 80% in adults + 97%
in children; transcatheter embolization
Healing: 1-6-15 months
DDx: (1) beam-hardening artifact from adjacent ribs/from air-contrast level in stomach
(2) Focal fatty infiltration
Blunt Trauma to Gallbladder (2%)
Associated with: injury to liver, duodenum
  • pericholecystic fluid (extraperitoneal location of GB)
  • free intraperitoneal fluid
CECT:
  • blurred contour of GB
  • focal thickening/discontinuity of GB wall
  • intraluminal enhancing mucosal flap
  • hyperattenuating blood within GB lumen
  • mass effect on adjacent duodenum
  • collapsed GB = GB rupture
  • focal periportal tracking = GB rupture
US:
  • focal hypoechoic thickening
  • echogenic mass within GB lumen
Blunt Trauma to GI Tract (5%)
Cause in children: MVA (lap belts), bicycle handle bar, child abuse
May be associated with: Chance fracture; traumatic hernia (disruption of the rectus abdominis muscle)
Location: jejunum distal to ligament of Treitz > duodenum > ascending colon at ileocecal valve > descending colon
  • abdominal tenderness (100% sensitive)
  • increased temperature + heart rate
  • decreased urine output over 24 hours
  • lap belt ecchymosis
NECT:
  • pneumoperitoneum (15–32%):
  • small gas bubbles anteriorly near liver/trapped within leaves of mesentery (with small bowel perforation)
  • retroperitoneal air (with disruption of duodenum/colon)
  • hypodense free fluid (58–85%), particularly in interloop location due to perforation
    DDx: parenchymal organ injury/osseous injury/large vessel injury/bladder perforation
  • sentinel clot sign adjacent to bowel
CECT (88–92% sensitive):
  • focal discontinuity of bowel wall = direct evidence
  • focal bowel wall thickening > 3 mm (= intramural hematoma (75%)/vascular compromise and inflammation due to spilling of bowel contents):
    • ± intestinal obstruction
  • hyperdense contrast enhancement of injured bowel wall = delayed venous transit time (20%)
  • stranding of mesentery = streaky hyperattenuating infiltration/fluid at mesenteric root (due to hemorrhage + inflammatory response)
  • mesenteric hematoma (39%)
  • extravasation of oral contrast material (uncommon), most dense near perforation
    DDx: hyperattenuating blood, extravasating vascular contrast material, leak of contrast material from urinary tract
  • mesenteric pseudoaneurysm
US:
  • nonspecific free fluid (98% sensitive)
N.B.: clinical signs + symptoms may be delayed for 24 hours (increasing mortality to 65%)
Blunt Trauma to Pancreas (3%)
Mechanism: compression against vertebral column with shear across pancreatic neck
Incidence: <10% of childhood trauma
Cause: motor vehicle accident, fall onto handle bars of a bicycle, child abuse
Associated with: injury to liver, duodenum
Classification:
I minor contusion/hematoma, capsule + major duct intact
II parenchymal injury without major duct injury
III major ductal injury
IV severe crush injury
Location: junction of body + tail
  • posttraumatic pancreatitis:
    • edema/fluid in peripancreatic fat
    • focal/diffuse pancreatic enlargement
    • irregularity of pancreatic contour
  • area of low-attenuation = contusion/laceration (actual site of laceration difficult to visualize)
  • fluid around superior mesenteric artery
  • fluid in transverse mesocolon/lesser sac
  • fluid between pancreas and splenic vein
  • thickening of anterior pararenal fascia
N.B.: 24–48-hour delayed scans uncover findings not present earlier
Rx: I + II conservative management;
III + IV need surgery within 24 hours
Cx: recurrent pancreatitis, pseudocyst, pseudoaneurysm, fistula, abscess (attendant mortality of 20%)
P.810

Boerhaave Syndrome
  • = complete transmural disruption of esophageal wall with extrusion of gastric content into mediastinum/pleural space secondary to food bolus impaction
  • • forceful vomiting with sudden onset of pain (substernal, left chest, in neck, pleuritic, abdominal)
  • • dyspnea
  • • NO hematemesis (blood escapes outside esophageal lumen)
  • rent of 2–5 cm in length, 2–3 cm above GE junction, predominantly on left posterolateral wall
  • pleural effusion on left >> right side/hydropneumothorax
  • pneumomediastinum (single most important plain-film finding), pneumopericardium, subcutaneous air
  • “V sign of Naclerio” = localized mediastinal emphysema with air between lower thoracic aorta + diaphragm
  • mediastinal widening
  • air-fluid level within mediastinum
  • extravasation of contrast medium into mediastinum/pleura
Brunner Gland Hyperplasia
  • = BRUNNER GLAND HAMARTOMA
Incidence: 1.2% of all gastric polyps
Etiology: response to increased acid secretion
Histo: diffusely enlarged hyperplastic glands with Swiss cheese appearance
Physiology: secrete a clear viscous alkaline mucus into crypts of Lieberkühn
MORPHOLOGIC TYPES:
  • Diffuse nodular hyperplasia
  • Circumscribed nodular hyperplasia: in suprapapillary portion
  • Single adenomatous hyperplastic polyp: in duodenal bulb
Location: duodenum, prepyloric region (duodenal glands begin in vicinity of pylorus extending distally within proximal 2/3 of duodenum)
  • multiple nodular filling defects (usually limited to 1st portion of duodenum) with “cobblestone appearance” (most common finding)
    DDx: polyposis syndromes, lymphoid hyperplasia, heterotopic gastric mucosa, nodular duodenitis
  • occasionally single mass up to 5 cm ± central ulceration
    DDx: adenomatous polyp, various submucosal tumors
    Cx: GI bleeding, obstruction, intussusception
Burkitt Lymphoma
  • = most common type of pediatric non-Hodgkin lymphoma; initially described in a 7-year old Ugandan child in 1958 by Dennis Burkitt, a British surgeon
    Etiology: tumor from undifferentiated small noncleaved B-cell–derived lymphocytes
    Path: resemblance to Hodgkin disease
    Histo: characteristic “starry sky” pattern
  • • fastest growing tumor in humans with a potential doubling time of 24 hours
  • • paraplegia
  • • NO peripheral leukemia
  • conspicuous absence of lymph node disease
  • tendency to permeate/destroy bone
MR:
  • isointense to muscle on T1WI + T2WI
  • intense homogeneous enhancement
Rx: dramatic response to chemotherapy
Prognosis: long-term survival in 50%
Endemic Form of Burkitt Lymphoma
Endemic in areas with malaria:
  • sub-Saharan Africa, New Guinea (exposure to Plasmodium falciparum has a synergistic effect causing a marked decrease in T-cell surveillance)
Incidence in central Africa:
  • 50–80% of all childhood neoplasms
Associated with: Epstein-Barr virus infection in 95% (implicated as a B-cell mitogen in the oncogenesis)
Age: 3–10 years
  • @ Mandible (first)/maxilla/facial bones
    • • jaw mass
    • • exophthalmos (orbital extension)
    • grossly destructive lesion, spicules of bone growing at right angles
    • large soft-tissue mass
  • @ Other skeleton (multifocal in 10%)
    • reminiscent of Ewing tumor/reticulum cell sarcoma
    • lamellated periosteal reaction around major long bones
Sporadic Form of Burkitt Lymphoma
  • = NONENDEMIC FORM OF BURKITT LYMPHOMA
Incidence in Europe + North America:
  • 35–45% of all pediatric NHL; 3% of all childhood tumors
Age: 6–15 years
  • Epstein-Barr virus genome found in only a minority
  • @ Abdomen (69%)
    • tumors of small bowel (Peyer patches of terminal ileum), mesentery
    • • abdominal mass
    • • intestinal obstruction
    • usually intraabdominal extranodal involvement with sparing of spleen
    • well-defined sharply marginated homogeneous tumors (75%)
    • ascites (13%)
  • @ Genitourinary tract (20%)
    • ovary, uterus, kidneys, retroperitoneum
    • renal masses/diffuse enlargement (5%)
    • hydronephrosis (28%)
  • @ Chest
    • pleural effusion (most common chest abnormality)
  • @ CNS
    • meningeal infiltration (most commonly)
    • cavernous sinus invasion
    • supra- and parasellar tumor
    • epidural spinal mass ± spinal cord compression
  • @ Others
    • salivary glands, thyroid, bone marrow
P.811

Carcinoid
  • = most common primary tumor of small bowel + appendix (>95% of all carcinoids); belongs to APUDomas (like pheochromocytoma, medullary carcinoma of thyroid, islet cell tumors of pancreas)
Age: 5th–6th decade; M:F = 2:1
Path: firm yellow submucosal nodule arising from argentophil Kulchitsky cells in the crypts of Lieberkühn (= argentaffinoma due to affinity for silver stain); invasion into mesentery incites an intense fibrotic reaction
Histo: low-grade malignancy = resemble adeno-carcinomas but do not have their aggressive behavior; malignant through invasion of muscularis
Biochemistry:
  • tumor elaborates (1) ACTH, (2) histamine, (3) bradykinin (4) kallikrein, (5) prostaglandin, (6) serotonin = 5-hydroxytryptamine (from tryptophan over 5-hydroxytryptophan), which is metabolized in liver by monamine oxidase into 5-hydroxyindole acetic acid (5-HIAA) and excreted in urine; 5-hydroxytryptophan is destroyed in pulmonary circulation
Associated with: other synchronous/metachronous malignancies (36% at necropsy); neurofibromatosis type 1
  • asymptomatic (66%)
  • abdominal pain/obstruction (19%)
  • nausea, weight loss (16%)
  • palpable mass (14%)
  • GI bleeding
  • Carcinoid syndrome (in 7% of small bowel carcinoids):
    • = constellation of clinical findings related to hormone secretion by tumor
    Cause: excess serotonin levels when the metabolic pathway to 5-HIAA (in liver) is bypassed
    (a) with liver metastases
    (b) with primary pulmonary/ovarian carcinoids
  • recurrent diarrhea (70%)
  • right-sided endocardial fibroelastosis (35%) resulting in tricuspid regurgitation + pulmonary valve stenosis + right heart failure
  • attacks precipitated by ingestion of food/alcohol
  • asthmatic wheezing from bronchospasm (15%)
  • desquamative skin lesions (5%)
  • pellagra (7%) from niacin deficiency as a result of preferential conversion of dietary tryptophan to serotonin rather than niacin
  • multiple telangiectasias (25%)
  • nausea & vomiting, fever
  • hypotension (vasomotor instability)
  • cutaneous facial flushing (rare)
  • excess 5-HIAA in urine
Prognosis: carcinoid syndrome has a higher morbidity & mortality than does the tumor itself!
RULE OF 1/3: ⋄ 1/3 occur in small bowel
⋄ 1/3 have metastases
⋄ 1/3 are multiple
⋄ 1/3 have a second malignancy
Metastases:
  • to mesenteric lymph nodes, liver (in 90% of patients with carcinoid syndrome), lung, bone (osteoblastic), peritoneum
  • incidence versus tumor size
    tumor of <1 cm (in 75%) metastasizes in 2%
    tumor of 1–2 cm (in 20%) metastasizes in 50%
    tumor of >2 cm (in 5%) metastasizes in 85%
  • incidence versus location
    tumor in ileum (in 28%) metastasizes in 35%
    tumor in appendix (in 46%) metastasizes in 3%
    tumor in rectum (in 17%) metastasizes in 1%
Liver metastases seen: best/ (only) on:
(a) NECT 35% (3%)
(b) CECT in HAP 35% (14%)
(c) CECT in PVP 30% (3%)
HAP = hepatic arterial-dominant phase of triple phase CT
PVP = portal venous-dominant phase of triple phase CT
Location: between gastric cardia and anus (85% in GI tract; 15% in lungs + bronchi)
  • @ Appendix (30–45%)
    Commonly benign: slow growth, rarely metastasizing
    Incidence at surgery: 0.03–0.7%
    Site: tip (70%), middle (20%), base (10%) of appendix
    • • symptoms of appendicitis
    • invasion of mesoappendix (11%)
  • @ Small bowel (25–35%)
    Incidence: 25% of all small bowel tumors
    Location: ileum (91%); jejunum (7%), duodenum (2%); multiple in 15–29–41%
    • 75% of patients with symptomatic spread have midgut carcinoids
    • 30% have a second primary malignancy of GI tract
    • Duodenal carcinoids are associated with multiple endocrine neoplasia
    • Periampullary carcinoids are associated with neurofibromatosis type 1 + often contain somatostatin-producing δ cells
  • @ Rectum (10–15%): metastasize in 10%
  • @ Colon (5%): ascending colon, often malignant
  • @ Stomach (<3%): lesser curvature of distal antrum
    • one/more 1–4-cm submucosal masses:
      • bull’s eye appearance when ulcerated
    • one/more sessile/pedunculated polyps
  • @ Other organs (5%): bronchus, thyroid, pancreas, biliary tract, teratomas (ovarian, sacrococcygeal, testicular)
  • @ may be multicentric
UGI:
  • small smooth submucosal mass (usually <2 cm) impinging eccentrically on lumen
  • desmoplastic response of mesentery from locally high levels of serotonin causes:
    • angulation + kinking of loops leading to obstruction (DIAGNOSTIC)
    • spiculated/tethered appearance of mucosal folds
    • matting of multiple loops
  • separation of loops due to large mesenteric metastases
CT:
  • submucosal vascular lesion (dual-phase imaging with water as oral contrast)
  • focal calcified mesenteric mass surrounded by thickened mesentery:
    • stellate radiating pattern + beading of mesenteric neurovascular bundles (desmoplastic reaction)
    • retraction + shortening of mesentery
    • P.812

    • displacement + kinking + separation of adjacent bowel loops
    • segmental thickening of adjacent bowel loops (encasement of mesenteric vessels leads to chronic ischemia)
  • low-density lymphadenopathy (due to necrosis)
  • characteristically hyperattenuating liver metastases in early arterial phase
  • may become isodense after slow contrast infusion/in portal-venous phase
Angio:
  • “sunburst” appearance:
    • kinking of small- and medium-sized vessels with a stellate configuration
    • simulated hypervascularity with thickening + foreshortening of mesenteric vessels secondary to fibrotic retraction
  • mesenteric ischemia:
    • arterial branch stenoses from encasement of mediumsized vessels (due to elastic vascular sclerosis with locally elevated serotonin levels)
    • venous occlusion/mesenteric varices
  • tumor may be identified as hypervascular mass
NUC (I-123 MIBG imaging):
  • uptake in 44-63% (higher frequency of radiotracer uptake in midgut carcinoids + with elevated serotonin levels)
US:
  • persistent fluid-distended appendix without typical signs of appendicitis
Prognosis: slow progression with average survival time of 3.2 years after diagnosis of liver metastases; 5-year survival of 65% for localized disease + 36% for distant metastatic disease
Rx: resection; somatostatin/SMS 201-995; chemoembolization of hepatic arteries
DDx: oat-cell carcinoma, pancreatic carcinoma, medullary thyroid carcinoma, retractile mesenteritis, desmoplastic carcinoma/lymphoma
Cathartic Colon
  • = prolonged use of stimulant-irritant cathartics (>15 years) resulting in neuromuscular incoordination from chronically increased muscular activity + tonus
    Agents: castor oil, senna, phenolphthalein, cascara, podophyllum, aloin
    Location: involvement of colon proximal to splenic flexure
  • effaced mucosa with flattened smooth surface
  • diminished/absent haustrations
  • “pseudostrictures” = smoothly tapered areas of narrowing are typical (sustained tonus of circular muscles)
  • poor evacuation of barium
  • flattened + gaping ileocecal valve
  • shortened but distensible ascending colon
DDx: “burned-out” ulcerative colitis with right-sided predominance (very similar)
Chagas Disease
[Carlos Chagas (1879-1934), physician in Rio de Janeiro, Brazil]
  • = damage of ganglion cells by neurotoxin liberated from protozoa Trypanosoma cruzi resulting in aperistalsis of GI tract + dilatation
Endemic to Central + South America (esp. eastern Brazil)
Histo: decreased number of cells in medullary dorsal motor nucleus + Wallerian degeneration of vagus + decrease/loss of argyrophilic cells in myenteric plexus of Auerbach
Peak age: 30–50 years; M:F = 1:1
  • • intermittent/persistent dysphagia
  • • odynophagia (= fear of swallowing)
  • • foul breath, regurgitation, aspiration
  • • Mecholyl test: abnormal response indicative of deficient innervation; 2.5–10 mg methacholine subcutaneously followed by severe tetanic nonperistaltic contraction 2–5 minutes after injection, commonly in distal half of esophagus, accompanied by severe pain
  • @ Dilatative cardiomyopathy (myocarditis)
  • @ Megacolon (bowels move at intervals of 8 days to 5 months)
    Cx: impacted feces, sigmoid volvulus
  • @ Esophagus: changes as in achalasia
Chalasia
  • = continuously relaxed sphincter with free reflux in the absence of a sliding hernia
    Etiology: elevated submerged segment
Causes:
  • Delayed development of esophagogastric region in newborns
  • Scleroderma, Raynaud disease
  • S/P forceful dilatation/myotomy for achalasia
  • free/easily induced reflux
Colitis Cystica Profunda
  • = rare benign condition characterized by submucosal mucus-containing cysts lined by normal colonic epithelium
    Etiology: probably related to chronic inflammation
    Associated with: solitary rectal ulcer syndrome (in localized form)
    Age: primarily disease of young adults
  • • brief periods of bright red rectal bleeding
  • • mucous/bloody discharge
  • • intermittent diarrhea
Location:
  • (a) localized to rectum (most commonly)/sigmoid
  • (b) generalized colonic process (less common)
  • nodular polypoid/cauliflower-like lesions <2 cm in size, containing no gas
  • spiculations mimicking ulcers (barium-filled clefts between nodules)
DDx: pneumatosis (rarely affects rectum)
Colonic Atresia
Incidence: less common than ileal atresia
Plain radiograph:
  • massive dilatation of colon proximal to obstruction
  • mottled pattern of gas + feces proximal to point of atresia
DDx: often indistinguishable from obstruction of distal ileum
BE:
  • functional microcolon
  • obstruction to retrograde flow of barium
P.813

US:
  • dilated hyperechoic distal small bowel + proximal colon (from retained meconium)
Colorectal Carcinoma
  • Most common cancer of GI tract; 3rd most commonly diagnosed malignancy in developed countries in men (after lung + prostate cancer) and women (after lung + breast cancer); 2nd leading cause of cancer deaths
Incidence: 11% of all newly diagnosed cancers; 13% of all cancer deaths; 150,000 new cases/year with 57,000 deaths in United States (1999); 6% lifetime probability of any White person to develop colorectal cancer; 3:100,000 in 30–34-year-olds; 532:100,000 for >85-year-olds
Lifetime probability: 4%
Risk factors:
  • Personal history of colonic adenoma/carcinoma
    • malignancy in 5% of tubular adenomas
    • malignancy in 30–40% of villous adenomas
    Proof of adenoma-carcinoma sequence:
    • frequent coexistence of adenoma + carcinoma
    • similar distribution within colon
    • consistent proportional prevalence in population having varied magnitudes of colon cancer risk
    • increased frequency of carcinoma in patients with adenomas
    • reduction of cancer incidence following endoscopic removal of polyps
    • all patients with familial adenomatous polyposis syndrome develop colon carcinoma if colon not removed
    • similarity of DNA + chromosomal constitution
    • 93% of colorectal carcinomas arise from adenomatous polyp!
    • A patient with one adenoma has a 9% chance of having a colorectal carcinoma in next 15 years!
    • It takes about 7 years for a 1-cm adenoma to become an invasive cancer!
    • 5% of adenomas 5 mm in size develop into invasive cancers (5 mm is considered critical mass of intraepithelial neoplasia)!
  • Family history of benign/malignant colorectal tumors in first-degree relatives (3–5 × risk)
  • Personal history of ovarian/endometrial/breast cancer
  • Dysplasia of colon within flat mucosa
  • Inflammatory bowel disease:
    • Ulcerative colitis (3–5% incidence; cumulative incidence of 26% after 25 years of colitic symptoms)
    • Crohn disease affecting the colon + rectum (particularly in bypassed loops/in vicinity of chronic fistula)
    Time delay: >8–10 years of colitis
    Underlying lesion: dysplasia within flat mucosa
  • Prominent lymphoid follicular pattern
  • Pelvic irradiation
  • Ureterosigmoidostomy
Environmental risk factors:
  • low fiber diet: prevents rapid transit time thus increasing contact time between potential toxins and colonic mucosa
  • increased ingestion of fat + animal protein
  • obesity
  • asbestos worker
Genetic risk factors (6% of colorectal carcinomas):
  • familial adenomatous polyposis syndrome: familial polyposis, Gardner syndrome, Turcot syndrome
    Age: approximately at 40 years
  • certain hamartomatous polyposis syndromes:Peutz-Jeghers syndrome, juvenile polyposis, Cowden disease
  • hereditary nonpolyposis colon cancer syndrome
    • = Lynch syndrome (see below)
Screening recommendations (American Cancer Society):
  • as/more effective than mammographic screening
  • (a) for persons >50 years of age: annual fecal occult-blood test + sigmoidoscopy/BE every 3–5 years
  • (b) for first-degree relatives of patients with colon cancer screening should start at age 40
Age: median age of 71 years for colon cancer; median age of 69 years for rectal cancer; M:F = 3:2
Histo:
  • Adenocarcinoma with varied degrees of differentiation
  • Mucinous carcinoma (uncommon)
  • Squamous cell carcinoma + adenoacanthoma (rare)
Metastases (lymphatic/hematogenous venous):
  • Liver (75%; 15–20% at time of surgery) due to portal venous drainage route
  • Mesentery + mesenteric nodes (10–15%)
  • Adrenal (10–14%)
  • Lung (5–50%)
  • Ovary (3–8%) = Krukenberg tumor
  • Psoas muscle tumor deposit
  • Peritoneal metastases:
    • malignant ascites: usually associated with poorly differentiated colonic carcinoma
    • pseudomyxoma peritonei (<5%): low-grade colonic adenocarcinoma
  • Bone (5%)
  • Brain (5%)
    • Because of absence of lymphatics in lamina propria colon cancer will not metastasize until it penetrates the muscularis mucosa!
  • rectal bleeding, iron deficiency anemia
  • change in bowel habits/caliber of stools
  • obstruction (poor prognostic indicator)
  • hydronephrosis (13%)
  • positive fecal occult blood testing (2–6% positive-result rate; 5–10% positive predictive value; fails to detect 30–50% of colorectal carcinomas + up to 75% of adenomas):
    • Hemoccult (hematein), HemoQuant® (porphyrins), Haemselect (hemoglobin)
  • progressive elevation of carcinoembryonic antigen (CEA) >10 μg/L indicative of recurrent/metastatic disease
  • watery diarrhea + potassium depletion/excessive secretion of mucus + hypoalbuminemia (in large mucin-secreting villous tumor)
Location: “aging gut” = number of right-sided lesions increasing with age (“changing distribution”)
P.814

  • left colon (52–61%):
    • rectum (15–33–41%), sigmoid (20–37%), descending colon (10–11%)
    • commonly annular strictures with obstruction
  • right colon:
    • transverse colon (12%), ascending colon (8–16%), cecum (8–10%)
      • commonly polypoid lesions with chronic bleeding + intussusception
Colonoscopy: cecum not visualized in 10–36%; fails to detect 12% of colonic polyps (10% in areas never reached by colonoscope)
Cx: perforation in 0.2% (0.02% for BE); death in 1:5,000 (1:50,000 for BE)
BE (sensitivities in detection of polyps >1 cm: SCBE 77–94%, DCBE 82–97%; for polyps <1 cm: SCBE 18–72%, DCBE 61–83%):
  • fungating polypoid carcinoma:
    • chronic bleeding, intussusception
  • annular ulcerating carcinoma = “apple core lesion”
    • = annular constriction is a result of tumor growing along the lymphatic channels, which parallel the circular muscle fibers of the inner layer of the muscularis propria; longitudinal growth is limited with abrupt transition to normal mucosa
    • • colonic obstruction
  • “saddle lesion” = growth characteristics between polypoid mass + annular constricting lesion
  • scirrhous carcinoma (signet-ring type)
    • = long-segment stricture without significant mucosal abnormality similar to linitis plastica due to diffuse circumferential + longitudinal tumor infiltration within the loose submucosal tissue between muscularis mucosa + muscularis propria
    • • often seen in ulcerative colitis
  • curvilinear/mottled calcifications (rare) are CHARACTERISTIC of mucinous adenocarcinoma
CT (48–90% staging accuracy, 25–73% for lymph node metastases):
  • CT staging (poor accuracy compared with Astler-Coller classification):
    Stage 1 intramural polypoid mass
    Stage 2 thickening of bowel wall
    Stage 3 slight invasion of surrounding tissues
    Stage 4 massive invasion of surrounding tissue + adjacent organs/distant metastases
    Staging of colorectal cancer
    (modified Dukes = Astler-Coller classification):
    Stage Findings
    A limited to mucosa
    B involvement of muscularis propria
        B1 extension into muscularis propria
        B2 extension through muscularis propria into serosa/mesenteric fat (35%)
    C lymph node metastases (50%)
        C1 + growth limited to bowel wall
        C2 + growth extending into adipose tissue
    D distant metastases
    Staging of Colorectal Cancer
    (UICC-AJCC Colorectal Cancer Staging System)
    Stage Grouping 5-year Survival
    0 Tis N0 M0 >95%
    I T1 N0 M0 75-100%
    T2 N0 M0
    II T3 N0 M0 50-75%
    T4 N0 M0
    III any T N1 M0 30-50%
    any T N2,3 M0
    IV any T any N M1 <10%
    Legend:
    Tis carcinoma in situ
    T1 invasion of submucosa
    T2 invasion of muscularis propria
    T3 invasion of subserosa/pericolic tissue
    T4 invasion of visceral peritoneum/other organs
    N1 1–3 pericolic Lnn
    N2 >4 pericolic Lnn
    N3 any Lnn along course of a vascular trunk
  • low-density mass + low-density lymph nodes in mucinous adenocarcinoma (= >50% of tumor composed of extracellular mucin)
  • psammomatous calcifications in mucinous adenocarcinoma
  • signs of Lnn involvement: single lymph node >1 cm in diameter/cluster of ≥3 nodes <1 cm/node of any size within mesentery
MR (staging accuracy of 73%, 40% sensitivity for lymph node metastases)
Prognosis:
  • Survival rate of 40–50% overall in 5 years (unchanged over past 40 years); 80–90% with Duke A; 70% with Duke B; 33% with Duke C; 5% with Duke D
  • Recurrence in 1/3 of patients:
    • local recurrence at line of anastomosis (60%) within 1 year after resection in 50%, within 2 years after resection in 70–80%
    • distant metastases (26%)
    • local recurrence + metastases (14%)
  • Risk after detection of colon cancer:
    5% for synchronous colon cancer
    14% for synchronous cancer with “sentinel polyp”
    35% for additional adenomatous polyp
    3% for metachronous colon cancer
    4% for extracolonic malignancy
Cx: (1) Obstruction (frequently in descending + sigmoid colon)
(2) Perforation
(3) Intussusception
(4) Abscess formation
(5) Fistula formation
(6) Pneumatosis cystoides intestinalis
(7) Pseudomyxoma peritonei (from low-grade adenocarcinoma of colon)
Rx: (1) Local surgical excision/polypectomy for stage I disease
(2) Right/left hemicolectomy with eventual anastomosis of proximal + distal excision sites
(3) Low anterior resection: >2 cm of rectum must remain to anastomose the colon
(4) Abdominoperineal resection with colostomy for low rectal carcinoma
(5) Adjuvant chemotherapy for stage II disease (fluorouracil/levamisole)
DDx: (1) Prolapsing ileocecal valve (change on palpation)
(2) Spasm (intact mucosa, released by propantheline bromide)
(3) Diverticulitis
P.815

Lynch Syndrome
  • = HEREDITARY NONPOLYPOSIS COLORECTAL CANCER SYNDROME
  • = families with high incidence of colorectal cancers + increased incidence of synchronous and metachronous colorectal cancers
Amsterdam criteria:
  • ≥3 family members of whom 2 are 1st degree relatives of the third
  • family members in ≥2 generations
  • one family member diagnosed <50 years of age
Lynch I = no associated extracolonic cancer
Lynch II = associated with extracolonic malignancy: transitional cell carcinoma of ureter + renal pelvis; adenocarcinoma of endometrium, stomach, small bowel, pancreas, biliary tract, brain; hematologic malignancy; carcinoma of skin + larynx
Etiology: autosomal dominant abnormality of chromosome 2 with defect in DNA replication-repair process
(a) accelerated adenoma-carcinoma sequence
(b) dysplasia in flat mucosa of colon
Prevalence: 5-10% of patients with colon cancer;
5 × more common than familial adenomatous polyposis syndrome
Mean age: 45 years
Location: 70% proximal to splenic flexure
Prognosis: better stage for stage than in other cancers
(5-year survival rate of 65% versus 44% in sporadic cases)
Surveillance: colonoscopy every 1-2 years from ages 22-35 years
Pathologic staging of rectal cancer
Astler-Coller/TNM Description 5-year Survival
A T1,N0,M0 limited to submucosa 80%
B1 T2,N0,M0 limited to muscularis propria 70%
B2 T3,N0,M0 transmural extension 60-65%
C1 T2,N1,M0 nodes (+), into muscularis 35-45%
C2 T3,N1,M0 nodes (+), transmural 25%
T4 invasion of adjacent organs
D M1 distant metastasis <25%
Rectal Cancer
Incidence: 45,000 rectal cancers/year in United States
Hematogenous metastasis:
  • dual venous drainage into portal + systemic veins
    • may have lung without liver metastases
Risk of recurrence:
5% for T1  
10% for T2 33% for T1, N1 + T2N1
25% for T3 66% for T3N1
50% for T4  
Staging accuracy:
  • Digital rectal examination: 68-75-83%; limited to lesions within 10 cm of anal verge
  • CT: 48-72-92%, better for more extensive regional spread; 25-73% for lymph node involvement
  • MR: 74-84-93% with tendency for overstaging
  • Transrectal ultrasound: 64-77-94% with tendency for overstaging; limited to lesions <14 cm from anal verge + nonstenotic lesions; 50-83% sensitivity for lymph node involvement
Transrectal US (81% accuracy):
Normal layers:
  • hyperechoic interface of balloon + mucosa
  • hypoechoic mucosa + muscularis mucosa
  • hyperechoic submucosa
  • hypoechoic muscularis propria
  • hyperechoic serosa
  • hypoechoic mass disrupting rectal wall:
    • no interruption of hyperechoic submucosa = tumor confined to mucosa + submucosa
    • no interruption of hyperechoic serosa = tumor confined to rectal wall
    • break in outermost hyperechoic layer = tumor penetrates into perirectal fat
    • irregular serrated outer border of muscularis propria (pseudopodia through serosa)
  • hypoechoic perirectal lymph nodes (= tumor involvement)
Colonic Volvulus
  • = most common form of volvulus
Incidence: 10% of large-bowel obstruction
Cecal Volvulus
  • = VOLVULUS OF CECUM
Incidence: 40% of colonic volvulus
Cause: sudden distension by trauma, pressure, constipation, distal colonic obstruction
Associated with: malrotation + long mesentery resulting in poor fixation of right colon (10-25% of population)
Pathophysiology of vascular compromise:
  • Acute mesenteric torsion + strangulation causes arterial + venous obstruction
  • Gradual distension + increase in intraluminal pressure interferes with blood supply; perforation in 65%
Age peak: 20–40 years; M > F
  • cecal gaseous distension:
    • cecum rotates anterior to ascending colon =cecal bascule [French = seesaw] (type I cecal volvulus)
    • “kidney-shaped” distended cecum rotates into left upper quadrant (type II cecal volvulus)
  • tapered end of barium column points toward torsion
Cx: (1) cecal distension >10–12 cm means risk of bowel perforation/infarction
(2) Abdominal compartment syndrome= increase in abdominal pressure diminishes respiratory function + cardiac output
P.816

Sigmoid Volvulus
  • = VOLVULUS OF SIGMOID
Cause: sigmoid twists on mesenteric axis
Age: usually in elderly/psychiatrically disturbed
Degree of torsion: 360° (50%), 180° (35%), 540° (10%)
  • greatly distended paralyzed loop with fluid-fluid levels, mainly on left side, extending toward diaphragm (erect film)
  • “coffee-bean sign” = distinct midline crease corresponding to mesenteric root in largely gas-distended loop (supine)
  • “bird-of-prey sign” = tapered hooklike end of barium column
CT:
  • “whirl sign” = tightly torsioned mesentery formed by twisted afferent + efferent loop
Congenital Esophageal Atresia & Tracheoesophageal Fistula
  • = complex of congenital anomalies characterized by failed/incomplete formation of the tubular esophagus or an abnormal communication between esophagus + trachea
Cause: developmental disorder in formation and separation of primitive foregut into trachea + esophagus/vascular compromise
Embryology:
  • primitive foregut tube develops lateral wall folds that may incompletely connect at any point leaving a fistulous communication; occurs at 3rd–5th week of intrauterine life
Incidence: 1:2,000–4,000 livebirths; most common sporadic congenital anomaly diagnosed in childhood
Risk of recurrence in sibling: 1%
Associated anomalies (17–56–70%):
  • Gastrointestinal (20–25%): imperforate anus, pyloric stenosis, duodenal atresia, annular pancreas
  • Cardiac (15–39%): patent ductus arteriosus, ASD, VSD, right-sided aortic arch (5%)
  • Musculoskeletal (24%): radial ray hypoplasia, vertebral anomalies
  • Genitourinary (12%): unilateral renal agenesis
  • Chromosomal (3–19%): trisomy 18, 21, 13
    • Trisomy 18 is present in 75–100% of fetuses + in 3–4% of neonates with esophageal atresia!
mnemonic: ARTICLES
  • Anal atresia
  • Renal anomalies
  • TE fistula
  • Intestinal atresia/malrotation
  • Cardiac anomaly (PDA, VSD)
  • Limb anomalies (radial ray hypoplasia, polydactyly)
  • Esophageal atresia
  • Spinal anomalies
mnemonic: VACTERL
  • Vertebral anomalies
  • Anorectal anomaly
  • Cardiovascular anomalies
  • Tracheo-
  • Esophageal fistula
  • Renal anomalies
  • Limb anomalies
  • drooling from excessive accumulation of pharyngeal secretions (esophageal atresia = EA)
  • obligatory regurgitation of ingested fluids (EA)
  • aspiration with coughing + choking during feeding (TEF)
  • recurrent pneumonia + progressive respiratory distress of variable severity (tracheoesophageal fistula = TEF) in neonate
Location: between upper 1/3 + lower 1/3 of esophagus just above carina
  • @ Mediastinum
    • “coiled tube” = inability to pass feeding tube into stomach (esophageal atresia)
    • retrotracheal air-distended pouch of proximal esophagus causing compression/displacement of trachea
    • non-/hypoperistaltic esophageal segment (6–15 cm) in midesophagus
    • food impaction
  • @ Abdomen
    • gasless abdomen (esophageal atresia ± proximal TE fistula = types A + B)
    • abdomen distended by bowel gas in 90% (distal TE fistula/H-type fistula = types C + D)
  • @ Chest
    • bronchopneumonia with patchy airspace opacity, esp. in dependent upper lobes (in 50%)
OB-US (anomalies not identified before 24 weeks GA):
  • polyhydramnios in 33–60%:
    • TE-fistula with esophageal atresia is cause of polyhydramnios in only 3%!
  • absence of fluid-distended stomach (in 10–41%; in remaining cases TE-fistula/gastric secretions allow some gastric distension)
  • reduced intraluminal fluid in fetal gut
  • small abdomen (birth weight <10th percentile in 40%)
  • distended proximal pouch of atretic esophagus
Cx after repair:
  • Anastomotic leak
  • Recurrent TE fistula
  • Aspiration pneumonia secondary to
    • esophageal stricture
    • disordered esophageal motility distal to TE fistula
    • gastroesophageal reflux
DDx: pharyngeal pseudodiverticulum (traumatic perforation of posterior pharynx from finger insertion into oropharynx during delivery/tube insertion)
Esophageal Atresia without Fistula = Type A
Frequency: 8–10%
  • Associated anomalies in 17% (mostly Down syndrome + other atresias of GI tract)
Esophageal Atresia with Fistula
Associated anomalies in 30% (mostly cardiovascular)
Type B = esophageal atresia + proximal TE fistula
Frequency: 0.9–1%
Type C = esophageal atresia + distal TE fistula
Frequency: 53–86%
Type D = esophageal atresia + proximal and distal TE fistula
Frequency: 1–2.1%
P.817

Tracheoesophageal Fistula without Atresia
image
Esophageal Atresia With Tracheo-esophageal Fistula
  • = H-shaped fistula =Type E
Frequency: 6–10%
Associated anomalies in 23% (mostly cardiovascular)
  • • feeding difficulties with choking
  • • diagnosis may not be made for several years
  • fistula courses forward and upward from esophagus
mnemonic: NO PD, P+D No
type A =esophageal atresia NO fistula = 10%
type B = esophageal atresia Prox fistula = 1%
type C = esophageal atresia Dist fistula = 80%
type D = esophageal atresia Prox + Dist = 1%
type E = H-type fistula NO atresia = 10%
Congenital Intestinal Atresia
Incidence: 1:300 livebirths
Cause: usually sporadic vascular accidents (primary/secondary to volvulus or gastroschisis)
Location: jejunum + ileum (70%), duodenum (25%), colon (5%); may involve multiple sites
  • “triple bubble sign” = intraluminal gas in stomach + duodenal bulb + proximal jejunum as pathognomonic sign for jejunal atresia
  • bulbous bowel segment sign = dilated loop of bowel just proximal to site of atresia (due to prolonged impaction of intestinal contents) with curvilinear termination
  • gasless lower abdomen (gut usually air-filled by 4 hours after birth)
  • meconium peritonitis (6%)
  • polyhydramnios (in 50% with duodenal/proximal jejunal atresia; rarely in ileal/colonic atresia)
Prognosis: 88% survival for isolated atresia
Cricopharyngeal Achalasia
  • = hypertrophy of cricopharyngeus muscle (= upper esophageal sphincter) with failure of complete relaxation
Etiology:
  • Normal variant without symptoms: seen in 5–10% of adults
  • Compensatory mechanism to gastroesophageal reflux
  • Neuromuscular dysfunction of deglutition
    • primary neural disorders: brainstem disorder (bulbar poliomyelitis, syringomyelia, multiple sclerosis, amyotrophic lateral sclerosis); central/peripheral nerve palsy; cerebrovascular occlusive disease; Huntington chorea
    • primary muscle disorder: myotonic dystrophy; polymyositis; dermatomyositis; sarcoidosis; myopathies secondary to steroids/thyroid dysfunction; oculopharyngeal myopathy
    • myoneural junction disorder: myasthenia gravis; diphtheria; tetanus
  • • mostly asymptomatic
  • • dysphagia
  • Cineradiography/videotape recording required for demonstration!
  • distension of proximal esophagus + pharynx
  • smoothly outlined shelf-/liplike projection posteriorly at level of cricoid (= pharyngoesophageal junction) = level of C5-6
  • barium may overflow into larynx + trachea
Cx: Zenker diverticula
Rx: cricopharyngeal myotomy
Cowden Disease
  • = MULTIPLE HAMARTOMA SYNDROME
  • = autosomal dominant disease with high penetrance characterized by multiple hamartomas + neoplasms of endodermal, ectodermal, mesodermal origin
Incidence: 160 cases reported
Cause: susceptibility gene on long arm of chromosome 10 (10q23)
Age: 2nd decade
  • @ Mucocutaneous tumors
    • facial papules
    • oral papillomas (lips, gingiva, tongue)
    • palmoplantar keratosis, acral keratosis
  • P.818

  • @ CNS neoplasia
    • meningioma; glioma
      Associated with: dysplastic cerebellar gangliocytoma
    • • macrocephaly
  • @ Breast lesions (in 50%):
    • fibrocystic disease + fibroadenomas
    • breast cancer (20–30%): often bilateral + ductal
  • @ GI tract
    • multiple hamartomatous polyps (in 30–60%, commonly in rectosigmoid)
  • @ Thyroid abnormalities (in 60–70%):
    • adenomas + goiter
    • follicular thyroid adenocarcinoma (3–4%)
  • @ Genitourinary lesions
  • @ Skeletal abnormalities
Crohn Disease
  • [Burrill Crohn (1884–1983), gastroenterologist in New York, USA]
  • = REGIONAL ENTERITIS
  • = disease with prolonged + unpredictable course characterized by discontinuous + asymmetric involvement of entire GI tract
Genetic susceptibility:
  • homozygosity for Nod-2 gene (intracellular protein in lymphocytes) responsible for binding bacterial endotoxins + initiating a cascade that produces TNF-alpha;(tumor necrosis factor-alpha)
  • increased mucosal permeability for enteric bacteria
Prevalence: 2–3:100,000 white adults
Path: transmural inflammation (noncaseating granuloma with Langhans giant cells and epithelioid cells, edema, fibrosis); obstructive lymphedema + enlargement of submucosal lymphoid follicles; ulceration of mucosa overlying lymphoid follicles
Age: onset between 15 and 30 years; M:F = 1:1
  • recurrent episodes of diarrhea
  • colicky/steady abdominal pain
  • low-grade fever
  • weight loss, anorexia
  • occult blood + anemia
  • perianal abscess/fistula (40%)
  • malabsorption (30%)
Associated with: erythema nodosum, pyoderma gangrenosum
Rx: probiotics + antibiotics (modulation of enteric flora); purine synthesis inhibitors like azathioprine + 6-mercaptopurine (downregulation of inflammatory response); infliximab (chimeric antibody binding to TNF-α)
Intestinal Manifestations of Crohn Disease
  • @ Esophagus (3%)
    • “aphthous” ulcers (early)
    • esophagitis, stricture, fistula (late)
  • @ Stomach (1–2%) = granulomatous gastritis
    • aphthous ulcers (= pinpoint erosions)
    • pseudo–post Billroth-I appearance
    • “ram’s horn sign” = poorly distensible smooth tubular narrowed antrum + widened pylorus + narrow duodenal bulb
    • cobblestone appearance of mucosa
    • antral-duodenal fistula
  • @ Duodenum (4–10%)
    • almost always associated with gastric involvement
    Location: duodenal bulb + proximal half of duodenum
    • superficial erosions/aphthoid ulcers (early lesion)
    • thickened duodenal folds
  • @ Small bowel (80%) = REGIONAL ENTERITIS
    • terminal ileum (alone/in combination in 95%); jejunum/ileum (15–55%)
    • thickening + slight nodularity of circular folds
    • aphthous ulcers
    • cobblestone mucosa/ulceration
    • commonly associated with medial cecal defect
  • @ Colon (22–55%) = GRANULOMATOUS COLITIS
    Location: particularly on right side with rectum + sigmoid frequently spared
    • tiny 1–2-mm nodular filling defects (lymphoid follicular pattern)
    • aphthous ulcers with “target/bull’s-eye” appearance
    • “transverse stripe sign” = 1-cm-long straight stripes representing contrast medium within deep grooves of coarse mucosal folds
    • long fistulous tracts parallel to bowel lumen
  • @ Appendicitis (20%)
  • @ Rectum (14–50%)
    • deep/collarbutton ulcers
    • rectal sinus tracts
Phases:
  • Earliest changes
    • nodular enlargement of lymphoid follicles
    • blunting/flattening/distortion/straightening/thickening of valvulae conniventes (obstructive lymphedema, usually first seen in terminal ileum)
    • aphthous ulcers = nodules with shallow central barium collection up to 5 mm in diameter
    Location: duodenal bulb, second portion of duodenum, terminal ileum
  • Advanced nonstenotic phase
    • skip lesions (90%) = discontinuous involvement with intervening normal areas
    • cobblestone appearance = serpiginous longitudinal + transverse ulcers separated by areas of edema
    • thick + blunted small bowel folds (inflammatory infiltration of lamina propria + submucosa)
    • straightening + rigidity of small bowel loops with luminal narrowing (spasm + submucosal edema)
    • separation + displacement of small bowel loops (from lymphedematous wall thickening/increase in mesenteric fat/enlarged mesenteric lymph nodes/perforation with abscess formation)
    • pseudopolyps = islands of hyperplastic mucosa between denuded mucosa
    • inflammatory polypoid masses
    • sessile/pedunculated/filiform postinflammatory polyps
    • diffuse mucosal granularity due to 0.5–1-mm round lucencies (= blunted + fused villi seen en face)
    • linear ulcers on mesenteric border (nearly PATHOGNOMONIC)
    • P.819

    • pseudodiverticula = pseudosacculations = bulging area of normal wall opposite affected scarred wall on antimesenteric side
  • Stenotic phase
    • “string sign” = strictures (in 21%, most frequently in terminal ileum)/marked narrowing of rigid loops
    • normal proximal loops may be dilated with stasis ulcers + fecoliths
CT:
  • @ bowel wall:
    • mucosal hyperenhancement (best seen with bowel lumen distended by negative contrast material):
      • “target sign” of active inflammation = mural stratification = hyperenhancement of mucosa + muscularis propria sandwiching an edematous/fatty submucosa of decreased attenuation
      • “comb sign” = hyperemic engorged tortuous vasa recta leading to actively inflamed bowel segment
    • homogeneous density of thickened bowel wall (DDx: ulcerative colitis with heterogeneous attenuation):
      • “double halo configuration” (50%) = intestinal lumen surrounded by inner ring of low attenuation (= edematous mucosa) + outer ring of soft-tissue density (= thickened fibrotic muscularis + serosa) (DDx: radiation enteritis, ischemia, mesenteric venous thrombosis, acute pancreatitis)
      • skip areas of asymmetric bowel wall thickening of 11 (range 10–20) mm in 82% (DDx: ulcerative colitis with a mean thickness of 8 mm)
    • luminal narrowing + proximal dilatation
  • @ paraenteric findings
    • “creeping fat” = massive proliferation of mesenteric fat along mesenteric border (40%):
      • fat attenuation elevated by 20–60 HU
      • separation of small bowel loops (mass effect)
    • mild mesenteric adenopathy (18%) with lymph nodes 3–8 mm small
      • Consider lymphoma/carcinoma with lymph nodes >10 mm!
    • fistula/sinus tract (15–40%)
    • mesenteric phlegmon/abscess in 15–20% (DDx: postoperative blind loop)
US:
  • “pseudokidney”/target sign = thickening of bowel wall (22–65–89%) of 5–20 mm (DDx: ulcerative colitis)
  • circumferential diffusely hypoechoic bowel wall with loss of normal layering (due to transmural edema, inflammation, fibrosis)
  • rigid + noncompressible bowel segment with reduction/loss of peristalsis
  • hyperemia of gut wall + adjacent fat on color Doppler
  • inflammatory mass = phlegmon (14%), abscess (4%)
  • distended fluid-filled loops (12%)
  • hypoechoic fistulous tract
Prognosis: recurrence rate of up to 39% after resection (commonly at the site of the new terminal ileum, most frequently during first 2 years after resection); mortality rate of 7% at 5 years, 12% at 10 years after 1st resection
Cx: (1) Fistula
(2) Intramural sinus tracts
(3) Abscess in up to 20% (DDx: acute appendicitis)
(4) Free perforation (1–2%)
(5) Toxic megacolon
(6) Small bowel obstruction (15%)
(7) Hydronephrosis (from ureteric compression, generally on right side)
(8) Adenocarcinoma in ileum/colon (particularly in bypassed loops/in vicinity of chronic fistula)
♢ 4–20 × increased risk of colonic adeno-carcinoma compared with general population with a latency period of 25–30 years!
(9) Lymphoma in large + small bowel
DDx: (1) Yersinia (in terminal ileum, resolution within 3–4 months)
(2) Tuberculosis (more severe involvement of cecum, pulmonary TB)
(3) Actinomycosis, histoplasmosis, blastomycosis, anisakiasis
(4) Segmental infarction (acute onset, elderly patient)
(5) Radiation ileitis (appropriate history)
(6) Lymphoma (no spasm, luminal narrowing is uncommon, tumor nodules)
(7) Carcinoid tumor (tumor nodules)
(8) Eosinophilic gastroenteritis
(9) Potassium stricture
Fistulizing Crohn Disease
Incidence: 33%
  • Crohn disease is 3rd most common cause of fistula/sinus tracts (DDx: iatrogenic [most common cause], diverticula [2nd most common cause])!
Types:
  • enterocolic:
    • most frequently between ileum and cecum
  • enterocutaneous (8–21%):
    • rectum-to-skin; rectum-to-vagina
  • perineal fistula + sinus tracts
image
Park’s Classification Of Perianal Fistulas
P.820

Extraintestinal Manifestations of Crohn Disease
  • @ Hepatobiliary
    • Fatty infiltration of liver (steroid therapy, hyperalimentation)
    • Hepatic abscess (rare): M:F = 3:1
    • Gallstones (15–34%): predominantly cholesterol;
      Risk: 3–5 × higher risk than expected; risk correlates with length of diseased ileum/resected ileum/duration of disease
      Cause: interrupted enterohepatic circulation with malabsorption of bile salts in terminal ileum
    • Acute cholecystitis
    • Primary sclerosing cholangitis (1%) + hepatoma
    • Bile duct + gallbladder carcinoma
    • Pancreatitis
  • @ Genitourinary
    • Urolithiasis (5–10%): oxalate (steatorrhea leads to excess colonic absorption of oxalate)/urate stones
    • Hydronephrosis
    • Renal amyloidosis
    • Focal cystitis
    • Ileoureteral/ileovesical fistula (5–20%)
  • @ Musculoskeletal
    • digital clubbing (11–40%)
    • mild self-limiting seronegative peripheral migratory arthritis (15–22%): may precede bowel disease in 10%; severity + course correlates well with severity of intestinal disease; resection of diseased bowel leads to regression of symptoms
    • Hypertrophic osteoarthropathy
    • Ankylosing spondylitis (in 3–16%)
      • Axial skeletal involvement usually precedes onset of GI symptoms!
      • • unrelated in severity/course to activity level of bowel disease
      • symmetric bilateral sacroiliitis
      • spondylitis with syndesmophytes
    • Peripheral erosive arthritis
      • small marginal erosions
      • periostitis
      • propensity for osseous ankylosis
    • Avascular necrosis of femoral head (steroid Rx)
    • Pelvic osteomyelitis (contiguous involvement)
    • Septic arthritis
    • Muscle abscess
    • Retarded skeletal growth + maturation
  • @ Erythema nodosum, uveitis
Cronkhite-Canada Syndrome
  • = nonneoplastic nonhereditary polyps (as in juvenile polyposis) associated with ectodermal abnormalities; no familial predisposition
Incidence: >100 cases described
Histo: hamartomatous polyps resembling juvenile/retention polyps = multiple cystic spaces filled with mucin secondary to degenerative changes; expansion + inflammation of lamina propria
Age: 62 years (range 42–75 years); M < F
  • • exudative protein-losing enteropathy
  • • diarrhea (disaccharidase deficiency, bacterial overgrowth in small intestine)
  • • severe weight loss, anorexia
  • • abdominal pain
  • • nail atrophy
  • • brownish macules of hand + feet
  • • alopecia
  • multiple polyps
  • thickened gastric rugae
Location: stomach (100%); small bowel (>50%); colon (100%)
Prognosis: rapidly fatal in women within 6–18 months (cachexia); tendency toward remission in men
Desmoplastic Small Round Cell Tumor
  • = INTRAABDOMINAL DESMOPLASTIC SMALL ROUND CELL TUMOR OF PERITONEUM
  • = highly malignant tumor belonging to a generic group of small round blue cell tumors (Ewing sarcoma, neuroblastoma, Wilms tumor, rhabdomyosarcoma, primitive neuroendocrine tumor)
Incidence: <50 cases in literature
Median age: 21 years; affects children + young adults; up to 6th decade; M:F = 4:1
Origin: mesothelial/submesothelial/subserosal mesenchyme of the abdominal cavity
Histo: islands of small blue cells surrounded by fibrous stroma; immunohistochemically positive for epithelial, neural, muscular markers (cytoplasmic keratin + desmin); abnormal chromosome 11
  • gastrointestinal/genitourinary discomfort/pain
  • abdominal distension
  • palpable abdominal mass
Location: mesentery (spread to omentum), retroperitoneum, paratesticular, posterior mediastinum, pleura, meninges
  • multiple scattered necrotic tumor masses in abdomen + pelvis with no definite visceral organ of origin:
    • nodular peritoneal thickening
    • serosal hepatic metastases
    • punctate peritoneal calcifications
  • enlarged lymph nodes
  • scant ascites
Cx: hydronephrosis, bowel obstruction
Prognosis: mean survival time of 17 months
DDx:
  • in infants/adolescents: rhabdomyosarcoma; neuroblastoma; mesenteric carcinoid; Burkitt lymphoma
  • in adults: diffuse omental/peritoneal carcinomatosis (carcinoma of stomach, colon, ovary, pancreas); melanoma; leiomyosarcoma; lymphoma; desmoid tumor; mesothelioma; tumefactive tuberculosis; actinomycosis; Castleman disease
Diaphragm Disease
  • = small bowel webs due to NSAIDs
Effect of NSAID: gastric irritation, ulceration of small intestines
Frequency: in 10% of patients receiving long-term NSAID therapy
Path: foci of submucosal fibrosis with interruption of adjacent muscularis mucosae
  • blood + protein loss
  • intermittent intestinal obstruction
Location: ileum > jejunum
P.821

Enteroclysis:
  • multiple concentric diaphragm-like strictures
DDx: Crohn disease
Disaccharidase Deficiency
  • = enzyme deficiencies for any of the disaccharides (maltose, lactose, etc.)
  • PRIMARY
  • SECONDARY to other diseases (eg, Crohn disease)
Pathophysiology:
  • unabsorbed disaccharides produce osmotic diarrhea
  • bacterial fermentation produces short-chain volatile fatty acids causing further osmotic + irritant diarrhea
  • normal small bowel series without added lactose
  • abnormal small bowel series done with lactose (50 g added to 600 cm3 of barium suspension)
  • small + large bowel distension
  • dilution of barium
  • shortening of transit time
Distal Intestinal Obstruction Syndrome
  • = MECONIUM ILEUS EQUIVALENT
  • = impaction of inspissated stool in distal part of ileum + proximal part of colon
Prevalence: 7–15–41% of children/adolescents with cystic fibrosis; 2% in patients <5 years of age
Cause: tenacious intestinal mucus, steatorrhea due to pancreatic insufficiency, undigested food residue, disordered intestinal motility with increase in intestinal transit time, fecal stasis, dehydration
Age: 2nd–3rd decade of life
  • • recurrent bouts of colicky abdominal pain (from fecal impaction/constipation) in RLQ
  • • palpable cecal mass
  • bubbly granular ileocecal soft-tissue mass in RLQ
  • partial/complete small bowel obstruction (due to puttylike fecal material in terminal ileum/right colon)
  • thickening of mucosal folds
  • cystic fibrosis of lung
image
Cross Section Through Colon
CT:
Location: cecum > ascending colon > transverse colon > descending colon (contiguous involvement)
  • diffuse colonic thickening
  • mural striation (50%)
  • mesenteric soft-tissue infiltration (100%)
  • increased pericolonic fat (60%)
Cx: intussusception, volvulus
Rx: stool softeners, oral polyethylene glycol-electrolyte solution (Golytely®), increasing dose of pancreatic enzyme supplements, mucolytic agents (N-acetylcysteine) orally/with Gastrografin® enema
DDx: appendicitis, partial intestinal obstruction (adhesion/stricture from previous bowel surgery)
Diverticular Disease of Colon
  • = overactivity of smooth muscle causing herniation of mucosa + submucosa through muscle layers
Incidence: 5–10% in 5th decade; 33–48% over age 50; 50–65% past 7th decade; M:F = 1:1; most common affliction of colon in developed countries
Cause: decreased fecal bulk (diet high in refined fiber + low in roughage)
Location: in 80% in sigmoid (= narrowest colonic segment with highest pressure); in 17% distributed over entire colon; in 4–12% isolated to cecum/ascending colon
Prediverticular Disease of Colon
  • = longitudinal + circular smooth muscle thickening with redundancy of folds secondary to myostatic contracture
  • “saw-tooth sign” = crowding + thickening of haustral folds (shortening of colonic segment)
  • plump marginal indentations
  • superimposed muscle spasm (relieved by antispasmodics)
DDx: hemorrhage; ischemia; radiation changes; pseudomembranous colitis
Colonic Diverticulosis
  • = acquired herniations of mucosa + muscularis mucosae through the muscularis propria with wall components of mucosa, submucosa, serosa = false diverticula of pulsion type
Location: predominantly left-sided colon
Site:
  • lateral diverticula arise between mesenteric + antimesenteric teniae on opposite sides
  • antimesenteric intertaenial diverticula opposite of mesenteric side
  • Intramural type vasa recta (= nutrient arteries) pass through the circular muscle (weakness in muscular wall) and are carried over the fundus of the diverticula as it enlarges
  • size: initially tiny (3–10-mm) V-shaped protrusions increasing up to several cm in diameter
  • bubbly appearance of air-containing diverticula
  • residual barium within diverticula from previous study
  • P.822

  • spiky irregular outline (antimesenteric intertaenial ridge is typical site for intramural diverticula)
  • smooth dome-shaped appendages with a short neck
  • may be pointed, attenuated, irregular with variable filling
  • circular line with sharp outer edge + fuzzy blurred inner edge (en face view in double contrast BE)
  • Giant sigmoid diverticulum = large gas-containing cyst (air entrapment secondary to ball-valve mechanism) arising in left iliac fossa
CT:
  • rounded outpouchings containing air ± contrast material (= diverticula)
  • circumferential sawtooth-like thickening of colonic haustra + distorted luminal contour (= muscular hypertrophy)
Cx: bleeding (usually right colon), diverticulitis (usually sigmoid colon)
Colonic Diverticulitis
  • = perforation of diverticulum with intramural/localized pericolic inflammatory mass
Incidence: 5% of population; in 10–35% of diverticular disease; increasing frequency with age (in 5–10% >45 years of age, in 80% >85 years of age)
Pathogenesis: mucosal abrasion from inspissated fecal material leads to perforation of thin wall
  • pain + local tenderness + mass in LLQ
  • fever (25%), leukocytosis (36%)
  • clinical misdiagnosis rate of 34–67%
Location: sigmoid colon (95%), cecum (4%)
  • localized ileus
  • ± pattern of small bowel obstruction (kinking/edema if small bowel adheres to abscess)
  • extraluminal gas in abscess/fistula
  • pneumoperitoneum (rare)
BE (77–86% sensitive):
  • focal area of eccentric luminal narrowing caused by pericolic/intramural inflammatory mass:
    • annular lesion mimicking carcinoma
  • marked thickening + distortion of mucosal folds
  • tethered spiculated mucosal folds
  • centrally amputated diverticulum
  • extraluminal contrast = peridiverticulitis:
    • “double-tracking” = pericolonic longitudinal sinus tract
    • pericolonic collection = peridiverticular abscess
    • fistula to bladder/small bowel/vagina
CT (79–93% sensitive, 77% specific):
  • inflamed diverticulum:
    • pericolic fat stranding = poorly marginated hazy area of increased attenuation ± fine linear strands within pericolic fat (98%)
    • diverticula (84%) = flask-shaped structures projecting through colonic wall + filled with air/barium/fecal material
    • “centipede” sign = hyperemic engorged vasa recta
  • bowel wall thickening:
    • circumferential bowel wall thickening of >4 mm (70%)
    • focally thickened + inflamed colonic wall
    • “arrowhead sign” = funnel of intraluminal contrast medium/air in focally thickened colonic wall centering about occluded orifice of inflamed diverticulum (27%)
  • fluid collection:
    • frank abscess (47%) = central liquid/gas
    • fluid ± air of peritonitis (16%)
    • fluid at root of sigmoid mesentery
  • tract formation:
    • fistula formation (14%): most commonly colovesical, also colovaginal, coloenteric, colocutaneous
    • intramural sinus tracts (9%)
  • fecolith
  • colonic obstruction (12%)
  • ureteral obstruction (7%)
US (85–98% sensitive, 80–97% specific):
  • thickening of bowel wall = >4 mm distance between echogenic lumen interface and serosa
  • diverticula = round/oval hypo-/hyperechoic foci protruding from colonic wall with focal disruption of normal layer continuity ± internal acoustic shadowing
  • inflammatory pericolic fat = regionally increased echogenicity adjacent to colonic wall ± ill-defined hypoechoic zones
  • pericolic abscess
Prognosis: (a) self-limiting (usually)
(b) transmural perforation
(c) superficial ulceration
(d) chronic abscess
Cx: (1) Colonic obstruction
(2) Fistula to bladder/vagina/small bowel
(3) Free perforation (rare)
DDx: (1) Colonic neoplasm (shorter segment, heaped-up margins, ulcerated mucosa)
(2) Crohn colitis (double-tracking longer than 10 cm)
Rx: antibiotics, surgery (in 25%), percutaneous abscess drainage
Right Colonic Diverticulitis
  • = congenital true diverticulum
Frequency: 1:34–1:300 appendectomies
Age: any; peak prevalence at 35–45 years of age
  • • protracted mild pain; palpable mass in 33%
  • solitary diverticulum containing a 12-mm fecolith surrounded by inflamed fat
  • marked circumferential colonic wall thickening
Cx: pericolonic abscess
Prognosis: spontaneous evacuation into colonic lumen
Rx: conservative
DDx: appendicitis
Colonic Diverticular Hemorrhage
  • Not related to diverticulitis
Incidence: in 3–47% of diverticulosis
Location: 75% located in ascending colon (larger neck + dome of diverticula)
  • • massive rectal hemorrhage without pain
  • extravasation of radionuclide tracers
  • angiographic contrast pooling in bowel lumen
Rx: (1) transcatheter infusion of vasoconstrictive agents (Pitressin®)
(2) embolization with Gelfoam®
P.823

Dumping Syndrome
  • = early postprandial vascular symptomatology of sweating, flushing, palpitation, feeling of weakness and dizziness
Pathophysiology: rapid entering of hypertonic solution into jejunum resulting in fluid shift from blood compartment into small bowel
Incidence: 1–5%; M:F = 2:1
  • Roentgenologic findings not diagnostic!
  • rapid emptying of barium into small bowel (= loss of gastric reservoir function)
Rx: lying down, diet
DDx: late postprandial hypoglycemia (90–120 minutes after eating)
Duodenal Atresia
  • = most common cause of congenital duodenal obstruction; second most common site of gastrointestinal atresias after ileum
Incidence: 1:10,000; M:F = 1:1
Etiology: defective vacuolization of duodenum between 6th and 11th weeks of fetal life; rarely from vascular insult (extent of obstruction usually involves larger regions with vascular insult)
Age at presentation: first few days of life
  • • persistent bilious vomiting a few hours after birth/following 1st feeding (75%)
  • • rapid deterioration secondary to loss of fluids + electrolytes
  • Isolated sporadic anomaly (30–52%)
Associated anomalies (in 50–60%):
  • Down syndrome (20–33%);
    • 25% of fetuses with duodenal atresia have Down syndrome!
    • <5% of fetuses with Down syndrome have duodenal atresia!
  • CHD (8–30–50%): endocardial cushion defect, VSD
  • Gastrointestinal anomalies (26%):
    • esophageal atresia, biliary atresia, duodenal duplication, imperforate anus, small bowel atresia, malrotation, Ladd bands, Meckel diverticulum, transposed liver, annular pancreas (20%), preduodenal portal vein
  • Urinary tract anomalies (8%)
  • Vertebral + rib anomalies (37%)
Location: (a) usually distal to ampulla of Vater (80%)
(b) proximal duodenum (20%)
  • “double bubble sign” = gas-fluid levels in duodenal bulb + gastric fundus
  • total absence of intestinal gas in small/large bowel
  • colon of normal caliber
OB-US (usually not identified prior to 24 weeks GA):
  • • ± elevated AFP
  • “double bubble sign” = simultaneous distension of stomach + 1st portion of duodenum, continuity of fluid between stomach + duodenum must be demonstrated
  • increased gastric peristalsis
  • polyhydramnios in 3rd trimester (100%)
Prognosis: 36% mortality in neonates
DDx: (1) Prominent incisura angularis causing bidissection of stomach
(2) Choledochal cyst
(3) Annular pancreas
(4) Peritoneal bands
(5) Intestinal duplication
Cx: prematurity (40%) secondary to preterm labor related to polyhydramnios
image
Duodenal Diverticula
Duodenal Diverticulum
Incidence: 1–5% of GI studies; 22% of autopsies
  • PRIMARY DIVERTICULUM
    • = mucosal prolapse through muscularis propria
    • posteriorly (8%), lateral wall (4%)
  • SECONDARY DIVERTICULUM
    • = all layers of duodenal wall = true diverticulum as complication of duodenal/periduodenal inflammation
Location: almost invariably in 1st portion of duodenum
  • mostly asymptomatic
Cx: (1) Perforation + peritonitis
(2) Bowel obstruction
(3) Biliary obstruction
(4) Bleeding
(5) Diverticulitis
Duodenal Ulcer
Incidence: 200,000 cases/year; 2–3 × more frequent than gastric ulcers; M:F = 3:1
Pathophysiology: too much acid in duodenum from
(a) abnormally high gastric secretion
(b) inadequate neutralization
Predisposed: cortisone therapy, severe cerebral injury, after surgery, chronic obstructive pulmonary disease
Location:
  • bulbar (95%):
    • anterior wall (50%), posterior wall (23%), inferior wall (22%), superior wall (5%)
    • bulbar deformity in 85%
  • postbulbar (3–5%):
    • M:F = 7:1; majority on medial wall above papilla
    • • hemorrhage in 66%
    • edema + spasm may obscure ulcer
    • smooth rounded indentation of lateral wall
  • frequently <1 cm round/ovoid (5% linear) ulcer niche
  • “kissing ulcers” = ulcers opposite from each other on anterior + posterior wall
  • P.824

  • giant duodenal ulcer >2 cm (rare) with higher morbidity + mortality; may be overlooked by simulating a normal/deformed scarred duodenal bulb
  • “cloverleaf deformity, hourglass stenosis” (healed stage) with prestenotic dilatation of recesses
Cx: (1) Obstruction (5%)
(2) Perforation (<10%): anterior > posterior wall; fistula to gallbladder
(3) Penetration (<5%) = sealed perforation
(4) Hemorrhage (15%): melena > hematemesis
Rx: antral resection (Billroth I) + vagotomy
Duodenal Varices
  • = dilated collateral veins secondary to portal hypertension (posterior superior pancreaticoduodenal vein)
  • lobulated filling defects (best demonstrated in prone position, maximal luminal distension will obliterate them)
  • commonly associated with fundal + esophageal varices
Duplication Cyst
  • = uncommon congenital anomaly found anywhere along alimentary tract from tongue to anus
Incidence: 15% of pediatric abdominal masses are gastrointestinal duplication cysts
Theories of formation:
  • Abortive twinning
  • Persistent embryologic diverticula
  • Split notochord
  • Aberrant luminal recanalization (Bremer): foregut epithelium grows and obliterates lumen (solid stage for esophagus, small bowel, colon); later produces secretions that form vacuoles in the intercellular space; vacuoles line up longitudinally and coalesce to form new lumen; failure of an aberrant vacuole to coalesce creates a wall cyst
  • Intrauterine vascular accident (Favara) associated with alimentary tract atresia in 9%
Age: presentation often in infancy/early childhood
Path: spherical cyst/tubular structure located in/immediately adjacent to gastrointestinal tract; shares a common muscle wall + blood supply; has a separate mucosal lining; cyst contents are usually serous
Histo: smooth muscle wall + lined with alimentary tract mucosa; ectopic mucosa; squamous, transitional, ciliated mucosa; lymphoid aggregates; ganglion cells
♢Gastric mucosa + pancreatic tissue are the only ectopic tissues of clinical importance!
  • respiratory distress (with esophageal duplication)
  • palpable abdominal mass
  • nausea, emesis (due to partial/complete obstruction)
Location: ileum (30–33%), esophagus (17–20%), colon (13–30%), jejunum (10–13%), stomach (7%), pylorus (4%), duodenum (4–5%), ileocecal junction (4%), rectum (4%)
♢In 7–15% concomitant duplications elsewhere in the alimentary tract!
Site: on mesenteric aspect of alimentary canal
Morphology:
  • large spherical/saccular cyst (82%)
  • small intramural cyst
  • tubular sausage-shaped cyst (18%): commonly along small + large bowel; frequently communicates with lumen of adjacent gut
BE:
  • mass extrinsic to bowel lumen
US:
  • elongated tubular/spherical cystic mass:
    • sonolucent mass with good through transmission (due to clear fluid content)
    • echogenic mass (due to hemorrhage + inspissated material)
  • muscular rim sign (= echogenic inner mucosal lining + hypoechoic outer rim) in 47%
  • cyst paralleling normal bowel lumen
CT:
  • smoothly rounded fluid-filled cyst/tubular structure
  • thin slightly enhancing wall
MR:
  • heterogeneous signal intensity of intracystic fluid on T1WI + homogeneous high signal intensity on T2WI
Cx: bowel obstruction, intussusception (due to cyst at ileocecal junction), small bowel volvulus (due to weight of duplication), bleeding (due to presence of gastric mucosa/pressure necrosis of adjacent mucosa by cyst expansion/from intussusception)
DDx:
  • Omental cyst (greater omentum/lesser sac, multilocular)
  • Mesenteric cyst (between leaves of small bowel mesentery)
  • Choledochal cyst
  • Ovarian cyst
  • Pancreatic pseudocyst
  • Cystic renal tumor
  • Abscess
  • Meckel diverticulum (communicates with GI tract)
  • Lymphangioma
  • Mesenteric lymphoma
  • Intramural tumor
Colonic Duplication Cyst
Incidence: 13% of all alimentary tract duplications
Cystic Colonic Duplication (7%)
Path: closed spherical cyst; contains gastric mucosa in 2% + ectopic pancreatic tissue in 5%
  • abdominal mass, bowel obstruction/constipation
  • GI hemorrhage
Location: cecum (40%) ± intussusception
  • air/intestinal matter can enter cyst (20%)
Colorectal Tubular Duplication (6%)
  • = DUPLICATION OF THE HINDGUT
  • = double-barreled duplication involving part/all of large bowel with “twin” segment on mesenteric/antimesenteric side
Symptomatic age: neonatal period/infancy; M:F = 1:2
May be associated with:
  • rectogenital/rectourinary fistula, duplication of internal/external genitalia, vertebral anomalies, multisystem congenital anomaly complex
  • • bowel obstruction/constipation
  • P.825

  • • passage of feces through vagina
  • simultaneous opacification of true + twin colon
  • duplication may terminate at
    • 2nd functional anus
    • imperforate perineal orifice
    • fistulous communication with GU tract
Double Appendix
Duodenal Duplication Cyst
Incidence: 5% of all alimentary tract duplications
Path: noncommunicating spherical cyst; may contain ectopic gastric mucosa in 21%, small bowel mucosa, pancreatic tissue
  • obstructive symptoms, palpable abdominal mass
  • hemorrhage (due to peptic ulceration)
  • jaundice (due to biliary obstruction)
  • pancreatitis (due to ectopic pancreatic tissue)
Site: on mesenteric side of anterior wall of 1st + 2nd portion of duodenum
  • mass in concavity of duodenal C-loop
  • compression + displacement of 1st/2nd portion of duodenum superiorly + anteriorly
Cholangiography:
  • may communicate with pancreatic ductal system through the aberrant duct of an accessory lobe
Cx: pancreatitis from perforation of duplication cyst
DDx: pancreatic cyst, pancreatic pseudocyst, choledochal cyst, choledochocele, duodenal intramural tumor, pancreatic tumor
Esophageal Duplication Cyst
  • arises from foregut
Incidence: 10–20% of all alimentary tract duplications; 0.5–2.5% of all esophageal masses; M:F = 2:1
Path: contains ectopic gastric mucosa in 43%
Histo: contains no cartilage, lined by alimentary tract mucosa
Associated with: vertebral anomalies (spina bifida, hemivertebra, fusion defects), esophageal atresia, small bowel duplication (18%)
Location: adjacent to esophagus/within esophageal musculature at any level, paraspinal position; R:L = 2:1; in right pleural space detached from esophagus (rare)
  • CERVICAL ESOPHAGUS (23%)
    • asymptomatic enlarging lateral neck mass
    • upper airway obstruction in newborn
    DDx: thyroglossal duct cyst, branchial cleft cyst, cystic hygroma, cervical tumor, cervical lymphadenopathy
  • MIDESOPHAGUS (17%)
    • severe upper airway obstruction in early infancy
    DDx: bronchogenic cyst, neurenteric cyst, intramural esophageal tumor
  • DISTAL ESOPHAGUS (60%)
    • frequently asymptomatic
    Location: paraspinal
    DDx: bronchogenic cyst, neurenteric cyst, intramural esophageal tumor
    • thick-walled closed spherical cyst, almost never communicating
CXR:
  • posterior mediastinal mass ± air-fluid level
  • lobar consolidation + central cavitation (from autodigestion of lung tissue by gastric secretions)
  • thoracic vertebral anomalies
UGI:
  • displacement of esophagus by paraesophageal mass
  • intramural extramucosal mass
US:
  • hypoechoic fluid-filled cyst + inner mucosal lining
CT:
  • sharply marginated homogeneous near-water density mass without enhancement
Cx: (1) Peptic ulceration (secondary to gastric mucosa)
(2) Perforation (secondary to penetrating ulcer)
(3) Hematemesis (from erosion into esophagus)
(4) Hemoptysis + autodigestion of pulmonary tissue (from erosion into tracheobronchial tree)
Gastric Duplication Cyst
  • = intramural gastric cyst lined with secretory epithelium
Incidence: 7% of all alimentary tract duplications
Path: noncommunicating spherical cyst (majority); may communicate with aberrant pancreatic duct; ectopic pancreatic tissue found in 37%
Symptomatic age: infancy; in 75% detected before age 12; M:F = 1:2
  • pain (from overdistension of cyst, rupture with peritonitis, peptic ulcer formation, internal pancreatitis)
  • vomiting, anemia, fever
  • symptoms mimicking congenital hypertrophic pyloric stenosis (if duplication in antrum/pylorus)
Most common site: greater curvature (65%)
  • paragastric cystic mass up to 12 cm in size, indenting greater curvature
  • seldom communicates with main gastric lumen at one or both ends
  • may enlarge + ulcerate
  • Tc-99m uptake
US:
  • cyst with two wall layers: inner echogenic layer of mucosa + outer hypoechoic layer of muscle
  • clear/debris-containing fluid
Cx: (1) Partial/complete small bowel obstruction
(2) Relapsing pancreatitis (with ductal communication)
(3) Ulceration, perforation, fistula formation
DDx: pancreatic cyst, pancreatic pseudocyst, mesenteric cyst, leiomyoma, adenomatous polyp, hamartoma, lipoma, neurofibroma, teratoma
Rectal Duplication Cyst
Incidence: 4% of all alimentary tract duplications
Path: spherical fluid-filled cyst; may contain duodenal/gastric mucosa + pancreatic tissue
Site: posterior to rectum/anus
  • communication with rectum/perianal fistula (in 20%)
Symptomatic age: childhood
P.826

  • • constipation + fecal soiling
  • • palpable retrorectal/retroanal mass
  • • intractable excoriation of perianal skin (with chronic perianal fistula)
  • cystic mass; may be echogenic (due to solid material ± gas from communication with rectum)
DDx: anterior meningocele, sacrococcygeal teratoma, retrorectal abscess, pilonidal cyst, sacral bone tumor
Small Bowel Duplication Cyst
Incidence: most common of all alimentary tract duplications
Symptomatic age: neonatal period (1/3); <2 years of age (in 72%)
Path: contains ectopic gastric mucosa in 24%; ectopic pancreatic tissue in jejunum (8%)
May be associated with: small bowel atresia
  • neonatal bowel obstruction
  • intussusception, palpable mass
  • acute abdominal pain
  • GI hemorrhage (may be painless)
Location: ileum (33%), jejunum (10%), ileocecal (4%)
Site: on mesenteric side
  • low small bowel obstruction ± soft-tissue mass
  • cyst may serve as lead point for intussusception
DDx: mesenteric cyst, pancreatic pseudocyst, omental cyst, exophytic hepatic cyst, ovarian cyst
Thoracoabdominal Duplication
  • = FOREGUT DUPLICATION
  • = long tubular cyst closed at its cranial end, passing through diaphragm through its own hiatus, in 60% communicating with normal duodenum/jejunum/ileum
Incidence: 2% of all alimentary tract duplications
Associated with: thoracic vertebral anomalies
Histo: gastric mucosa in 29%
Symptomatic age: 50% during neonatal period; 80% within 1st year of life
  • • severe respiratory distress
  • • chest pain, GI bleeding, anemia
  • tubular right posterior mediastinal mass ± air
  • thoracic vertebral anomaly
  • contrast material may enter through distal connection
Ectopic Pancreas
  • = PANCREATIC REST = MYOEPITHELIAL HAMARTOMA
Incidence: 2–10% of autopsies; M:F = 2:1
  • asymptomatic
Location: lesions may be multiple
(a) greater curvature of antrum 1–6 cm from pylorus, pylorus, duodenal bulb, proximal jejunum (in 80%)
(b) ileum, Meckel diverticulum
  • smooth cone-/nipple-shaped submucosal nodule 1–5 cm in size
  • central umbilication representing orifice of filiform duct
Enteric Cyst
  • = cyst lined by gastrointestinal mucosa without bowel wall
Etiology: migration of small bowel/colonic diverticulum into mesentery/mesocolon
Path: unilocular thin smooth-walled cyst with serous contents lined by enteric epithelium + thin fibrous wall
US:
  • hypoechoic cystic mass, occasionally with septations
DDx: duplication cyst (reduplication of bowel wall)
Eosinophilic Gastroenteritis
  • = uncommon self-limited form of gastroenteritis with remissions + exacerbations characterized by infiltration of eosinophilic leukocytes into stomach/small bowel wall + usually marked peripheral eosinophilia
Cause: unknown
Histo: fibrous tissue + eosinophilic infiltrate of gastrointestinal mucosa
Age: in children + young adults with allergy + eosinophilia
  • EOSINOPHILIC GRANULOMA
    • = FIBROUS POLYPOID LESION
    • = INFLAMMATORY PSEUDOTUMOR
    • = localized form/circumscribed type
      Location: almost exclusively in stomach (most common in antrum + pylorus)
    • submucosal polypoid mass/pedunculated polyp
  • EOSINOPHILIC GASTROENTERITIS
    • = diffuse type
    • = eosinophilic infiltration of mucosa, submucosa, and muscular layers of small intestine ± stomach by mature eosinophils (¿ gastric pendant to Löffler syndrome)
  • recurrent episodes of abdominal pain, diarrhea, vomiting
  • weight loss
  • hematemesis (from ulceration)
  • peripheral eosinophilia, anemia
  • history of systemic allergy/food allergy
Location: entire small bowel (particularly jejunum), distal stomach, omentum, mesentery
Site: (a) mucosal
(b) muscular
(c) serosal (rare)
  • @ Stomach (almost always limited to antrum)
    • “wet stomach”
    • ulcers are rare
    • mucosal type
      • enlarged gastric rugae/cobblestone nodules/polyps
    • muscular type
      • thickened + rigid wall with narrowed gastric antrum/pylorus
      • bulky intraluminal mass up to 9 cm in size
      Cx: pyloric obstruction
      DDx: hypertrophic gastritis, lymphoma, carcinoma
  • @ Small bowel (involved in 50%)
    • separation of small bowel loops
    • mucosal type
      • • malabsorption + hypoproteinemia
      • thickening + distortion of folds predominantly in jejunum
    • submucosal/muscular type
      • motility disturbance
      • small-bowel obstruction
      • effacement of mucosal pattern + narrowing of lumen
    • serosal type
      • ascites
P.827

Prognosis: tendency toward spontaneous remission
Rx: steroids/removal of sensitizing agent
Epiploic Appendagitis
  • = rare inflammation of one of the 100 epiploic/omental appendages, between 5 and 50 mm long, arising from serosal surface of colon
Cause: (a) primary: torsion (exercise), venous thrombosis
(b) secondary: inflammation of adjacent organ (eg, diverticulitis, appendicitis)
Associated with: obesity, hernia, unaccustomed exercise
Age: 4th–5th decade; M>F
Histo: acute infarction with fat necrosis, inflammation, thrombosed vessels with hemorrhagic suffusion
  • • abrupt onset of localized abdominal pain (RLQ in 50%), gradually resolving over 3–7 days
  • • palpable mass (10–30%)
  • • ± peritoneal signs
  • • normal/mildly increased WBCs; NO fever
  • Almost never suspected preoperatively!
Location: anterolaterally/(occasionally) anteromedially to sigmoid > descending > ascending colon
US:
  • solid hyperechoic noncompressible oval mass at site of maximal tenderness
  • hypoechoic margin (93%)
  • absence of central blood flow
CT:
  • pericolic oval-shaped pedunculated mass, 1–5 cm in diameter, with fat attenuation (approx.–60 HU):
    • hyperattenuating peripheral rim
    • internal fat stranding
  • periappendigeal fat infiltration
  • thickening of adjacent visceral peritoneal lining (93%)
MR:
  • foal lesion with signal intensity of fat
  • enhancing rim
Cx: adhesion, bowel obstruction, intussusception, intraperitoneal loose body, peritonitis, abscess
Prognosis: spontaneous resolution within 2 weeks clinically + within 6 months on CT
Rx: conservative management with NSAID
DDx: torsion/infarction of greater omentum, sclerosing mesenteritis, diverticulitis, appendicitis, primary tumor of mesocolon
Esophageal Cancer
Incidence: <1% of all cancers; 4–10% of all GI malignancies; 11,000 cases/year (USA in 1994); M:F = 4:1; Blacks:Whites = 2:1
High-risk regions: Iran, parts of Africa, Italy, China
Predisposing factors:
  • achalasia (risk factor of 1,000 x), asbestosis, Barrett esophagus, celiac disease, radiation exposure, caustic stricture (risk factor of 1,000 x), Plummer-Vinson syndrome, tannins, alcohol, tobacco, history of oral/pharyngeal cancer, tylosis palmaris et plantaris
mnemonic: BELCH SPAT
  • Barrett esophagus
  • EtOH abuse
  • Lye stricture
  • Celiac disease
  • Head and neck tumor
  • Smoking
  • Plummer-Vinson syndrome
  • Achalasia, Asbestosis
  • Tylosis
Cancer Staging:
  • TNM system:
    T1 tumor invades lamina propria/submucosa
    T2 tumor invades muscularis propria
    T3 tumor invades adventitia
    T4 tumor invades adjacent structures
    Stage I = T1,N0,M0
    Stage IIA = T2/3,N0,M0
    Stage IIB = T1/2,N1,M0
    Stage III = T3,N1,M0
    or T4,N0/1,M0
    Stage IV = T1-4,N0/1,M1
  • CT staging (Moss):
    Stage 1 intraluminal tumor/localized wall thickening of 3–5 mm
    Stage 2 localized/circumferential wall thickening >5 mm
    Stage 3 contiguous spread into adjacent mediastinum (trachea, bronchi, aorta, pericardium)
    √ loss of fat planes (nonspecific due to cachexia, often still resectable)
    √ mass in contact with aorta >90° arc (in 20–70% still resectable)
    √ displacement/compression of airway (90–100% accuracy for invasion)
    √ esophagotracheal/-bronchial fistula (unresectable)
    Stage 4 distant metastases
    √ enlarged abdominal lymph nodes >10 mm (12–85% accuracy)
    √ hepatic, pulmonary, adrenal metastases√ direct erosion of vertebral body
    √ tumor >3 cm wide = high frequency of extraesophageal spread
Histo:
  • Squamous cell carcinoma (50–70%)
  • Adenocarcinoma (30–50%) arising from mucosal/submucosal glands or heterotopic gastric mucosa or columnar-lined epithelium (Barrett)
    • in 70% from Barrett esophagus
    • gastric adenocarcinoma involving GE junction
    • in submucosal/deep esophageal glands
    • ectopic gastric mucosa in esophagus
    • 2,500 new cases each year; M:F = 7:1
    • tendency to invade gastric cardia + fundus
  • Spindle-cell squamous carcinoma = carcinosarcoma = pseudosarcoma
    Histo: squamous + sarcomatous elements
    Age: in men >45 years
    Location: usually middle third of esophagus
    • large bulky polypoid smooth, lobulated, scalloped intraluminal mass; may be pedunculated
    DDx: lymphoma, other sarcomas
  • Mucoepidermoid ca., adenoid cystic carcinoma
  • Leiomyosarcoma, rhabdomyosarcoma, fibrosarcoma, malignant lymphoma
  • P.828

  • Secondary tumor involvement from: thyroid, larynx
  • Metastasis from: breast, melanoma, GI tract
  • dysphagia (87–95%) of <6 months’ duration
  • weight loss (71%)
  • retrosternal pain (46%)
  • regurgitation (29%)
Location: upper 1/3 (15–20%); middle 1/3 (37–44%); lower 1/3 (38–43%)
Radiologic types:
  • Polypoid/fungating form (most common)
    • sessile/pedunculated tumor with lobulated surface
    • protruding, irregular, polycyclic, overhanging, steplike “apple core” lesion
  • Ulcerating form
    • large ulcer niche within bulging mass
  • Infiltrating form
    • gradual narrowing with smooth transition
    • (DDx: benign stricture)
  • Varicoid form = superficial spreading carcinoma
    Histo: longitudinal extension confined to mucosa/submucosa
    • focal area of confluent mucosal nodules/plaques
    DDx: Candida esophagitis
Metastases:
  • lymphogenic: anterior jugular chain + supraclavicular nodes (primary in upper 1/3); paraesophageal + subdiaphragmatic nodes (primary in middle 1/3); mediastinal + paracardial + celiac trunk nodes (primary in lower 1/3)
  • hematogenous: lung, liver, adrenal gland
CXR:
  • widened azygoesophageal recess with convexity toward right lung (in 30% of distal + midesophageal cancers)
  • thickening of posterior tracheal stripe + right paratracheal stripe >4 mm (if tumor located in upper third of esophagus)
  • widened mediastinum
  • tracheal deviation
  • posterior tracheal indentation/mass
  • retrocardiac mass
  • esophageal air-fluid level
  • lobulated mass extending into gastric air bubble
  • repeated aspiration pneumonia (with tracheoesophageal fistula)
Cx: fistula formation to trachea (5–10%)/bronchi/mediastinum
Prognosis: 3–5–20% 5-year survival rate; 0% 5-year survival rate for cancer of cervical esophagus
Mean survival time:
  • 90 days with subdiaphragmatic lymphadenopathy
  • 180 days with local invasion + abdominal metastases
  • 480 days without evidence of invasion/metastases
Rx: (1) chemotherapy (fluorouracil, cisplatin, bleomycin sulfate, mitomycin) + surgery
(2) chemotherapy + irradiation (∼4,000 cGy)
(3) chemotherapy + irradiation + surgery
Operative mortality: 3–8%
Esophageal Intramural Pseudodiverticulosis
  • = dilated excretory ducts of deep mucous glands
Etiology: uncertain
Incidence: about 100 cases in world literature
In 90% associated with:
  • diabetes, alcoholism, any severe esophagitis (most often reflux/Candida), esophageal stricture
Site: diffuse/segmental involvement
  • multiple tiny rounded/flask-shaped barium collections in longitudinal rows parallel to long axis of esophagus:
    • appear to “float” outside esophagus without apparent communication with lumen
  • esophageal stricture:
    • short stricture in distal esophagus (common)
    • long stricture in cervical/upper thoracic esophagus (classic)
Esophageal Perforation
  • = ESOPHAGEAL RUPTURE
Cause:
  • Iatrogenic injury (most common cause, 55%): complication of endoscopy, dilatation of stricture, bougie, disruption of suture line following surgical anastomosis, attempted intubation
  • Spontaneous rupture = Boerhaave syndrome (15%): emetogenic injury of the esophagus from sudden increase in intraabdominal pressure + relaxation of distal esophageal sphincter in the presence of a moderate to large amount of gastric contents
  • Closed chest trauma (10%)
    Incidence: 1% of all blunt chest trauma
    • Location:
      • cervical/upper thoracic esophagus (82%)
      • just above gastroesophageal junction along posterolateral wall on the left side
  • Esophageal carcinoma
  • Retained foreign body (14%): coin, aluminum pop-tops, metallic button, safety pin, invisible plastic toy) leading to perforation (in pediatric age group)
  • Barrett ulcer
  • pain, dysphagia, odynophagia
  • rapid onset of overwhelming sepsis: fever, tachycardia, hypotension, shock
Plain film (normal in 9–12%):
  • extensive pneumomediastinum
  • V sign of Naclerio = extrapleural air within lower mediastinum between parietal pleura + diaphragm (usually on left)
  • subcutaneous emphysema of the neck
  • delayed widening of the mediastinum (secondary to mediastinitis)
  • hydrothorax (after rupture into pleural cavity), usually unilateral on left side
  • hydropneumothorax (often not initially seen)
  • left lower lobe atelectasis
  • confirmation with contrast study (90% of contrast esophagograms are positive)
CT:
  • focal extraluminal air collection at site of tear (92%; most useful sign)
  • periesophageal/mediastinal hematoma/fluid (92%)
  • pleural effusion (75%)
  • P.829

  • esophageal wall thickening
  • extravasation of oral contrast material
Esophagography with:
  • water-soluble contrast material (10% false-negative results)
  • barium (if result with water-soluble material negative)
Cx: (1) Acute mediastinitis
(2) Obstruction of SVC
(3) Mediastinal abscess
Prognosis: 20–60% mortality
Upper/Midesophageal Perforation
Location: at level of cricopharyngeus muscle (most frequent)
  • widening of upper mediastinum
  • right-sided hydrothorax
Distal Esophageal Perforation
Incidence: more common (but not in blunt chest trauma)
Cause: biopsy, dilatation of stricture, Boerhaave syndrome
  • left-sided hydrothorax
  • little mediastinal changes
Esophageal Varices
  • = plexuses formed by dilated subepithelial veins + submucosal veins + dilated venae commitantes of the vagus nerves outside the tunica muscularis
Anatomy:
  • anterior branch connected to left gastric vein
  • posterior branch connected to azygos + hemiazygos system
Examination Technique:
  • small amount of barium (not to obscure varices)
  • relaxation of esophagus (not to compress varices): refrain from swallowing because succeeding swallow initiates a primary peristaltic wave that lasts for 10–30 seconds; sustained Valsalva maneuver precludes from swallowing
  • in LAO projection with patient recumbent/in Trendelenburg position ± Valsalva maneuver/deep inspiration
Plain film:
  • lobulated masses in posterior mediastinum (visible in 5–8% of patients with varices)
  • silhouetting of descending aorta
  • abnormal convex contour of azygoesophageal recess at level of gastroesophageal junction
UGI:
  • thickened sinuous interrupted mucosal folds (earliest sign)
  • tortuous radiolucencies of variable size + location
  • “worm-eaten” smooth lobulated filling defects
  • findings may be accentuated after sclerotherapy
CT:
  • thickened esophageal wall + lobulated outer contour
  • scalloped esophageal luminal masses
  • right-/left-sided soft-tissue masses (= paraesophageal varices)
  • marked enhancement following dynamic CT
Cx: bleeding in 28% within 3 years; exsanguination in 10–15%
DDx: varicoid carcinoma of esophagus
Uphill Esophageal Varices
  • = collateral blood flow from portal vein via azygos vein into SVC (usually lower esophagus drains via left gastric vein into portal vein)
Cause:
  • intrahepatic obstruction from cirrhosis
    • In <5% of patients with portal hypertension
  • splenic vein thrombosis (usually gastric varices)
  • obstruction of hepatic veins
  • IVC obstruction below hepatic veins
  • IVC obstruction above hepatic vein entrance/CHF
  • marked splenomegaly/splenic hemangiomatosis (rare)
  • varices in lower half of esophagus
Downhill Esophageal Varices
  • = collateral blood flow from SVC via azygos vein into IVC/portal venous system (upper esophagus usually drains via azygos vein into SVC)
Cause: obstruction of superior vena cava distal to entry of azygos vein (= superior vena cava syndrome) most commonly due to lung cancer, lymphoma, retrosternal goiter, thymoma, mediastinal fibrosis
  • varices in upper 1/3 of esophagus
Esophageal Web
  • = complete/incomplete circumferential narrowing caused by 1–2-mm thick (vertical length) mucosal membrane projecting into esophageal lumen; covered by squamous epithelium on superior + inferior surfaces
Age: middle-aged females
¿ Association with:
  • Plummer-Vinson syndrome = Paterson-Kelly syndrome (iron deficiency anemia, stomatitis, glossitis, dysphagia, thyroid disorder, spoon-shaped nails)
Cause:
mnemonic: BIEP
  • B-ring (Schatzki ring)
  • Idiopathic (= transverse mucosal fold)
  • Epidermolysis bullosa
  • Plummer-Vinson disease
Path: hyperkeratosis + chronic inflammation of submucosa
  • mostly asymptomatic (unless severely stenosing)
Location: in cervical esophagus near cricopharyngeus (most common) > thoracic esophagus; occasionally multiple
  • visualized during maximal distension (in one-tenth of a second)
  • arises at right angles from anterior esophageal wall
  • thin delicate membrane of uniform thickness of <3 mm
Cx: high risk of upper esophageal + hypopharyngeal carcinoma
Rx: (1) balloon dilatation
(2) bougienage during esophagoscopy
DDx: stricture (circumferential + thicker = 1–2-mm thick [vertical length] area of complete/incomplete circumferential narrowing
P.830

Esophagitis
Acute Esophagitis
Cause:
mnemonic: CRIER
  • Corrosives, Crohn disease
  • Reflux
  • Infection, Intubation
  • Epidermolysis bullosa
  • Radiation therapy
  • thickened >3-mm-wide folds with irregular lobulated contour
  • mucosal nodularity (= multiple ulcerations + intervening edema)
  • erosions
  • vertically oriented ulcers usually 3–10 mm in length
  • inflammatory esophagogastric polyp = proximal gastric fold extending across esophagogastric junction (rare)
  • abnormal motility
Candida Esophagitis
  • = MONILIASIS = CANDIDIASIS
  • Most common cause of infectious esophagitis!
Organism: C. albicans, C. tropicalis; endogenous (majority)/transmitted by another human/animal; often discovered in diseased skin, GI tract, sputum, female genital tract, urine with an indwelling Foley catheter
Predisposed:
  • individuals with depressed immunity: hematologic disease, renal transplant, leukemia, chronic debilitating disease, diabetes mellitus, steroids, chemotherapy, radiotherapy, AIDS
    • Most common type of fungi found with opportunistic infections!
  • delayed esophageal emptying: scleroderma, strictures, achalasia, S/P fundoplication
  • antibiotics
Path: patchy, creamy-white plaques covering a friable erythematous mucosa
Histo: mucosal plaques = necrotic epithelial debris + fungal colonies
  • dysphagia (= difficulty swallowing)
  • severe odynophagia (= painful swallowing from segmental spasm)
  • intense retro-/substernal pain
  • associated with thrush (= oropharyngeal moniliasis) in 20–50–80%
Location: predilection for upper 1/2 of esophagus
  • involvement of long esophageal segments:
    • “cobblestone” appearance = mucosal nodularity in early stage (from growth of colonies on surface)
    • longitudinal plaques = grouping of tiny 1–2-mm nodular filling defects with linear orientation (= heaped-up areas of mucosal plaques)
    • shaggy/fuzzy/serrated contour (from coalescent plaques, pseudomembranes, erosions, ulcerations, intramural hemorrhage) in fulminant candidiasis of AIDS
  • narrowed lumen (from spasm, pseudomembranes, marked edema)
  • “intramural diverticulosis” = multiple tiny indentations + protrusions
  • sluggish/absent primary peristalsis
  • strictures (rare)
  • mycetoma resembling large intraluminal tumor (rare)
Diagnostic sensitivity: endoscopy (97%), double contrast (88%), single contrast (55%)
Cx: (1) Systemic candidiasis (“microabscesses” in liver, spleen, kidney)
(2) Gastric bezoar due to large fungus ball (after long-standing esophageal candidiasis)
Rx: ketoconazole/fluconazole
DDx: glycogen acanthosis, reflux esophagitis, superficial spreading carcinoma, artifacts (undissolved effervescent crystals, air bubbles, retained food particles), herpes esophagitis, acute caustic ingestion, intramural pseudo-diverticulosis, squamous papillomatosis, Barrett esophagus, epidermolysis bullosa, varices
Caustic Esophagitis
  • = CORROSIVE ESOPHAGITIS
Corrosive agents:
  • lye (sodium hydroxide), washing soda (sodium carbonate), household cleaners, iodine, silver nitrate, household bleaches, Clinitest® tablets (tend to be neutralized by gastric acid)
    • Severity of injury dependent on contact time + concentration of corrosive material!
Associated with: injury to pharynx + stomach (7–8%): antral burns more common with acid (buffering effect of gastric acid on alkali)
Location: middle + lower thirds of esophagus
Stage I: acute necrosis from protein coagulation
√ mucosal blurring (edema)
√ diffusely atonic + dilated esophagus√ tertiary contractions/spasm
Stage II: frank ulceration in 3–5 days
√ ulceration + pseudomembranes
Stage III: scarring + stricture from fibroblastic activity
√ long segmental stricture after 10 days when acute edema subsides (7–30%)
Cx: (1) Esophageal/gastric perforation during ulcerative stage
(2) Squamous cell carcinoma in injured segment
Rx: dilatation procedure/esophageal replacement surgery
Chronic Esophagitis
  • luminal narrowing with tapered transition to normal + proximal dilatation
  • circumferential/eccentric stricture
  • sacculations = pseudodiverticula
Drug-induced Esophagitis
  • = contact esophagitis due to oral medications = “pill esophagitis”
Agents: antibiotics (tetracycline, doxycycline), quinidine, potassium chloride, nonsteroidal antiinflammatory agents (aspirin), ascorbic acid, alprenolol chloride, emepronium bromide, alendronate (= inhibitor of osteoclastic activity)
P.831

  • severe odynophagia
  • history of taking medication with little/no water immediately before going to bed
  • rapid clinical improvement after withdrawal of offending agent
Location: midesophagus at site of normal extrinsic impressions by aortic arch/left mainstem bronchus/left atrium
  • localized cluster of tiny ulcers distributed circumferentially (most commonly)
  • superficial solitary/several discrete ulcers
Prognosis: ulcers heal within 7–10 days after cessation of offending medication
DDx: herpes esophagitis (immunosuppressed patient, less localized); reflux esophagitis (heartburn, distal esophagus near esophagogastric junction)
Reflux Esophagitis
  • = esophageal inflammation secondary to reflux of acid-peptic contents of the stomach; reflux occurs if resting pressure of LES <5 mm Hg (may be normal event if followed by rapid clearing)
Prevalence: in 20% of gastroesophageal reflux
Histo: basal cell hyperplasia with wall thickening + thinning of epithelium, mucosal edema + erosions, inflammatory infiltrate
Determinants: (1) Frequency of reflux
(2) Adequacy of clearing mechanism
(3) Volume of refluxed material
(4) Potency of refluxed material
(5) Tissue resistance
Reflux preventing features:
  • Lower esophageal sphincter
  • Phrenoesophageal membrane
  • Length of subdiaphragmatic esophagus
  • Gastroesophageal angle of His (70–110°)
May be associated with: sliding hiatal hernia (in most patients), scleroderma, nasogastric intubation
  • heartburn, epigastric discomfort
  • choking, globus hystericus
  • retrosternal pain
  • thoracic/cervical dysphagia
Site: usually lower 1/3/lower 1/2 with continuous disease extending proximally from GE junction
  • segmental esophageal narrowing (edema/spasm/stricture)
  • poorly defined tiny mucosal elevations (“mucosal granularity”) on thickened/nodular longitudinal folds (mucosal edema + inflammation) in early stages
  • single marginal ulcer/erosion at or adjacent to gastroesophageal junction
  • multiple areas of superficial ulceration in distal esophagus
  • prominent mucosal fold ending in polypoid protuberance within hiatal hernia/cardia
  • interruption of primary peristalsis at inflamed segment
  • nonperistaltic waves in distal esophagus following deglutition (85%)
  • incomplete relaxation of LES (75%), incompetent sphincter (33%)
  • acid test = abnormal motility elicited by acid barium (pH 1.7)
  • “felinization” = transverse ridges of esophagus secondary to contraction of muscularis mucosae (similar to cat esophagus)
NUC (pertechnetate):
  • esophageal activity (Barrett esophagus similar to ectopic gastric mucosa)
Reflux tests:
  • Reflux of barium in RPO position, may be elicited by coughing/deep respiratory movements/swallowing of saliva + water/anteflexion in erect position: only in 50% accurate
  • Water-siphon test: in 5% false negative; large number of false positives
  • Tuttle test = measurement of esophageal pH: 96% accurate
  • Radionuclide gastroesophageal reflux test (typically combined with gastric emptying test):
    Technique: ROI drawn over distal esophagus + compared with time-activity curve over stomach, scaled to 4%
    • esophageal activity >4% stomach activity
Cx of reflux:
  • from acid + pepsin acting on esophageal mucosa:
    • Motility disturbance
    • Stricture
    • Schatzki ring
    • Barrett esophagus
    • Iron-deficiency anemia
    • Reflux/peptic esophagitis
  • from aspiration of gastric contents
    • Acute aspiration pneumonia
    • Mendelson syndrome
    • Pulmonary fibrosis
Viral Esophagitis
Predisposed: immunocompromised, eg, underlying malignancy, debilitating illness, radiation treatment, steroids, chemotherapy, AIDS
Cytomegalovirus Esophagitis
Organism: member of herpesvirus group
Associated with: AIDS
  • • severe odynophagia
  • diffusely normal mucosal background
  • one/more giant ovoid flat ulcers (up to several cm in size) near gastroesophageal junction
  • discrete small superficial ulcers indistinguishable from herpes esophagitis (uncommon)
Rx: ganciclovir (relatively toxic)
Dx: endoscopic brushings, biopsy specimen, cultures
Herpes Esophagitis
  • 2nd most common cause of opportunistic infection!
Organism: Herpes simplex virus type I (DNA core virus) secreted in saliva of 2% of healthy population
Age: 15–30 years; usually males
Predisposed: immunosuppressed patient
  • history of recent exposure to sexual partners with herpetic lesions on lips/buccal mucosa
  • P.832

  • flulike prodrome of 3–10 days (headaches, fever, sore throat, upper respiratory symptoms, myalgia)
  • severe acute dysphagia/odynophagia
May be associated with: oropharyngeal herpetic lesions/oropharyngeal candidiasis
Location: midesophagus (level of left main bronchus)
  • initially vesicles/blisters that subsequently rupture
  • multiple small discrete superficial punctate/round/linear/serpentine/stellate (often “diamond-shaped”) ulcers surrounded by radiolucent halos of edematous mucosa (in >50%)
  • intervening mucosa normal (without plaques)
  • multiple plaquelike lesions (only with severe infection)
Dx: rising serum titer for HSV type I, viral culture, biopsy (immunofluorescent staining for HSV antigen, demonstration of intranuclear inclusions)
Rx: oral/intravenous acyclovir
Prognosis: resolution of symptoms in 3–14 days
DDx: drug-induced esophagitis, Crohn disease, esophageal intramural pseudodiverticulosis
Human Immunodeficiency Virus Esophagitis
  • • maculopapular rash + ulcers of soft palate (occasionally)
  • • recent seroconversion/known AIDS
  • one/more giant (>1 cm) flat ovoid/diamond-shaped ulcers (at time of seroconversion) indistinguishable from CMV esophagitis
Dx: per exclusion (brushings, biopsies, cultures negative for CMV)
Rx: oral steroids
DDx: CMV esophagitis, mycobacterial esophagitis, actinomycosis, potassium chloride, quinidine, caustic ingestion, nasogastric intubation, radiation therapy, endoscopic sclerotherapy
Familial Adenomatous Polyposis
  • = FAMILIAL MULTIPLE POLYPOSIS
  • = autosomal dominant disease with 80% penetrance (gene for familial polyposis localized on chromosome 5); sporadic occurrence in 1/3
Incidence: 1:7,000 to 1:24,000 live births
Histo: tubular/villotubular adenomatous polyps; usually about 1,000 adenomas
Age: polyps appear around puberty
  • family history of colonic polyps (66%)
    • Screening of family members after puberty!
  • clinical symptoms begin during 3rd–4th decade (range 5–55 years)
  • vague abdominal pain, weight loss
  • diarrhea, bloody stools
  • protein-losing enteropathy (occasionally)
Associated with: (1) Hamartomas of stomach in 49%
(2) Adenomas of duodenum in 25%
(3) Periampullary carcinoma
  • “carpet of polyps” = myriad of 2–3 mm (up to 2 cm) polypoid lesions
  • @ Colon (100%): more numerous in distal colon; always affecting rectum
    • normal haustral pattern
  • @ Stomach (5%)
  • @ Small bowel (<5%)
Cx: malignant transformation of adenomas in: colon > stomach > small bowel (in 12% by 5 years; in 30% by 10 years; in 100% by 20 years after diagnosis; age at carcinomatous development usually 20–40 years; multiple carcinomas in 48%)
♢331-fold increased risk of small bowel adenocarcinoma compared to general population after colectomy
♢ Periampullary carcinoma is the most common cause of death after prophylactic colectomy!
Rx: prophylactic total colectomy in late teens/early twenties before symptoms develop
(1) Permanent ileostomy
(2) Continent endorectal pull-through pouch
(3) Kock pouch (= distal ileum formed into a one-way valve by invaginating the bowel at skin site)
DDx: other polyposes, lymphoid hyperplasia, lymphosarcoma, ulcerative colitis with inflammatory pseudopolyps
Gallstone Ileus
Incidence: 0.4–5% of all intestinal obstructions (20% of obstruction in patients >65 years; 24% of obstructions in patients >70 years); develops in <1% of patients with cholelithiasis; in 1 of 6 perforations; risk increases with age
Etiology: biliary disease (90%), peptic ulcer disease, cancer, trauma
Age: average 65–75 years; M:F = 1:4–1:7
  • • previous history of gallbladder disease
  • • intermittent episodes of acute colicky abdominal pain (20–30%)
  • • nausea, vomiting, fever, distension, obstipation
  • Rigler triad on plain film (in 10%):
    • Partial/complete intestinal obstruction (usually small bowel), “string of rosary beads” = multiple small amounts of air trapped between dilated + stretched valvulae conniventes (in 86%)
    • Gas in biliary tree (in 69%)
    • Ectopic calcified gallstone (in 25%): stones are commonly >2.5 cm in diameter
  • change in position of previously identified gallstone
UGI/BE:
  • well-contained localized barium collection lateral to first portion of duodenum (barium-filled collapsed GB + possibly biliary ducts)
    • Fistulous communication:
      • cholecystoduodenal (60%), choledochoduodenal, cholecystocolic, choledochocolic, cholecystogastric
  • identification of site of obstruction: terminal ileum (60–70%), proximal ileum (25%), distal ileum (10%), pylorus, sigmoid, duodenum (Bouveret syndrome)
Cx: recurrent gallstone ileus in 5–10% (additional silent calculi more proximally)
Prognosis: high mortality
Gangliocytic Paraganglioma
  • = rare benign tumor of the GI tract
Frequency: <100 cases reported
Origin: pancreatic endocrine rest that remained when the ventral primordium rotated around the duodenum
Age: 50–60 years of age; M:F = 2:1
Location: almost exclusively in 2nd portion of duodenum near the ampulla of Vater on the medial/lateral wall of duodenum
P.833

  • • GI hemorrhage, abdominal pain
  • polypoid smooth-surfaced intraluminal mass
  • homogeneously enhancing mural/extrinsic solid mass of soft-tissue attenuation
  • well-circumscribed hypoechoic mass contiguous with bowel
  • no biliary duct dilatation
DDx: adenocarcinoma (biliary duct dilatation, hypovascular), leiomyosarcoma (cystic internal hemorrhage/necrosis), hemangioma, duplication cyst, choledochal cyst, lipoma, hamartoma, inflammatory fibroid polyp (distal small bowel), lymphoma (isolated in stomach and ileum)
Gardner Syndrome
  • = autosomal dominant disease (¿ variant of familial polyposis) characterized by a triad of
    • colonic polyposis
    • osteomas
    • soft-tissue tumors
Cause: adenomatous polyposis gene on chromosome 5-q21; in 20% new mutations
♢Familial polyposis + Gardner syndrome may occur in the same family!
Histo: adenomatous polyps
Age: 15–30 years (2 months–70 years)
Associated with: ¿ MEA complex
  • periampullary/duodenal carcinoma (12%)
  • papillary thyroid carcinoma (often multicentric)
  • adrenal adenoma/carcinoma
  • parathyroid adenoma
  • pituitary chromophobe adenoma
  • carcinoid, adenoma of small bowel
  • retroperitoneal leiomyoma
  • Extraintestinal manifestations occur usually earlier than in intestinal polyposis!
  • • skin pigmentation
  • • cramping abdominal pain
  • • weight loss, diarrhea
  • @ Polyposis
    Location: colon (100%), stomach (5–68%), duodenum (90%), small bowel (<5%)
    • multiple colonic polyps appearing during puberty, increasing in number during 3rd–4th decade
    • lymphoid hyperplasia of terminal ileum
    • hamartomas of stomach
    • intussusception
    Cx: small bowel/colonic obstruction
  • @ Soft-tissue tumors
    • sebaceous/epidermoid inclusion cysts (scalp, back, face, extremities)
    • fibroma, lipoma, leiomyoma, neurofibroma
    • desmoid tumors (3–29%); peritoneal adhesions (desmoplastic tendency); mesenteric fibrosis, retroperitoneal fibrosis
      • urinary tract obstruction
    • mammary fibromatosis
    • marked keloid formation, hypertrophied scars (anterior abdominal wall) arise 1–3 years after surgery
  • @ Osteomatosis of membranous bone (50%)
    Location: calvarium, mandible (81%), maxilla, ribs, long bones
  • @ Long bones
    • localized wavy cortical thickening/exostoses
    • slight shortening + bowing
  • @ Teeth
    • odontoma, unerupted/supernumerary teeth, hypercementosis
    • tendency toward numerous caries (dental prosthesis at early age)
Cx: malignant transformation of colonic polyps in 100% (average age at death is 41 years if untreated)
Prophylaxis: gastrointestinal surveillance, thyroid screening, ophthalmologic evaluation for retinal pigmentation anomalies; screening of family members starting at age 15
Rx: prophylactic total colectomy at about 20 years of age
Gastric Carcinoma
  • 3rd most common GI malignancy after colorectal + pancreatic cancer, 6th leading cause of cancer deaths
Prevalence: declining; 24,000 cases/year in USA
Risk factors: smoking, nitrites, nitrates, pickled vegetables
Predisposing factors:
  • H. pylori gastritis, chronic atrophic gastritis, adenomatous + villous polyp (7–27% are malignant), gastrojejunostomy, partial gastrectomy (Billroth II > Billroth I), pernicious anemia (risk factor of 2), Ménétrier disease (¿)
Histo: adenocarcinoma (95%); rarely squamous cell carcinoma/adenoacanthoma
Staging:
T1 tumor limited to mucosa/submucosa
T2 tumor involves muscle/serosa
T3 tumor penetrates through serosa
T4a invasion of adjacent contiguous tissues
T4b invasion of adjacent organs, diaphragm, abdominal wall
N1 involvement of perigastric nodes within 3 cm of primary along greater/lesser curvature
N2 involvement of regional nodes >3 cm from primary along branches of celiac axis
N3 paraaortic, hepatoduodenal, retropancreatic, mesenteric nodes
M1 distant metastases
Location: mostly distal third of stomach + cardia; 60% on lesser curvature, 10% on greater curvature; esophagogastric junction in 30%; transpyloric spread in 5–25% (for lymphoma 40%)
Probability of malignancy of an ulcer:
  • at lesser curvature 10–15%, at greater curvature 70%, in fundus 90%
Morphology:
  • Polypoid/fungating carcinoma
  • Ulcerating/penetrating carcinoma (70%)
  • Infiltrating/scirrhous carcinoma (5–15%)
    • = linitis plastica
    Histo: frequently signet ring cell type + increase in fibrous tissue
    Location: antrum, fundus + body (38%)
    P.834

    • firmness, rigidity, reduced capacity of stomach, aperistalsis in involved area
    • granular/polypoid folds with encircling growth
  • Superficial spreading carcinoma
    • = confined to mucosa/submucosa; 5-year survival of 90%
    • patch of nodularity
    • little loss of elasticity
  • Advanced bulky carcinoma
  • GI bleeding, abdominal pain, weight loss
UGI:
  • rigidity
  • filling defect
  • amputation of folds ± ulceration ± stenosis
  • miliary/punctate calcifications (mucinous adenocarcinoma)
CT:
  • irregular nodular luminal surface
  • asymmetric thickening of folds
  • mass of uniform density/varying attenuation
  • wall thickness >6 mm with gas distension + 13 mm with positive contrast material distension:
    • diffuse low attenuation in mucinous carcinoma
  • increased density in perigastric fat
  • enhancement exclusively in linitis plastica type
  • nodules of serosal surface (= dilated surface lymphatics)
  • diameter of esophagus at gastroesophageal junction larger than adjacent aorta (DDx: hiatal hernia)
  • lymphadenopathy below level of renal pedicle (3%)
Metastases:
  • along peritoneal ligaments
    • gastrocolic lig.: transverse colon, pancreas
    • gastrohepatic + hepatoduodenal lig.: liver
  • local lymph nodes
  • hematogenous: liver (most common), adrenals, ovaries, bone (1.8%), lymphangitic carcinomatosis of lung (rare)
  • peritoneal seeding:
    on rectal wall = Blumer shelf
    on ovaries = Krukenberg tumor
  • left supraclavicular lymph node = Virchow node
Prognosis:
  • overall 5-year survival rate of 5–18%, mean survival time of 7–8 months;
— 85% 5-year survival in stage T1
— 52% 5-year survival in stage T2
— 47% 5-year survival in stage T3
— 17% 5-year survival in stage N1-2
— 5% 5-year survival in stage N3
Early Gastric Cancer (20%)
  • = invasion limited to mucosa + submucosa (T1 lesion) regardless of lymph node involvement
Classification of Japan Research Society for Gastric Cancer:
Type I protruded type = >5 mm in height with protrusion into gastric lumen (10–20%)
Type II superficial type = <5 mm in height
    IIa slightly elevated surface (10–20%)
    IIb flat/almost unrecognizable (2%)
    IIc slightly depressed surface (50–60%)
Type III excavated/ulcerated type (5–10%)
Advanced Gastric Cancer (T2 lesion and higher)
Bormann classification:
Type 1 broad-based elevated polypoid lesion
Type 2 elevated lesion + ulceration + well-demarcated margin
Type 3 elevated lesion + ulceration + ill-defined margin
Type 4 ill-defined flat lesion
Type 5 unclassified, no apparent elevation
Gastric Diverticulum
  • Stomach is least common site of diverticula
Incidence: 1:600–2,400 of UGI studies
Etiology: (a) traction secondary to scarring/periantral inflammation = true diverticulum
(b) pulsion (less common) = false diverticulum
Age: beyond 40 years
Often associated with: aberrant pancreas in antral location
Location: juxtacardiac on posterior wall (75%), prepyloric (15–22%), greater curve (3%)
  • pliability + varying degrees of distension
  • NO mass, edema or rigidity of adjacent folds
DDx: small ulcer in intramural-extramucosal mass
Gastric Polyp
Incidence: 1.5–5%, most common benign gastric tumor
Associated with: hyperacidity + ulcers, chronic atrophic gastritis, gastric carcinoma
  • NONNEOPLASTIC
    • Inflammatory polyp of stomach (75–90%)
      • = HYPERPLASTIC POLYP = REGENERATIVE POLYP
      Histo: cystically dilated glands lined by gastric epithelium + acute and chronic inflammatory infiltrates in lamina propria
      Associated with: chronic atrophic gastritis, pernicious anemia
      Location: predominantly in fundus + body; usually multiple
      • sharply delineated polyp with smooth circular border
      • “Mexican hat sign” = stalk seen en face overlying the head of polyp
      • sessile/pedunculated
      • usually <2 cm in diameter without progression
      • no contour defect of stomach
      Prognosis: no malignant potential
    • Hamartomatous polyp of stomach (rare)
      Histo: densely packed gastric glands + bundles of smooth muscle
      Associated with: Peutz-Jeghers syndrome
      • sessile/pedunculated
      • usually <2 cm in diameter
    • Retention polyp of stomach (rare)
      Histo: dilated cystic glands + stroma
      Associated with: Cronkhite-Canada syndrome
  • NEOPLASTIC
    • Adenomatous polyp of stomach (10–20%)
      • = true neoplasm with malignant potential (10–80%, increasing with size)
      Age: increasing incidence with age; M:F = 2:1
      Histo: intestinal metaplasia (common) + marked cellular atypism
      Associated with: Gardner syndrome; coexistent with gastric carcinoma in 35%
      Location: more commonly in antrum (antrum spared in Gardner syndrome)
      P.835

      • broad-based elliptical/mushroom-shaped polyp ± pedicle; usually solitary
      • usually >2 cm in diameter (in 80%)
      • smooth/irregular lobulated contour
    • Villous polyp of stomach (rare)
      • trabeculated/lobulated slightly irregular contour
      Cx: malignant transformation
DDx: (1) Ménétrier disease (antrum spared)
(2) Eosinophilic polyp (peripheral eosinophilia, linitis plastica appearance, small bowel changes)
(3) Lymphoma
(4) Carcinoma
Gastric Ulcer
Benign Gastric Ulcer
  • 95% of all gastric ulcers
Cause:
  • HORMONAL
    • Zollinger-Ellison syndrome
    • Hyperparathyroidism (in 1.3–24%)
      • duodenum:stomach = 4:1; M:F = 3:1
      • Duodenal ulcers predominate in females!
      • Gastric ulcers predominate in males!
      • • absence of gastric hypersecretion
    • Steroid-induced ulcer
      • gastric > duodenal location;
      • frequently multiple + deep ulcers;
      • commonly associated with erosions
      • • bleeding (in 1/3)
    • Stress, severe prolonged illness
    • Cerebral disease = Cushing ulcer
    • Curling ulcer (burns) (in 0.09–2.6%)
    • Retained gastric antrum
    • Uremia
  • INFLAMMATION
    • Peptic ulcer disease
    • Gastritis
    • Radiation-induced ulcer
    • Intubation
    • Stasis ulcer proximal to pyloric/duodenal obstruction
  • BENIGN MASS
    • Leiomyoma
    • Granulomatous disease
    • Pseudolymphoma (lymphoid hyperplasia)
  • DRUGS
    ASA: greater curvature
Pathophysiology:
  • disrupted mucosal barrier (Helicobacter pylori) with vulnerability to acid + secretion of large volume of gastric juice containing little acid
Incidence: 5:10,000; 100,000/year (United States)
Age peak: 55–65 years; M:F = 1:1
Multiplicity:
  • multiple in 2–8% (17–24% at autopsy), especially in patients on aspirin
  • coexistent duodenal ulcer in 5–64%; gastric:duodenal = 1:3 (adults) = 1:7 (children)
  • abdominal pain: in 30% at night, in 25% precipitated by food
Location: lesser curvature at junction of corpus + antrum within 7 cm from pylorus; proximal half of stomach in older patients (geriatric ulcer); adjacent to GE junction within hiatal hernia
  • ulcer size usually <2 cm (range 1–250 mm); in 4% >40 mm
  • round/ovoid/linear shape
  • Haudek niche = conical/collar button-shaped barium collection projecting outside gastric contour (profile view)
  • Hampton line = 1-mm thin straight lucent line traversing the orifice of the ulcer niche (seen on profile view + with little gastric distension) = ledge of touching overhanging gastric mucosa of undermined benign ulcer
  • ulcer collar = smooth thick lucent band interposed between the niche and gastric lumen (thickened rim of edematous gastric wall) in well-distended stomach
  • ulcer mound = smooth, sharply delineated, gently sloping extensive tissue mass surrounding a benign ulcer (edema + lack of wall distensibility) in well-distended stomach
  • ulcer crater = round/oval barium collection with smooth border on dependent side (en face view)
  • halo defect = wide lucent band symmetrically surrounding ulcer resembling extensive ulcer mound (viewed en face)
  • ring shadow: ulcer on nondependent side (en face view)
  • radiating thick folds extending directly to crater edge fusing with the effaced marginal fold of the ulcer collar/halo of ulcer mound
  • incisura defect = smooth, deep, narrow, sharp indentation on greater curvature opposite a niche on lesser curvature at/slightly below the level of the ulcer (spastic contraction of circular muscle fibers)
Prognosis: healing in 50% by 3 weeks, in 100% by 6–8 weeks; slower healing in older patients; only complete healing proves benignancy
Cx: bleeding, perforation, fistula
♢Most common cause of gastrocolic fistula!
Gastric Ulcer
Sign Benign Malignant
Crater round, ovoid irregular
Radiating folds symmetric nodular, clubbed, fused
Areae gastricae preserved destroyed
Projection outside lumen inside lumen
Ulcer mound smooth rolled edge
Malignant Gastric Ulcer
Incidence: 5% of ulcers are malignant
Cause:
  • Gastric carcinoma
  • Lymphoma (2% of all gastric neoplasms)
    • multiple ulcers with aneurysmal appearance
  • P.836

  • Leiomyosarcoma, neurogenic sarcoma, fibrosarcoma, liposarcoma
  • Metastases
    • hematogenic: malignant melanoma, breast cancer, lung cancer
    • per continuum: pancreas, colon, kidney
Prognosis: partial healing may occur
Location: anywhere within stomach; fundal ulcers above level of cardia are usually malignant
  • ulcer location within gastric lumen, ie, not projecting beyond expected margin of stomach (profile view)
  • eccentrically located ulcer within the tumor
  • irregularly shaped ulcer
  • shallow ulcer with width greater than depth
  • nodular ulcer floor
  • abrupt transition between normal mucosa + abnormal tissue at some distance (usually 2–4 cm) from ulcer edge
  • rolled/rounded/shouldered edges surrounding ulcer
  • nodular irregular folds approaching ulcer with fused/clubbed/amputated tips
  • rigidity/lack of distensibility
  • associated large irregular mass
  • Carman meniscus sign = curvilinear lens-shaped intraluminal form of crater with convexity of crescent toward gastric wall and concavity toward gastric lumen (profile view, usually under compression) found in specific type of ulcerating carcinoma, seen only infrequently; wall aspect can also be concave/flat
  • Kirklin meniscus complex = Carman sign (appearance of crater) + radiolucent slightly elevated rolled border
Gastric Varices
Cause: portal hypertension (varices seen in 2–78%); splenic vein obstruction (from pancreatitis, pancreatic carcinoma, pseudocyst)
Location: (a) esophagogastric junction (most common)
(b) along lesser curvature (in 11–75% of patients with portal hypertension/cirrhosis)
Feeding vessels:
  • Left gastric vein (between splenic vein + stomach)
  • Short gastric veins (between spleen + fundus)
  • Retrogastric vein (between splenic vein + esophagogastric junction)
  • • increased prevalence of portosystemic encephalopathy
  • barium study: 65–89% rate of detection:
    • lobulated folds/polypoid masses in fundus
  • endoscopy: most practical method
  • splenic portography
  • hepatofugal blood flow along SMV into left gastric + splenic vein
Cx: variceal bleeding in 3–10–36%
♢Gastric varices bleed less frequently but more severely than esophageal varices!
Gastric Volvulus
  • SURGICAL EMERGENCY
  • = abnormal degree of rotation of one part of stomach around another part, usually requires >180° twisting to produce complete obstruction
Degrees of rotation:
  • Partial Volvulus
    • = rotation of stomach <180 degrees without vascular compromise
  • Complete volvulus
    • = rotation of stomach >180 degrees
Etiology:
  • abnormality of suspensory ligaments
  • unusually long gastrohepatic + gastrocolic mesenteries
Anatomy of ligaments:
  • gastrohepatic at lesser curvature; gastrosplenic + gastrocolic at greater curvature; gastrophrenic at posterior fundus; attachment to esophagus at gastroesophageal junction; attachment to duodenum at pylorus
Predisposing factors:
  • sliding/paraesophageal hernia (33%), ligamentous laxity, eventration of diaphragm, phrenic nerve paralysis, splenic abnormalities (asplenia, polysplenia, splenomegaly, prior splenectomy)
Age: 40–50 years (in 20% in infants <1 year of age); M:F = 1:1
Types:
  • ORGANOAXIAL VOLVULUS (more common)
    • = rotation around a line from cardia to pylorus
    • • more common in elderly
    • • high correlation with hiatal hernia
    • mirror-image stomach:
      • reversal of locations of greater + lesser curvatures (in transversely oriented stomach)
      • greater curvature to right of lesser curvature (in vertically oriented stomach)
  • MESENTEROAXIAL VOLVULUS (less common)
    • = rotation around an axis from lesser to greater curvature coinciding with axis of mesenteric attachments
    • • associated with severe obstruction + strangulation
    • upside-down stomach (= antrum + pylorus superior to fundus + proximal body)
  • COMBINATION (rare)
  • • Borchordt triad:
    • sudden onset of severe epigastric pain
    • intractable retching (= vigorous attempts to vomit) without production of vomitus
    • inability to pass nasogastric tube into stomach
  • • chronic volvulus: asymptomatic/postprandial pain, belching, bloating, vomiting, early satiety
  • massively distended stomach in LUQ extending into chest
  • unexpected location of stomach gas bubble
  • air-fluid levels in mediastinum/upper abdomen
  • incomplete/absent entrance of barium into stomach
  • displaced gastroesophageal junction
  • barium demonstrates area of twist
Cx: intramural emphysema, gastric ischemia, necrosis, perforation, peritonitis, shock, gastric ulceration, hemorrhage, pancreatic necrosis, omental avulsion, splenic rupture
Mortality: 42–80% in acute volvulus;
10–13% in chronic volvulus
Rx: open/laparoscopic gastropexy
DDx: gastric atony, acute gastric dilatation, pyloric obstruction
P.837

Gastritis
Corrosive Gastritis
Agents:
  • acid, formaldehyde
    • clinically usually silent
    Location: esophagus usually unharmed, severe gastric damage, duodenum may be involved (newer potent materials cause atypical distribution)
  • alkaline
    Location: pylorus + antrum most frequently involved
  • ACUTE CHANGES (edema + mucosal sloughing)
    • marked enlargement of gastric rugae + erosions/ulceration
    • complete cessation of motor activity
    • gas in portal venous system
    Cx: perforation
  • CHRONIC CHANGES
    • firm thick nonpliable wall
    • stenotic/incontinent pylorus (if involved)
    • gastric outlet obstruction (cicatrization) after 3–10 weeks
Emphysematous Gastritis
  • = rare but severe form of widespread phlegmonous gastritis subsequent to mucosal disruption characterized by gas in wall of stomach
Cause of mucosal disruption:
  • ingestion of toxic/corrosive substances (37%), alcohol abuse (22%), gastroenteritis (15%), recent abdominal surgery (15%), gastric infarction, necrotizing enterocolitis, ulcer, acute pancreatitis, adenocarcinoma of stomach, phytobezoar, leukemia, diabetes mellitus, disseminated strongyloidiasis, gastric mucormycosis, after ingestion of large amounts of carbonated beverages
Histo: bacterial invasion of submucosa + subserosa
Organism: hemolytic streptococcus, Clostridium welchii, Clostridium perfringens, E. coli, S. aureus, enterobacter, P. aeruginosa
  • explosive onset of severe abdominal pain
  • nausea, diarrhea, chills, fever, leukocytosis
  • bloody foul-smelling emesis ± PATHOGNOMONIC vomiting of a necrotic cast of stomach (due to dissection along plane of muscularis mucosae)
CT:
  • gastric wall thickening (DDx: emphysematous gastritis)
Plain radiographs:
  • innumerable small gas bubbles silhouetting the stomach in a mottled fashion without positional change
  • thickening of rugal folds
  • ± portal venous gas
GI:
  • cobblestone appearance of mucosa on upper GI
  • intramural penetration of contrast material
Cx: cicatricial stenosis (21%), sinus tract formation
Prognosis: 60–80% mortality
Rx: broad-spectrum antibiotics + intravenous fluids; emergent surgery for acute perforation
Erosive Gastritis
  • = HEMORRHAGIC GASTRITIS
Incidence: 0.5–10% of GI studies
Etiology (in 50% without causative factors):
  • Peptic disease: emotional stress, alcohol, acid, corrosives, severe burns, anti-inflammatory agents (aspirin, steroids, phenylbutazone, indomethacin)
  • Infection: herpes simplex virus, CMV, Candida
  • Crohn disease: aphthoid ulcers identical in appearance to varioliform erosions
Histo: epithelial defect not penetrating beyond muscularis mucosae
  • 10–20% of all GI hemorrhages (usually without significant blood loss)
  • vague dyspepsia, ulcerlike symptoms
Location: antrum, rarely extending into fundus; aligned on surface of gastric rugal folds
  • varioliform complete erosion (95%) = tiny fleck of barium surrounded by radiolucent halo (“target lesion”) <5 mm, usually multiple
  • incomplete erosion (5%) = linear streaks/dots of barium without surrounding mound of edema/inflammation
  • nodularity/scalloping of prominent antral folds
  • contiguous duodenal disease may be present
  • limited distensibility, poor peristalsis/atony, delayed gastric emptying
Phlegmonous Gastritis
Etiology: septicemia, local abscess, postoperative stomach, complication of gastric ulcer/cancer
Organism: Streptococcus
Path: multiple gastric wall abscesses, which may communicate with lumen
  • severe fulminating illness
  • patient may vomit pus
Location: usually limited to stomach not extending beyond pylorus; submucosa is the most severely affected gastric layer
  • barium dissection into submucosa + serosa
Gastrointestinal stromal tumor
  • = GIST = SPINDLE CELL/EPITHELOID TUMOR
Origin: KIT-positive gut pacemaker cell = precursor of the interstitial cell of Cajal of myenteric plexus
  • Most common mesenchymal neoplasm of GI tract
Incidence: 4500–6000 new cases per year (USA)
Age: >50 years
Histo: spindle cell (70–80%)/epithelioid (20–30%) morphology/mixture of both
Location:
  • GI tract anywhere between esophagus and anus:
    • stomach (37–70%), small intestine (20–33%), duodenum (9%), anorectum (5–7%) > colon (4%) > esophagus (2%)
    • 75% of mesenchymal tumors in the esophagus are leiomyomas, 25% GIST
    • Stomach is the most common location of GIST = 2–3% of all gastric tumors
  • peritoneum (4%), omentum; mesentery; retroperitoneum
Site: muscularis propria (leiomyomas arise from muscularis mucosae)
P.838

  • • early satiety, indigestion, bloating, vague abdominal pain
  • often not detected until late in their progression
  • • gastrointestinal bleeding (from mucosal ulceration)
  • • expresses transmembrane receptor tyrosine kinase encoded by KIT gene (CD117) in 95%; 70% of GISTs coexpress CD34
Associated with: neurofibromatosis type 1
Spread: (in 50% at presentation)
  • adjacent organ invasion, ascites, omentum, peritoneum, liver metastasis
  • Lymphadenopathy is NOT a feature!
  • large hypervascular enhancing mass in prominent extraluminal location
  • ± heterogeneous texture due to necrosis, hemorrhage, cystic degeneration
  • ulceration + fistulization to GI lumen (common)
  • tumor vessels visible within tumor
  • displacement of adjacent organs + vessels
  • @ Stomach
    • well-circumscribed mass up to 30 cm in size
    • features of submucosal mass:
      • lesion margin obtuse/at right angle with gastric wall (in profile)
      • smoothly circumscribed (en face)
    • smooth mucosal surface (common)
    • mucosal ulceration (in up to 60%)
    • polypoid intraluminal mass (in 14%
CT:
  • extragastric extension into gastrohepatic/gastrosplenic ligament/lesser sac (in 86%)
  • peripheral enhancement in 92% (corresponding to viable tumor)
  • central areas of low attenuation (corresponding to hemorrhage, necrosis, cyst formation)
  • cavity containing air/air-fluid level/oral contrast medium communicates with gastric lumen
  • calcified in 3%
MR:
  • solid tumor portion hypointense on T1WI + hyperintense on T2WI + enhancement
  • tumoral hemorrhage varies from high to low signal intensity on T1WI + T2WI depending on age
DDx: leiomyoma, leiomyosarcoma, schwannoma, neurofibroma, carcinoid
  • @ Small intestine
  • @ Anorectum
Cx: bowel obstruction (rare)
Rx: (1) surgery for localized primary
(2) imatinib (= tyrosine kinase inhibitor) inhibits growth of GIST (paradoxical enlargement due to tumor hemorrhage/necrosis)
Giardiasis
  • = overgrowth of commensal parasite Giardia lamblia
Organism:
  • Giardia lamblia (flagellated protozoan); often harmless contaminant of duodenum + jejunum in motile form (= trophozoite) attached to mucosa by suction disk, nonmotile form (= cyst) shed in feces; capable of pathogenic behavior with invasion of gut wall
Incidence: 1.5–2% of population in United States, infests 4–16% of inhabitants of tropical countries, found in 3–20% of children in parts of southern USA
Predisposed: altered immune mechanism (dysgammaglobulinemia, nodular lymphoid hyperplasia of ileum)
Histo: blunted villi (may be misdiagnosed as celiac disease especially in children), cellular infiltrate of acute + chronic inflammation in lamina propria
  • abdominal pain, weight loss, failure to thrive (especially in children)
  • spectrum from asymptomatic to severe debilitating diarrhea, steatorrhea (related to number of organisms)
  • reduced fat absorption (simulating celiac disease)
Location: most pronounced in duodenum + jejunum
  • thickened distorted mucosal folds in duodenum + jejunum (mucosal edema) with normal ileum
  • marked spasm + irritability with rapid change in direction + configuration of folds
  • hypersecretion with blurring + indistinctness of folds
  • hyperperistalsis with rapid transit time
  • segmentation of barium (from motility disturbance + excess intraluminal fluid)
  • ± lymphoid hyperplasia (associated with immunoglobulin deficiency state)
Dx: (1) Detection of Giardia lamblia cysts in formed feces or trophozoites in diarrheal stools
(2) Trophozoites in duodenal aspirate/jejunal biopsy
DDx: Strongyloides/hookworm infection
Rx: quinacrine (Atabrine®)
Glomus Tumor of Stomach
  • Most common benign vascular gastric tumor
Histo: dilated irregularly shaped thin-walled vessels (= modified capillaries) covered by nests/strands/sheets of glomus cells
  • asymptomatic/upper GI bleeding
Location: gastric antrum
  • single smooth submucosal mass ± ulceration
  • tiny flecks of calcification (occasionally)
  • strong enhancement in early arterial phase
Glycogen Acanthosis
  • = benign degenerative condition with accumulation of cellular glycogen within squamous epithelial lining of esophagus
Incidence: in up to 15% of endoscoped patients
Etiology: unknown
Age: middle-aged/elderly individuals
Histo: hyperplasia + hypertrophy of squamous mucosal cells secondary to increased glycogen; no malignant potential
  • asymptomatic
  • white oval mucosal plaques of 2–15 mm in diameter on otherwise normal appearing mucosa
Location: middle (common)/upper esophagus, in random distribution
  • multiple 1–3-mm rounded nodules/plaques
Dx: biopsy
DDx: candida esophagitis (lesions disappear under treatment in contrast to glycogen acanthosis), reflux esophagitis
P.839

Graft-Versus-Host Disease
  • = T lymphocytes from donor bone marrow cause selected epithelial damage of recipient target organs
Bone marrow transplantation for treatment of:
  • leukemia, lymphoma, aplastic anemia, immunologic deficit, metabolic disorders of hematopoietic system, some metastatic disease
Incidence: 30–70% of patients with allogeneic (= donor genetically different from host) transplant
Target organs: GI tract (small bowel), skin, liver
  • @ Skin
    • maculopapular rash on face, trunk, extremities
  • @ Liver
    • elevation of hepatic enzymes ± liver failure
  • @ GI tract
    • profuse secretory diarrhea
    • abdominal cramping, fever, nausea, vomiting
Path: severe mucosal atrophy/destruction
  • shaggy fold thickening
  • “ribbon bowel” = small bowel fold effacement with tubular appearance (DDx: viral enteritis, ischemia, celiac disease, radiation, soybean allergy)
  • loss of haustration, spasm, edema, ulceration, granular mucosal pattern of colon (simulating ulcerative colitis)
  • small bowel “cast” = prolonged coating of abnormal bowel for hours to days
  • circular collections of contrast material on cross section + parallel tracks on longitudinal section
  • severely decreased transit time
CT:
  • abnormally enhancing thin layer of mucosa diffusely involving small + large bowel
  • fluid-filled distended poorly opacified bowel (oral contrast material not given!)
  • barium (from previous contrast enema) may become incorporated into bowel wall
Cx: infection with opportunistic organisms, eg, Candida albicans, herpes virus, invasive fungal organisms, CMV, Varicella-zoster virus, Epstein-Barr virus, hepatitis viruses, Rotavirus, Adenovirus, Coxsackie virus A and B, P. carinii, pneumococcus
Prognosis: fatal in up to 15% (due to opportunistic infections)
Rx: steroids + cyclosporine
DDx: superinfection with enteroviruses
Helicobacter Pylori Infection
Organism: worldwide gram-negative spiral-shaped bacillus [formerly Campylobacter pylori]
Prevalence: increasing with age; >50% of Americans >60 years of age
Path: surface epithelial damage + inflammation with mucosal infiltration by neutrophils, plasma cells, and lymphoid nodules
Location: gastric antrum > proximal half of stomach
Site: beneath mucus layer on surface epithelial cells
  • • asymptomatic (vast majority)
  • • dyspepsia, epigastric pain
  • gastritis (75% prevalence of H. pylori):
    • thickened gastric folds
    • polypoid gastritis mimicking malignant tumor
    • enlarged areae gastricae
  • gastric ulcer (60–80% prevalence of H. pylori)
  • duodenal ulcer (90–100% prevalence of H. pylori)
Dx: (1) Endoscopic brushings + biopsy
(2) Breath test measuring urease activity after ingestion of carbon-14–labeled urea
(3) Serologic test for IgG antibodies
Rx: triple therapy (= bismuth + metronidazole + tetracycline/amoxicillin) results in 95% cure rate after 2 weeks of therapy
Hemangioma of Small Bowel
Incidence: 7–10% of all benign small bowel tumors
Increased incidence in: Turner syndrome, tuberous sclerosis, Osler-Weber-Rendu disease
  • symptomatic (80%):
    • acute intermittent severe bleeding (melena)
    • acute/chronic life-threatening anemia
    • intestinal obstruction, intussusception, perforation
Path: submucosal soft infiltrative polypoid mass
Location: jejunum (55%), ileum (42%), duodenum (2%)
  • multiple sessile compressible intraluminal filling defects
  • nodular segmental mucosal abnormality
  • ± phleboliths in intestinal wall
CT:
  • well-circumscribed lobulated mass of mixed attenuation supplied by large artery
Henoch-Schönlein Purpura
  • = most common systemic allergic hypersensitivity-related acute small-vessel vasculitis in children
Precipitated by: bacterial/viral infection, allergies, insect sting, drugs (eg, penicillin, sulfonamides, aspirin), certain foods
Cause: deposition of IgA-dominant immune complexes in venules, capillaries, and arterioles
Age: children (peak age of 5, range 3–10 years) + adults >20 years (in up to 30%)
  • • most frequent manifestations:
    • purpuric skin rash on legs + extensor surfaces on arms
    • colicky abdominal pain + GI bleeding
    • microscopic hematuria + proteinuria in 50% (from proliferative glomerulonephritis with IgA deposits demonstrated by immunofluorescence)
  • • often begins as an upper respiratory tract infection
  • • arthralgias of large joints
  • multifocal bowel wall thickening (due to intramural hemorrhage + edema)
Cx: (1) Bowel infarct/perforation/irreducible intussusception (3–5%)
(2) Renal insufficiency (10–20%), end-stage renal disease (5%)
Rx: high doses of corticosteroids + azathioprine
Hernia
Prevalence: 10% of SBO; 2nd most common cause of small bowel obstruction!
Nomenclature: according to anatomic site of its orifice
P.840

External Hernia
  • = bowel extending outside the abdominal cavity
Incidence: 95% of all hernias
Location:
  • @ Ventral
    • Postoperative hernia
    • Trocar site hernia
      Incidence: 1–3.6%
      • often Richter type hernia
    • Umbilical hernia
      • see below
    • Paraumbilical hernia
      • large defect through linea alba from diastasis of rectus abdominis muscle at umbilicus
    • Epigastric/hypogastric hernia
      • in linea alba above/below umbilicus
    • Spigelian hernia
      Frequency: 2% of anterior abdominal hernias
      • = acquired ventrolateral hernia through defect in aponeurosis between transverse and rectus muscle of abdomen at junction of semilunar + arcuate lines below umbilicus
      • hernia sac dissects laterally to rectus abdominis muscle through a fibrous groove (= semicircular/spigelian line)
      • hernia sac lies beneath an intact external oblique aponeurosis
  • @ Diaphragm
    • Bochdalek hernia
    • Morgagni hernia
  • @ Lumbar
    Location: defect in lumbar muscles below 12th rib + above iliac cest
    • Grynflett-Lesshaft (upper)
      Borders: internal oblique m. (anteriorly), 12th rib (superiorly), erector spinae m. (posteriorly)
    • Inferior lumbar triangle (Petit) (lower)
      Borders: external oblique m. (anteriorly), iliac crest (inferiorly), latissimus dorsi m. (posteriorly)
  • @ Pelvic floor
    • Obturator foramen
      • hernia between pectineus + external obturator muscles
    • Sciatic notch
    • Perineal hernia (rare)
      • (a) anterior perineal hernia = defect of urogenital diaphragm anterior to superficial transverse perineal m. + lateral to bulbocavernosus m. + medial to ischiocavernosus m. (only in females)
      • (b) posterior perineal hernia = defect in levator ani m./between levator ani m. and coccygeus m. posterior to superficial transverse perineal m.
      • defecating proctography
  • @ Groin
    • Inguinal hernia
      • Most common type of abdominal wall hernia, M>F
      • direct inguinal hernia
        • = defect in Hesselbach triangle (bounded by inguinal ligament inferiorly, inferior epigastric artery superolaterally, fused aponeuroses of internal oblique + transverse abdominal muscles medially)
        • medial to inferior epigastric vessels
        • hernia contains bowel, mesenteric fat, vessels
      • indirect inguinal hernia
        • Most common hernia in children due to failure of obliteration of processus vaginalis accompanying the testis
        • lateral to inferior epigastric vessels originating at deep inguinal ring
      • Littre hernia = inguinal hernia containing Meckel diverticulum
    • Femoral hernia
      • M<F
      • medial to femoral vein within femoral canal
      • posterior to inguinal ligament
      Cx: high probability of incarceration
    • Richter hernia = entrapment of antimesenteric border of bowel in hernia orifice, usually seen in older women with femoral hernias
      • • no palpable mass = difficult to diagnose
      • partial obstruction with patent bowel lumen
Internal Hernia
  • = herniation of bowel through a developmental/surgically created defect of the peritoneum, omentum, mesentery or through an adhesive band
Incidence: 5% of all hernias, responsible for <1% of mechanical small bowel obstruction
  • Classification of internal hernias:
    • retroperitoneal: usually congenital containing a hernia sac
      • paraduodenal (ligament of Treitz)
      • foramen of Winslow
      • intersigmoid
      • pericecal/ileocolic
      • supravesical
    • anteperitoneal:
      • small group of hernias without a peritoneal sac
      • transmesenteric (transverse/sigmoid mesocolon)
      • transomental
      • pelvic (including broad ligament)
  • • intermittent nausea, abdominal pain, distension (made worse by eating + standing and relieved by fasting + assuming a recumbent position)
  • signs of bowel obstruction (only during symptomatic period)
  • mass effect with displacement of other abdominal organs
Cx: volvulus
Paraduodenal Hernia (53%)
  • = congenital defect in descending mesocolon
  • • frequently asymptomatic
P.841

  • LEFT through fossa of Landzert (75%)
    Location: to the left of 4th portion of duodenum at duodenojejunal junction (paraduodenal fossa = confluent zone of descending mesocolon + transverse mesocolon + small bowel mesentery
    • cluster of dilated small-bowel loops between pancreas + stomach
    • displacement of gastric wall anteriorly
    • displacement of duodenojejunal flexure + transverse colon inferiorly
    • engorged crowded vessels at entrance of hernia sac
    • CT:
      • encapsulated bowel loop displacing the inferior mesenteric vein (= landmark of the right margin of the descending mesocolon) anterolaterally
  • RIGHT through mesentericoparietal fossa of Waldeyer (25%)
    Predisposed: nonrotation of small bowel
    Location: behind the root of small bowel mesentery caudal to SMA and inferior to 3rd portion of duodenum on right side
    • CT:
      • encapsulated bowel loop displacing the right colic vein (= landmark of left margin of the ascending mesocolon) anteriorly
      • looping of small intestine behind SMA + SMV below transverse portion of duodenum
      • SMV located ventral + to left of SMA
      • absence of normal horizontal duodenum
Cx: partial/complete obstruction of small intestine (in 50%)
Lesser Sac Hernia (<10%)
  • through foramen of Winslow in retrogastric location
  • Invaginated gut:
    • ileum > jejunum, cecum, appendix, ascending colon, Meckel diverticulum, gallbladder, greater omentum
  • gas-containing bowel loops in center of upper abdomen
  • distended small bowel loops occupying space between stomach + liver
Iatrogenic Hernia
  • Transmesenteric Hernia
    Cause: fenestration of transverse mesocolon in construction of Roux-en-Y loop
    • cluster of small-bowel loops (70%)
    • clustered small bowel outside colon compressed against abdominal wall without overlying omental fat (85%)
    • central displacement of colon (92%)
    • displacement of mesenteric trunk (85%)
    • engorged mesenteric vessels (85%)
  • Hernia through Broad Ligament (very rare)
    • after laceration/fenestration during surgery or during pregnancy
Hiatal Hernia
Associated with: diverticulosis (25%), reflux esophagitis (25%), duodenal ulcer (20%), gallstones (18%)
Sliding Hiatal Hernia (99%)
  • = AXIAL HERNIA = CONCENTRIC HERNIA
  • = esophagogastric junction (= termination point of converging gastric folds) >1.5 cm above diaphragmatic hiatus (= pinched appearance of gastric folds) with portion of peritoneal sac forming part of wall of hernia
Etiology: rupture of phrenicoesophageal membrane due to repetitive stretching with swallowing
Incidence: increasing with age
  • reducible in erect position
  • epiphrenic bulge = entire vestibule + sleeve of stomach are intrathoracic
  • distance between B ring (if visible) and hiatal margin >2 cm
  • peristalsis ceases above hiatus (end of peristaltic wave delineates esophagogastric junction)
  • tortuous esophagus having an eccentric junction with hernia
  • numerous coarse thick gastric folds within suprahiatal pouch (>6 longitudinal folds)
  • ± gastroesophageal reflux
  • CT:
    • dehiscence of diaphragmatic crura >15 mm
    • pseudomass within/above esophageal hiatus
    • increase in fat surrounding distal esophagus (= herniation of omentum through phrenicoesophageal ligament)
DDx: normal temporary cephalad motion of esophagogastric junction by 1–2 cm into chest due to contraction of longitudinal muscle during esophageal peristalsis
Paraesophageal Hernia (1%)
  • = ROLLING HIATAL HERNIA = parahiatal HERNIA
  • = portion of stomach superiorly displaced into thorax with esophagogastric junction remaining in subdiaphragmatic position
  • cardia in normal position
  • herniation of portion of stomach anterior to esophagus
  • frequently nonreducible
  • may be associated with gastric ulcer of lesser curvature at level of diaphragmatic hiatus
Totally Intrathoracic Stomach
  • = defect in central tendon of diaphragm in combination with slight volvulus in transverse axis of stomach behind heart (organoaxial rotation)
  • cardia may be intrathoracic (usually)/subdiaphragmatic
  • great gastric curvature either on right/left side
Congenitally Short Esophagus
  • (not true hernia, very rare)
  • = gastric ectopy by lack of lengthening of esophagus
  • nonreducible intrathoracic gastric segment (in erect/supine position)
  • cylindrical/round intrathoracic segment with large sinuous folds
  • P.842

  • short straight esophagus
  • circular narrowing at gastroesophageal junction, frequently with ulcer
  • gastroesophageal reflux
Umbilical Hernia
  • = protrusion of abdominal contents/fat into anterior abdominal wall via umbilical ring
Prevalence: 4% of all hernias; M < F
Cause: failed closure of umbilical ring, obesity, multiple pregnancies, intraabdominal masses, liver failure, increased intraabdominal pressure, weak abdominal wall
  • may contain fat/small bowel/colon
Cx: strangulation, incarceration
DDx: paraumbilical, spigelian, epigastric, incisional hernia
Hirschsprung Disease
  • = AGANGLIONOSIS OF THE COLON = AGANGLIONIC MEGACOLON
  • = absence of parasympathetic ganglia in muscle (Meissner plexus) + submucosal layers (Auerbach plexus) secondary to an arrest of craniocaudal migration of neuroblasts along vagal trunks before 12th week leading to relaxation failure of the aganglionic segment
Incidence: 1:5,000–8,000 live births; 15–20% of all neonatal bowel obstructions; usually sporadic; familial in 4%
Age: during first 6 weeks of life of a full-term infant (70–80%); M:F = 4–9:1; extremely rare in premature infants
Associated with: trisomy 21 (in 2%)
Location: at varying distances proximal to anus, usually rectosigmoid (in 80%)
(a) ultrashort segment (= internal sphincter) (very rare)
(b) short segment disease (80%)
(c) long segment disease (15%)
(d) total colonic aganglionosis (5%)
(e) skip aganglionosis = sparing of rectum (very rare)
  • • failure to pass meconium within first 48 hours of life
  • • intermittent constipation + paradoxical diarrhea (25%)
  • • bilious vomiting, abdominal distention
  • • rectal manometry with absence of spike activity
  • generalized gaseous distention of bowel loops
  • BE:
    • short patent colon usually of normal caliber
    • inverted cone shape at transition between abnormal
      • + normal bowel (MOST CHARACTERISTIC):
      • “transition zone” = aganglionic segment appearing normal in size (seen in 50% during 1st week of life)
      • dilatation of large + small bowel aborally from transition zone
    • normal-appearing rectum in 33%
    • marked retention of barium on delayed postevacuation films after 12–24 hours
    • 10–15-cm segment of persistent corrugated/convoluted rectum (= abnormal uncoordinated contractions of the aganglionic portion of colon) in 31% (DDx: colitis, milk allergy, normal intermittent spasm of rectum)
    N.B.: avoid digital exam/cleansing enema prior to radiographic studies!
  • OB-US:
    • dilated small bowel/dilated colon
Cx:
  1. Necrotizing enterocolitis
  2. Cecal perforation (secondary to stasis, distension, ischemia)
  3. Obstructive uropathy
Dx: suction mucosal biopsy of rectum (increased acetylcholinesterase activity)
Rx:
  1. Swenson pull-through procedure
  2. Duhamel operation
  3. Soave procedure
Hyperplastic Polyp of Colon
  • = intestinal metaplasia consisting of mucous glands lined by a single layer of columnar epithelium; NO malignant potential
Path: infolding of epithelium into the glandular lumen
Location: rectosigmoid
  • smooth rounded sessile elevation
  • usually <5 mm in diameter
Hypertrophic Pyloric Stenosis
  • = idiopathic hypertrophy and hyperplasia of circular muscle fibers of pylorus with proximal extension into gastric antrum
Incidence: 3:1,000; M:F = 4–5:1
Etiology: inherited as a dominant polygenic trait; increased incidence in firstborn boys; acquired rather than congenital condition
image
Hypertrophic Pyloric Stenosis
Infantile Form of Hypertrophic Pyloric Stenosis
Age: manifestation between 2–8 weeks of life
  • • nonbilious projectile vomiting (sour formula/clear gastric contents) with progression over a period of several weeks after birth (15–20%)
  • • positive family history
  • • palpable olive-shaped mass (80% sensitive in experienced hands, up to 14% false positive)
  • • nasogastric aspirate >10 mL (92% sensitive, 86% specific)
  • UGI (95% sensitivity):
    Precautions:
    1. empty stomach via nasogastric tube before study
    2. remove contrast at end of study
    • elongation + narrowing of pyloric canal (2–4 cm in length):
      • “double/triple track sign” = crowding of mucosal folds in pyloric channel
      • “string sign” = passing of small barium streak through pyloric channel
      • P.843

      • Twining recess = “diamond sign” = transient triangular tentlike cleft/niche in midportion of pyloric canal with apex pointing inferiorly secondary to mucosal bulging between two separated hypertrophied muscle bundles on the greater curvature side within pyloric channel
    • abnormal configuration of antrum:
      • “pyloric teat” = outpouching along lesser curvature due to disruption of antral peristalsis
      • “antral beaking” = mass impression upon antrum with streak of barium pointing toward pyloric channel
      • Kirklin sign = “mushroom sign” = indentation of base of bulb (in 50%)
    • gastric distension with fluid
    • active gastric hyperperistalsis:
      • “caterpillar sign” = gastric hyperperistaltic waves
  • US:
    • “target sign” = hypoechoic ring of hypertrophied pyloric muscle around echogenic mucosa centrally on cross-section
    • elongated pylorus with thickened muscle:
      • pyloric muscle wall thickness ≥3 mm
      • pyloric volume >1.4 cm3 (= 1/4 π × [maximum pyloric diameter]2 × pyloric length); most criteria independent of contracted or relaxed state (33% false negative)
      • pyloric length (mm) + 3.64 × muscle thickness (mm) > 25
      • pyloric transverse diameter ≥13 mm with pyloric channel closed
      • elongated pyloric canal ≥17 mm in length
    • “cervix sign” = indentation of muscle mass on fluid-filled antrum on longitudinal section
    • “antral nipple sign” = redundant pyloric channel mucosa protruding into gastric antrum
    • exaggerated peristaltic waves
    • delayed gastric emptying of fluid into duodenum
    Cx: hypochloremic metabolic alkalosis
  • DDx: