3_primer_mankad_hoey_20150316195806 Flashcards
Hepatic Artery Variants
50-60% from CHA via Coeliac axis, then CHA divides to proper HA and GDA10% CHA divides into RHA and GDA10% CHA divides into LHA and GDANormal HA velocity 30-60 cm/s; RI 0.6±0.06; continuous diastolic flow
Portal Vein
Hepatopetal, non-pulsatile, mild respiratory variationFlow velocity 20-30 cm/sDiameter 12-14 mm
Hepatic Vein
Triphasic with respiratory and cardiac variationHV sampling occurs at its confluence
Cirrhotic nodules
Regenerative (hepatocytes and stroma; not seen on US unless large; on CT are high attenuation if siderotic)Cirrhotic (regenerative nodules with surrounding fibrosis)Dysplastic (hepatic adenomas with areas of dysplasia; due to HBV and HCV)
Imaging features of Cirrhosis
Decrease size of right lobe and medial left lobe, with caudate lobe hypertrophyMRI:Regenerative nodules: high T1W, low T2W;Dysplastic: high T1W, very low T2W, with post Gd enhancement;Neoplastic: arterial enhancement with PV washout; nodule-in-nodule on T2W (high T2W neoplastic within low T2W dysplastic nodule)
Haemochromatosis
Primary (AR) due to increased uptake of transferrinSecondary - erythrogenic, Bantu siderosis or transfusional (>30 units blood)CT - high attenuation liver with low attenuation PV branchesMR - Liver low T1W and T2W relative to muscle, with susceptibility on GRE; pancreas low late in disease, spleen normal in primary but low in secondary disease
Liver Abscess
Cause: 80-90% bacterial, 5% amoebic, 50%), ofetn contain gas and 60-70 y/o peakAmoebic: due to entamoeba histolytica, usually 30-50 y/o, usually single, in peripheral right lobe and often >5 cmImaging: raised right hemidiaphragm, hypoechoic initally, then developing thick reflective wallCT signs specific to pyogenic abscess: Double target sign (enhancing wall with surrounding oedema), cluster sign (clustered abcesses)MR: Low T2W, high T2W, enhancing wall, low signal wall on T2W with surrounding perilesional oedemaNM: Uptake of sulphur colloid; Gallium taken up by pyogenic but not amoebic
Hepatic Haemangioma
Commonest benign liver lesion (70 to 80%), usually 4 cm = giant cavernous haemangioma.Associations: FNH, HHT, Kasabach-Merritt Syndrome (Haemangioma and thrombocytopaenia).Supplied from hepatic artery, may rupture spontaneously.Usually hyperechoic on US, ± posterior acoustic enhancement, no flow on DopplerCT: low attenuation with early peripheral nodular enhancement, delayed centripetal fill in to maximal at 15 minutes.MR: Sharply defined, low T1W, very high T2W, central fibrous scar, similar enhancement to CT.
FNH
Second commonest benign liver lesion, usually right lobe, FCentral scar (containing AVM), usually on liver surface, non-encapsulated ± pedunculated,, very vascular, contains Kupffer cells, non-calcifiedUS: Homogeneously hyperechoic with hypoechoic central scar in 15-20%, displaces vessels around it, enlarged central artery and peripheral draining veins visible on DopplerCT: Ill-defined, transiently high attenuation in PV phase with gradual equilibration, central scar on delayed, ‘spoke-wheel’ pattern in 20-30%MR: Isointense on T1W and T2W, central scar hypointense on T1W and hyperintense (in 75%) on T2W; initial Gd avid enhancement with gradual equilibration (early enhancement of central scar); SPIOd (Kupffer specific) cause lesion enhancement
Hepatocellular adenoma
Women on COCP and men on anabolic steroids, 20-40 y/o, usually 5-10 cm, subcapsular in right lobeContain mixture of hepatocytes, Kupffer cells and fat, but no portal tracts; usually contains haemorrhage and necrosisUS: Heterogeneous, solid, with hypoechoic rimCT: well defined, ±hyperdense if areas of haemorrhageMR: can’t be distinguished from HCC, predominantly hyperintense T1W and isointense T2WNM: Photopaenic on sulphur colloid, no uptake on Gallium
HCC
Commonest visceral malignancy, peak 60-70 y/o;Solitary (30%), Multifocal (60-70%) and diffuse (5%) forms; invades PV in 50-60% and IVC in in siderotic noduleLarge HCC: Mosiac pattern (confluent nodules, small septae, best seen on T2W), tumour capsule (hypointense) in 60-80%, extracapsular extension with satellite nodules in 50-70%, tumour thrombus as high T1W and T1 GRE in PV, with arterial enhancementNM: photopaenic on sulphur colloid, avid uptake on Gallium
Fibrolamellar HCC
No RFs for HCC, 30-40 y/oSolitary lobulated lesion, central scar, pseudocapsule of hepatic tissue, central amorphous calcification in 30-40%Regional LNs 50-60%, rarely metastasises, no vascular invasionUS: Heterogeneous with hyperechoic central scarCT: Lobulated enhancing mass with non-enhancing central scarMR: Hypointense T1W, hyperintense T2W with heterogenous enhancement; scar hypointense on T1W and T2W and non-enhancing
Liver metastases
Usually colon, breast, lung or pancreas; solitary in 10%, both lobes in 75%US: variable, echogenic usually GIT or GU; no Doppler flow except with carcinoidExclusion criteria for metastatectomy - advanced primary, >4 metastases, extrahepatic metastases, <30% liver remaining post surgeryCalcified liver metastases: gastric, melanoma, RCC, colon, ovarianHypervascular metastases: thyroid, renal, carcinoid, melanoma, pancreatic islet cellHaemorrhagic metastases: Colon, thyroid, breast, choriocarcinoma, melanoma
Budd Chiari Syndrome
Hepatic vein of IVC obstruction, 60-70% idiopathicCauses of thrombotic obstruction (5 P’s): Pregnancy, Pill, Polycythaemia Rubra Vera, abnormal Platelets, PNHNon-thrombotic obstruction: Right heart failure, constrictive pericarditis, right atrial tumour, IVC membraneUS: Hepatosplenomegaly, ascites, caudate lobe hypertrophy, ascites, prominent portosystemic anastomoses and azygos/hemiazygos systems, absent / reversed flow in hepatic veins, hepatic arterial resistance index >0.7CT: Heterogenous liver enhancement, caudate large and normally enhancing, poor opacification of hepatic veins
Hepatic veno-occlusive disease
Post radiation / chemotherapyMR: occlusion of centrilobular venules without major hepatic vein thrombosisUS: Bidirectional flow in portal veins without hepatic vein / IVC obstruction, GB wall thickening
Portal vein thrombosis
Causes: idiopathic (neonates), malignancy (in 30% of HCC, also cholangioCa, pancreatic Ca, liver metastases), hypercoaguable, trauma (iatrogenic - umbilical vein catheter), peritonitis, pancreatitis, ascending cholangitisUS: Echogenic material on PV, increased PV diameter, thickened lesser omentum
Peliosis hepatis
Rare benign dilatation of sinusoidal blood filled spaces in reticuloendothelial system (liver, spleen, marrow, lymph nodes, lungs)Causes: AIDS, TB, Anabolic steroids, CRF, tamoxifenUS: Multiple hyper-/hypoechoic areasCT: Enhancing, round lesions in organs; initially low attenuation then isoattenuating with time
Biliary anatomy
RPHD into LHD 20%RPHD, RAHD, LHD trifluence 10%75% cystic duct inserts into middle third of extrahepatic CHD, 10% distal CHDCBD / PD / Ampulla - 75% Y, 25% V, 5% UCHD measured at level of HA, normal <7 mmSecretin transiently distends pancreatic duct (maximal at 2 minutes post injection) prior to MRCP
Choledochal cysts
Cystic dilatations of CBD; 30-40% present at <1 y/o.Clinical features: Intermittent obstructive jaundice, RUQ pain and RUQ mass (25% triad)Associations: Biliary, pancreatic anomalies and liver cysts
Caroli’s disease
Segmental dilatation of intrahepatic bile ducts, autosomal recessive, causes biliary stasis with intrahepatic calculi then secondary pyogenic cholangitis, intrahepatic abscesses, increased risk cholangiocarcinomaAssociations: Medullary sponge kidney (80%), Infantile polycystic kidney disease’Central dot sign’ - specific, portal radicals surrounded by abnormally dilated / ectatic bile ducts
Chemotherapy cholangitis
Most commonly associated with floxuridine; strictures of CHD and bifurcation, sparing of distal CBD
Cholelithiasis
Cholesterol (70-80%) but 70% mixed, 20% radiopaque, associated with cirrhosisPigment (30%) 2-5 mm, faceted, calcium bilirubinate, 50% radiopaqueWall-echo-shadow complex (double arc sign) when GB contracted over GS (but also seen with porcelain GB and emphysematous cholecystitis)Sludge (echogenic bile) - 100% fasting patients at 6 weeks (decreased CCK)
Biliary Enteric fistulae
Most commonly biliary-duodenal (70%; can cause GS ileus)Causes: Chronic cholecystitis with GS erosion into GIT (90%), Penetration of posterior DU into CHD (5%)
Bouveret syndrome
Obstruction of stomach or duodenum by GS
Mirizzi syndrome
Obstruction of CHD by stone in cystic duct; causes cholecystitis
Complications of Acute cholecystitis
Usually GB wall > 3 mm, lumen distended > 4 cmMurphy’s sign 60% sensitive, 90% specific95% calculous, 5% acalculous (GB dysmotility with bacterial superinfection)Gangrenous cholecystitis (rupture), 20% mortality but neural death causes 60% Murphy’s negativeEmphysematous cholecystitis (ischaemia due to inflammation / vasculitis, rare; pneumobilia and air around GB on PFA; 40% diabetic)EmpyemaGS ileus
Xanthogranulomatous cholecystitis
Thickened GB wall with intramural nodules; can mimic adenoCaUsually 70-80 y/o femaleComplications (30%) - perforation, abscess, fistulae
Porcelain GB
Usually due to chronic cholecystitis (GB doesn’t react to CCK)Increased risk GB Carcinoma (15% lifetime risk)
GB US in AIDS
Hepatosplenomegaly (30%), ascites (15%), lymphadenopathy (20%)GB wall thickening (7%; may be due to acalculous cholecystitis due to cryptosporidium, CMV)GS (6%)
Cholangitis
Infection of obstructed bile ducts E coli > klebsiella > pseudomonas; 80-90% supparative60% due to GS or post surgical strictures, but can be due to ampullary tumour
PSC
Chronic obliterative fibrosis of biliary tree, usually mostly intrahepatic, always involves CBDString of beads on cholangiogram, pruning of biliary tree10% risk cholangiocarcinoma; can also cause biliary cirrhosis.Associations: IBD, pancreatitis, Sjogrens, RPF, Peyronie’s
Strawberry GB
Deposition of triglycerides and macrophages in GB wall, studded ‘strawberry’ appearance of wall (<1 mm echogenic lipid deposits, multiple 0.5 mm polyps)
GB adenomyomatosis
Hyperplasia GB wall, enlarged Rokitansky-Aschoff sinuses, hypercontractile wall
GB adenomas
10% multiple, F>M, usually 5-20 mm, 60% associated with GSAssociated with Peutz Jeghers, FAP
Cholangiocarcinoma
Usually at hilum or distal CBD (30-40%)Associations: GS (90%), PSC, Caroli’s disease, Biliary atresia, IBD (UC > Crohns), Porcelain GB (15% risk), familial polyposis, adult polycystic kidney disease, clonarchis (asians), toluene exposureIntrahepatic: Mass with satellite nodules, dilated biliary tree with hyperechoic mass; Klatskin tumour - at confluence of RHD and LHD (causing segmental dilatation of main ducts, PV obstruction and lobar atrophy)Extrahepatic: 10% present with cholangitis, pure intrahepatic biliary dilatation
GB Adenocarcinoma spread
Direct invasion of liver (50%), liver metastases (5%)Direct invasion of duodenum (50%)Carcinomatosis (50%)
Von Meyenburg Complex
Bile duct hamartoma, usually 1-5 mm, composed of disorganised bile ducts and fibrocollagenous stroma
Pancreas Divisum
Lack of fusion of dorsal and ventral pancreatic ducts, 10% of population.Main pancreatic drainage is through the minor papilla (too small to handle secretions).25% of patients with recurrent idiopathic pancreatitis have pancreas divisum.
Annular Pancreas
Abnormal migration of the ventral pancreas, surrounds and obstructs second portion of duodenumERCP: pancreatic duct encircles the duodenum. Increased incidence of pancreatitis and peptic ulcer disease.
Complications of pancreatic trauma
Pancreatic fistula, 10%-20%Abscess, 10%-20%PancreatitisPseudocyst, 2%
Types of Pancreatitis
Acute pancreatitis Mild acute pancreatitis (interstitial edema)Severe acute pancreatitis (necrosis, fluid collections)Groove pancreatitis: inflammation localized to groove between duodenum and pancreatic headChronic pancreatitis
Pancreatic necrosis
Diffuse parenchymal (30% area) or focal (>3 cm) nonviable; CT 80-90% accuratePrognosis (necrosis/mortality): 30/8, 50/24, >90/50Infected necrosisRequires surgical debridement, can occur at any time, worse prognosis than pancreatic abscess.HamorrhageLate consequence, erosion into splenic or pancreaticoduodenal arteries or rupture of psuedoaneurysm
Acute fluid collections pancreatitis
40% of pancreatitisNo fibrous capsule, usually within and around pancreatic periphery50% spontaneously resolve, remainder bocome pseudocysts or develop other issue.
Pseudocyst
Encapsulated collection of pancreatic fluid due to microperforation of pancreatic duct (communication seen at ERCP in 50%), must persist at 6 weeks post onset.40% acute pancreatitis, 30% chronic pancreatitis
Pseudocyst prognosis
Prognosis (<5 cm - monitor; otherwise percutaneous drainage; 10% risk superinfection)50% resolve spontaneously20% stable30% other complicationsDissection into adjacent organsHaemorrhage (vessel erosion, thrombosis, pseudoaneurysm)Peritonitis (rupture)Biliary obstructionInfection (abscess) - forms at 2-4 weeks, usually E coli, polymicrobial or candida if immunosuppressed; Percutaneously drained.
Emphysematous pancreatitis
Pancreatitis with superinfection, usually E Coli; high morbidity and mortality but usually resolves with conservative treatment
Chronic pancreatitis Types
Calcifying (alcohol, hyperparathyroisim/hypercalcaemia, hyperlipidaemia, hereditary pancreatitis, juvenile tropical pancreatitis)Obstructive (Trauma, Renal failure, CF, Sclerosing cholangitis, Ampullary tumour, ampullary stenosis)FeaturesFatty replacement, fibrosis, parenchymal calcifications (usually start in head), intraductal calculi.Irregular dilatation pancreatic duct (Grade 1-3)
Complications of chronic pancreatitis
Malabsorption (50%)Pseudocyst (30%)Obstructed CBD (10%)Venous thrombosis (splenic, portal, mesenteric) (5%)Increased risk carcinoma
Autoimmune pancreatitis
Previously idiopathic pancreatitisHistologic diagnosis: dense lymphoplasmacytic infiltrate with scattered eosinophils. May be associated with autoimmune cholangitis. Treatment: steroids.Imaging: diffuse enlargement of pancreas, loss of normal surface indentations, tail retracted from splenic hilum, capsule-like rim enhancement around gland, peripancreatic adenopathy, no calcification, vascular encasement of CBD dilatation
Groove pancreatitis
Involves pancreatic groove (between pancreatic head, duodenum and CBD)Related to PUD, previous gastric resection, duodenal wall cysts, pancreatic heterotopiaBiliary strictures in 50%Imaging: Soft tissue in the pancreaticoduodenal groove with delayed enhancement; small cystic lesions along medial wall of duodenum
Tropical Pancreatitis
Young, no C2H5, usually malnutrition, rapidly progressive, large intraductal calculi (>5 cm), x15-25 increased risk adenoCa
Hereditary Pancreatitis
AD, cationic trypsinogen gene mutation, 50-70x risk pancreatic adenocarcinomaSimilar to tropical pancreatitis on imaging
Heterotopic pancreatic tissue
Duodenum (30%)Stomach (25%) - usually submucosal along greater curveJejunum (15%)Rarely - Meckel’s, ileum, GB, fallopian tubes, umbilicus, oesophagus, spleen, mediastinum, omentum
Pancreatic Ductal Adenocarcinoma
95% pancreatic cancer; Couvosier’s sign (enlarged, nontender GB) in 25%; 8% 1 year survival65% head (5% curable), 35% body and tail (incurable)May be subtle hypodense on NECT, then hypodense on bolus contrast CT; calcifications rare; inverted 3 on barium meal.
Pancreatic AdenoCa unresectability
Criteria for unresectabilitySMA encasedPortal vein or SMV largely encasedMetastases: Liver > LNs > pertioneal/serosal > lung
IPMN / IPMT
From epithelial lining pancreatic duct, secrete mucin, cluster of cysts 1-2 cm diameterPresents with abdominal pain ± pancreatitisCan be side branch (30%; usually in uncinate) or main duct or combined (70%)Associations - AdenoCa (25%), Hyperplasia (25%), Dysplasia (50%)Location: Head/uncinate (55%), Body/tail (10%), Multifocal/diffuse (35%)Increased risk of malignancy:Size > 3 cm or solitary and < 3cmSolid mass or mural noduleMain pancreatic duct > 10 mmIntraluminal calcificationsDiffuse or multifocalHx of DM
Pancreatoblastoma
Usually 1-8 y/o, rareSometimes associated with Beckwith-WiedemannLarge, well-defined, multilobulated with enhancing septa
Solid pseudopapillary neoplasm
Aka Frantz’s tumour, usually female <50 y/oLarge epithelial well-demarcated mixed solid/cystic haemorrhagic mass
Acinar cell carcinoma
Older males, usually larger and less desmoplastic than adenoCa, invades vessels, causes metastatic fat necrosis.
Insulinoma
Most common islet cell tumour, usually 40-60 y/o, 90% sporadicSingle 90%, multiple 10%, diffuse hyperplasia / extrapancreatic 10%Malignant 10%90% < 2 cm but 70% hypervascularDiagnostic accuracy: intraoperative US > venous sampling > angiography > MRI > othersWhipple’s triad at presentation: symptoms of hypoglycaemia, hypoglycaemia, relief with glucose
Gastrinoma
Second most common islet cell tumour, usually <20 y/o, 70% sporadic, presents with Zollinger-Ellison (diarrhoea, PUD)Usually benign (although 60% can have malignant transformation) but if MEN I then malignantUsually pancreatic head, but 30% ectopicGastrinoma triangle: Porta hepatis at apex, D2 and D3 as baseMean size = 3.5 cm
Non-functioning islet cell tumour
Third most common islet cell tumour, associated with MEN I, peak age > 20 y/o80-100% malignant transformation (5 year survival 45%)Usually in pancreatic head, > 5 cm, hypervascular with hyperenhancing liver metastases, and 20% show calcification
Glucagonoma
75% malignant, almost all symptomatic, associated with MEN IUsually 50-79 y/o, F>MUsually pancreatic body or tailPresents with Necrolytic Erythema Migrans (80%), Diarrhoea, DM, glossitis, VTE (25%)50% develop liver metastases
VIPoma
67% female, 60% malignant, 59% liver metastases at presentationUsually pancreatic body/tail but extrapancreatic sites - RP, mediastinum in children (usually from neurogenic tumour)Presents with Verner-Morrison’s syndrome: watery diarrhoea, hypokalaemia, hypochlorhydriaOften causes GB dilatation due to VIP causing smooth muscle paralysis
Somatostatinoma
90% malignant, usually pancreatic headPeak 50 y/o, presents with DM, steathorrhoea (suppresses insulin, TSH, GH secretion)
Pancreatic metastases
RCC (usually hypervascular), lung, breast, GIST, melanoma, carcinoid, adrenal, thyroid, angiosarcomaUsually head of pancreas
MEN
I (Wermer’s): PTH, pancreas (islet cell), anterior pituitary ± mutiple limpoas and angiofibromasIIA (Sipple’s): Commonest MEN, usually RET oncogene positive; causes medullary C cell thyroid carcinoma, phaeochromocytomas (70% bilateral), PTH gland hyperplasia; associated with carcinnoid and Cushing’s syndromesIIB: 5% of MEN II, marfanoid features, mucosal neuromas; medullary thyroid carcinoma, phaeochromocytomas, oral and intestinal mucosal neuromas, intussusception due to small bowel neuromas
Carney’s Complex
Rare form of MENPresents with primary pigmented adrenocortical disease, pituitary adenomas, sertoli cell tumours, thyroid nodules, cardiac myxomas, schwannomas
Whipple’s Surgery and complications
Resection of pancreatic head, duodenum and gastric antrum, usually with cholecystectomy;Usually jejunal loop used to anastomose resected portionsComplicationsDelayed gastric emptying (11-29%): NG tube required > 10 daysPancreatic fistula: surgical drain output of amylase rich fluid at >5 mL/day at >7-10 days (10-15% require percutaneous drainage, 5% require further surgery)Infection, abscess, haemorrhage, pancreatitis
Pancreatic transplant
Duodenal interposition between pancreas and bladder, duodenocystostomyComplications:Rejection (35%)Pancreatitis (35%)Peripancreatic abscess (35%)Peripancreatic haemorrhage (35%)Vascular thrombosis (20%)
Oesophageal atresia / Types of tracheo-oesophageal fistula
A: Atresia without fistula (10%)B: Atresia with proximal TOF (<1%)Polyhydramnios: 33% of fetuses with atresia and distal TOF, 100% of atresia without fistulaGasless stomach: Type A and BRight sided aortic arch in 5% of TOF patients
Iatrogenic TOF
Usually at carina, can be caused by ET cuff; also by blunt trauma
Malignant TOF
Usually oesophageal malignancy; less likely lung Ca, SCC larynx50% trachea, 40% bronchi
Oesophageal Cancer
4-10% GI malignacy, M/F = 4/1;SCC 50-70%, Adenocarcinoma 30-50%20/30-40/30-40 = upper/middle/lower thirdsT: 3=adventitia, 4=adjacent structuresEUS best for local staging
Oesophageal Cancer Unresectability Criteria
Pericardial effusionIntraluminal airway massTumour between arch and trachea or left main bronchus and descending aortaPleural thickening or pleural effusion adjacent to tumourMediastinal or coeliac axis nodes
Oesophageal perforation
55 % iatrogenicif upper oesophageal, usually at cricopharyngeus, causing widening of prevertebral fascia, air/fluid and a right pleural effusion
Boerhaave’s syndrome
Failure of cricopharyngeus to relax with pressure rise and ruptureUsually tear at left posterolateral wall of lower oesophagus 2-3 cm proximal to GOJSecond commonest rupture at upper thoracic area or subdiaphragmatic30% mortality but better surgery at 24, 90% at >48 hoursCXR 90% abnormal, usually a unilateral effusion
V sign of Naclerio
Only in 20% Boerhaave’s, but specific - air in space between heart and vertebral column, thus left paraspinal hyperlucency
Oesophageal ring
3-5 mm extension of 3 layers (mucosa, submucosa, muscle)A: 1.5 cm proximal to z lineB (Scatzki): technically web as only mucosa and submucosa, at z line, upper limit of HHC: Rare anatomical variant, represents indentation of diaphragmatic crura
Oesophageal strictures
Peptic (70-80%), originate from z line, 1 to 4 cm long, whites increased risk x10, M/F = 2.5/1Smooth: Inflammatory (peptic, scleroderma, corrosive), Neoplastic (Ca, leiomyoma), Achalasia, Skin (Epidermolysis Bullosa, pemphigus)Irregular: Neoplastic (Ca, leiomyosarcoma, lymphoma), Inflammatory (acid reflux, Crohn’s), Iatrogenic (Radiotx, fundoplication)
Oesophageal varices
Due to increase of portal pressure above normal (i.e. >10 mm Hg)Gastrooesophageal varices: Left gastric (coronary) vein and short gastric veins (via splenic hilum)Paraoesophageal varices: outside oesophageal wall
GORD and HH’s
Grades: I - erythema, II - linear non-confluent erosions, III - circular confluent erosions, IV - stricture, BOSliding HH - >1.5 cm difference between GOJ and diaphragmParaoesophageal HH - fundus herniates and GOJ remains below diaphragmType 3 HH - combined sliding and paraoesophagealType 4 HH - All / part of stomach with some organoaxial rotation
Barrett’s Oesophagus
Squamous to columnar metaplasia, 0.5%/year progression to AdenoCa (not reduced by fundoplication), thus oesophagectomy indicated if dysplasia confirmed by second pathologistRF: GORD, HH (75-90%), reduced LOS pressureReticular pattern on Ba swallow, strictures occurs at squamocolumnar junction (usually short, tight and eccentric)
Candida Oesophagitis
Usually oral thrush but absent in 25%Tends to be in upper oesophagus and longitudinally orientated plaques, progresses to ‘shaggy’ confluent plaques and pseudomembranes in AIDS patients, can dissect with contrast - ‘double barrel’ oesophagus
Tuberculous oesophagitis
Erosion of enlarged mediastinal nodes into oesophagus, causing shallow ulcers and heaped up lesions with extrinsic oesophageal compression
CMV Oesophagitis
Severe odynophagia and dysphagia, evidence of dissemination≥1 giant superficial diamond/ovoid/serpiginous erosion in mid/distal oesphagus, may be up to 5-10 cmCan have satellite ulcers and halo of oedematous tissue
HSV Oesophagitis
Second commonest, usually rounded 1-3 mm vesicles in mid-distal oesophagus with halo of oedemaCan be indistiguishable from candida if advanced (plaques, cobblestone, shaggy)VZV can be similar but has an associated skin rash (shingles)
HIV Oesophagitis
Acute onset odynophagia, maculopapular rashGiants flat ulcers ≥1 cm with satellite ulcers and rim of oedema (very similar to CMV)Can result in perforation, fistulae, superinfection
Oesophageal Leiomyoma
Commonest benign oesophageal tumour, usually distal oesophagus (smooth muscle)Can be associated with HPOA, can show calcification
Zenker’s diverticulum
Between inferior constrictor and cricopharyngeus, usually at posterior left oesophagus
Alport’s
Multiple oesophageal leiomyomas, sensorineural deafness, renal impairment
Grades of Candida oesophagitis
Grades - 1: Few raised plaques ≤2 mm, no ulceration2: Multiple raised white plaques >2 mm, no ulceration3: Confluent linear nodular elevated plaques with ulceration4: Grade 3 with stricturing, thus narrowed oesophageal lumen
Lateral pharyngeal pouch and diverticulum
Occurs in glass blowers and musicians through thyrohyoid membrane at anterolateral upper hypopharynx
Lateral cervical oesophageal pouch and diverticulum
Through Killian Jamieson space below cricopharyngeus, usually asymptomatic
Tertiary oesophageal contractions
Non-propulsive, usually due to muscle atrophy, in 25% >60 y/oCauses: Reflux, presbyoesophagus, neuropathy, DM, alcohol, malignant infiltration or gastric cardia obstruction, early achalasia
VACTERL
3 or more of following anomaliesVertebral: hemivertebrae, scoliosis, rib deformitiesAnorectal: Imperforate anus, cloacal deformityCardiovascular: VSD, tetralogy of Fallot, PDA, ASD, AV canal defects, aortic coarctation, right sided aortic arch, single umbilical arteryTracheo-oesophageal: Oesophageal atresiaRenal: renal agenesis (Potter’s syndrome, bilateral agenesis), horseshoe kidney, polycystic kidneys, urethral atresiaLimb: Radial dysplasia/absence, syndactyly, polydactyly, tibial deformities
Phlegmonous Gastritis
Rare, due to strep, staph, proteus, clostridium, E ColiUsually debilitated patients; often recent alcohol binge, URTI and AIDS
Emphysematous Gastritis
Widespread phlegmonous gastritis, with mucosal disruption and gas in stomach wallFoul smelling bloody vomit with necrotic cast of stomach (pathognomic)
Corrosive gastritis
Acid: Severe gastric damage, oesophagus unharmedAlkali: Pylorus and antrum usually involved
Gastric cancer
3rd commonest GI malignancy, 95% adenoCa, 5 year survival 5-18%Usually distal third or cardia; 60% lesser curve, 10% greater curve, 30% GOJT Stage: 3 penetrates serosa, 4a invades contiguous tissues, 4b adjacent organs / diaphragm / abdominal wallRFs: Smoking, nitrates, H Pylori, atrophic gastritis, pernicious anaemia, Menetriers, gastrojejunostomy/partial gastrectomyMetastases: Liver (25%), peritoneal seeding to rectum (Blumer’s shelf), ovaries (Krukenberg), left suprclavicular (Virchow’s node)
Peptic Ulcer
Risk of malignant transformation 2% in initial 3 yearsGastric: Pain after eating, if benign usually on lesser curve, project beyond stomach contour, mucosal folds radiating to ulcer marginMalignant ulcer - irregular, heaped up margins, protrude into lumen of stomachDuodenal: Pain relieved by food, occurs hours after meals and at night, 95% in D1, usually <1 cm
Gastric volvulus
Subdiaphragmatic (30%) or Supradiaphragmatic (60%; associated with paraoesophageal rolling HH)Axis: organoaxial (60%; axis of rotation parallel to lesser curve; 30% necrosis) or mesentroaxial (30%; axis perpendicular to lesser and greater curves; usually intermittent and vascular compromise rareSevere pain and retching without vomiting, can’t pass NG tube
Pyloric Stenosis
Inherited as dominant polygenic trait, higher incidence in first born malesCauses hypokalaemic, hypochloraemic metabolic alkalosisUsually presents at 2-8/52 with non-billous projectile vomiting and palpable olive shaped massUS: Target sign (hypoechoic ring of hypertrophied pylorus around echogenic central mucosa), elongated pylorus (≥17 mm), increased pyloric muscle wall thickness (≥3 mm), pyloric transverse diameter ≥13 mm
GIST
Commonest mesenchymal GI neoplasm, 50-70% in stomach, then SI, mesentery, omentumSubmucosal and endophyticAssociations: NF1, Carney’s triad (GISTs, pulmonary chondromas, extra-adrenal paragangliomas)CT: Rim or homogenous enhancement, ±calcification and necrosis
Causes of Linitis Plastica
Neoplastic: Gastric carcinoma, lymphoma, metastases, local pancreatic cancer invasionInflammatory: Corrosives, radiotherapy, granulomas, eosinophliic enteritis
Causes of gastric target lesions
Submucosal metastases (melanoma, lymphoma, carcinoma, carcinoid)LeiomyomaEctopic pancreatic tissue (pancreatic rest)Neurofibroma
Haemoperitoneum
Serum: 0-20 HUFresh unclotted: 30-45 HUClotted: 50-100 HUActive Bleed: >180 HUSentinel clot - highest attenuation clot, site of injury
CT Signs of hypovolaemia
Collapsed IVC (20 HU above liver, with peripancreatic oedema, mesenteric and RP fluid collectionsIntense adrenal enhancement (>IVC)Mucosal enhancement of GB and bowel (shock bowel - >psoas muscle, >3 mm mural thickening, fluid filled/dilated >2.5 cm)
Sites of blunt bowel trauma
In order of decreasing frquencyJejunum distal to ligament of TreitzDuodenumAscending colon at ICVDescending colon
Bowel injury signs on CT
Extraluminal contrast 100% Sp, low Sn; extraluminal air 40-50% Sn, usually duodenal injuryBowel wall thickening 75% transmural injuries, high Sn, may also be seen in isolated mesenteric lacerationsMesenteric stranding particularly on mesenteric borderHaemoperitoneum and haematoma in mesenteryFree fluid on three contiguous sections suggests significant bowel or mesenteric injury5% hepatic and splenic lacerations associated with major bowel injuryFocal discontinuity of bowel wall
Malrotation
Arrest of gut rotation and fixation, can cause midgut volvulus and duodenal obstructionCT: SMV on left of SMA in 80%
Spigelian hernia
Ventrolateral hernia through defect in aponeurosis of transverse and rectus muscles
Lumbar hernias
GrynfeltPetit’s lumbar triangle
Obturator hernia
Between pectineus and external obturator
Inguinal hernia
Direct: via defect in Hesselbach’s triangle, medial to inferior epigastric vesselsIndirect: via inguinal canal, lateral to inferior epigastric vessels
Richter’s hernia
Entrapment of anti-mesenteric border of bowel in hernial orifice, usually older women in femoral hernia
Internal hernias
Via developmental or surgical defect in peritoneumParaduodenal - congenital defect in descending mesocolonLesser sac - via foramen of Winslow in retrogastric locationHiatus hernia - 99% sliding (GOJ in chest), 1% paraoesophageal (GOJ below diaphragm, upper stomach in chest)
Duodenal diverticulum
Commonest at D1, can cause perforation, biliary or bowel obstruction, bleeding, diverticulitisPrimary: Mucosal prolapse through muscularis propriaSecondary: All layers of duodenal wall, due to duodenal inflammation
Cobblestone duodenal cap causes
Big cobblestones: Hypertrophy of Brunners glands, Crohn’s, Varices, Carcinoma, lymphomaSmall cobblestones: Food residue, duodenitis, nodular lymphoid hyperplasia, heterotopic gastric mucosa
Decreased or absent duodenal folds
AmyloidCrohn’sCFSclerodermaStrongyloidiasis
Thickened duodenal folds
Inflammation: Crohn’s, duodenitis/pancreatitis, Zollinger EllisonInfiltrative: Neoplastic (Metastases, lymphoma), eosinophilic enteritis, amyloid, mastocytosis, Whipple’sVascular: Intramural haematoma, ischaemiaOedema: Hypoproteinaemia, venous/lymphatic obstruction, angioneurotic oedemaInfective: Worms, giardiasis
Causes of duodenal dilatation
Mechanical obstruction (bands, atresia, annular pancreas, SMA syndrome)Paralytic ileusScleroderma
Intestinal lymphoma
Commonest SI malignancy, commonest cause of intussusception in children >6 y/oRFs: Coeliac, AIDS, SLE, Crohn’s, chemotherapyLarge cavitating ulcerating / nodular mass with aneurysmal SI dilatationPoor prognosis unless low grade, MALToma = low grade B cellCT: Polypoidal / nodular (47%), diffuse infiltrative (11%; reduced peristalsis), ulcerative (42%; can perforate)Staging: I - Bowel wall, II - local nodes, III - widespread nodes, IV - disseminated (e.g. liver, marrow)SI locations (arise from Peyer’s patches): 51% ileum, 47 % jejunum, 2% duodenumCan cause desmoplastic responeseEndoexoenteric lymphoma: large mass, small intramural component, can cause fistulation
Gastric lymphoma
Presentation of 2.5% of lymphomas, commonest site of extranodal spreadCan have nodular mass (25%), diffuse involvement without ulcers (50%), ulceration (8%)
Colonic lymphoma
85% caecum
Carcinoid
Commonest SI primary; 2% 2 cm metastasise (usually ileal)33% small bowel (81% ileum, 7% jejunum, 2% duodenum, 10% gastric), 45% appendix (rarely metastasises)33% second primarySecretes 5-HIAA, ACTH, histamine, serotonninGastric: Usually solitary fundal lesion, 50-70% metastases at presentationDuodenal: Intraluminal polypoid (50%) or intramural (40%), arterial enhancement with delayed washout (unlike ampullary tumours)Jejunal/ileal: Can cause invasion, fibrosis, ‘hairpin turn’ in bowelMetastases: Liver, LNs, lung, bone
Coeliac Disease
Bimodal: 1-3 y/o and 30-50 y/o, F/M = 2/1Primarily involves SI mucosa with atrophic villi with elongated crypts, typically worse in jejunum than ileumDiagnosis: Reversal of jejunal/ileal fold pattern (due to ileal hypertrophy; jejunal atrophy (≤3 folds per 2.5 cm in first jejunal loop, with increase in ileal folds) + 3 of: fold thickening, SI dilatation, flocculation (hypersecretion, 20-30%)Can cause gastric metaplasia in duodenum with mucosal nodules (bubbly bulb)Extraintestinal features: anaemia, osteopaenia, dermatitis herpetiformis, amenorrhoeaComplications: Ulcerative jejunitis (usually fatal), Intussusception, cavitating lymph node syndrome, hyposlenism and splenic atrophy (30-50%), small bowel lymphoma, adenoCa of SI/rectum/stomach, Oesophageal SCCAssociations (10%): Autoimmune thryoiditis, Sjogren’s
Whipple’s Disease
Gram positive tropheryma whippelii disordered host response, usually immunocompromised patients, M/F = 8/1Muscle wasting, arthralgia, fever, diarrhoea, pericarditisPositive periodic acid Schiff macrophagesFatal in <1 year if untreated by antibioticsMinimal bowel dilatation, thickened jejunal and ileal folds, bulky hypodense LNs
Radiation enteritis
Required dose: 45-60 Gy SI, 55-80 Gy colonAcute (within 6-24 months) severity function of dose, field and type; chronic of cumulative doseRFs: HTN, DM, PID, combination chemo-radiotherapy, previous abdominal surgerySubacute phase (2-12 months) due to obliterative endarteritis of small vesselsChronic (>1 year) fibrosis, adhesions, fistula, increased mesnteric attenuation
Radiation injury of stomach
Usually 45-60 Gy over 5 weeksAcute phase - 2-8 weeks post Rx; chronic 4 weeks to 7 months post RxTypes: 1. Prepyloric or Pyloric ulceration - Usually acute, indistiguishable from benign ulcers2. Antral narrowing - chronic injury, no ulceration, may mimic gastric cancer
Radiation injury colon and rectum
Increase presacral space >1 cm, thickening/effacement valves of Houston, halo effect on CT (increased attenuation prerectal fat and fibrous tissue)
GvHD
Loss of haustrations, tubular SI, persistent coating of bowel mucosa by barium, reduced transit
Appendicitis
Causes: faecolith obstruction (33%), lymphoid hyperplasia, foreign body, parasites, tumourUS: Wall thickness >2mm, graded compression 85% Sn, 92% SpCT: 87-100% Sn, 89-98% Sp, >7 mm diameter
Meckel’s Diverticulum
Persisting omphalomesenteric duct on antimesenteric ileal border; 50% contain ectopic mucosa (gastric, pancreatic, coloonic)Rule of two: 2% population, 2 inches long, 2 feet from ICV, symptomatic before 2 y/o (but 20-40% asymptomatic)Compilcations: Bleeding, intussusception, obstruction, malignancyTc99m: 85% Sn, 95% Sp (but drops with age as less gastric mucosa in Meckel’s with age)Angiogram: Identification of vitelline artery is pathognomic
Chronic mesenteric ischaemia
> 95% due to diffuse atherosclerotic disease, causes mesenteric anginaTreatment: Coeliac/SMA endartectomy, bypass, mesenteric artery reimplantation (not recommended)
Epiploic appendagitis
Abrupt onset pain in RLQ (50%), palpable mass 10-30%CT: pericolic oval 1-4 cm mass; hyperechoic on US with hypoechoic marginPrimary: due to torsion or venous thromboisSecondary: inflammation of adjacent organ
Infective TI lesions
TB, yersinia, Actinomycosis, histoplasmosis
Ischaemic Colitis
Non-occlusive but blood flow s point - anastomotic plexus between IMA and hypgastric supply at rectosigmoid junctionCT: Segmental thickening, portal/mesenteric gas
Pseudomembranous colitis
C Difficile - GPB, anaerobic and spore forming; Toxins A (enterotoxin) and B (cytotoxin), 25% mortality in elderlyUsually due to cephalosporins, ampoicillin, amoxicillin, clindamicinPancolitis (50%), right sided colitis (27%), isolated rectosigmoid (12%), but rectosigmoid spared in 67%Stool cytotoxin 94% Sn, 99% Sp; 2-10 m yellow pseudomembranes on endoscopyComplications: fulminant colitis (3%), toxic megacolon, colonic perforation, peritonitisCT: Mural thickening, bowel dilatation, paucity of pericolonic inflammation
Diverticular disease
Mucosal herniations through intestinal layers/smooth musclle via vasa recta apertures; 70-80% >80 y/o10-25% risk of diverticulitisComplications: Abscess, fistula (14%), perforation, sepsis, bleeding (more likely in diverticulosis)
Colonic polyps
Colonic mucosal outgrowths, 1.5 cm, have 10% risk of containing invasive cancerCT colonography detects 80% large polyps, colonoscopy 80-90% sensitive
Colorectal carcinoma
RFs: Family history, polyps (30-40% villous, 5% tubular), IBD, prominent lymphoid follicular pattern, obesity, asbestos, Lynch syndromeLocation: Rectum (30%), sigmoid (30%), descending (10%), transverse (10%), ascending (10%), caecum (10%)Metastases: Liver (75%), adrenal (10%), lung (5-50%), ovary (5%), bone (5%), brain (5%)Dukes staging (5 yr survival): A (85%) - mucosa, B (70%) - muscularis propria, C (33%) - lymph nodes, D (5%) - metastases33% recurrence, half within one year, 60% locally (risk reduced by radiotx)
Crohn’s disease
RFs: Family history, smoking, OCPComplications: sinus tracts (15%), bowel obstruction (20%), fistulae (50%), malignant transformation (usually adenoCa)Ulceration usually along mesenteric bordersCobblestoning causes reticular pattern’String sign’ due to stricturingMesenteric stranding does not necessarily correlate with disease activity
Ulcerative colitis
Crypt abscess formation, inflammation usually progresses proximally from rectum, can cause backwash ileitis (incompetent ICV), benign strictures in 10% with chronic diseaseCRC risk increases by 0.5-1% per year after 10 years;Toxic megacolon (2%) - dilatation >9 cm in caecum, 10 cm in transverse colon carries high risk perforationBa enema (while quiescent): rose thorn ulcers, collar button ulcers (undermining of edges), CT: Rectal narrowing causes increased presacral space, target sign (alternating high and low attenuation colonic wall due to oedema), submucosal fat deposition UC>Crohn’sUS: Can differentiate UC from Crohn’s in skilled hands because transmural inflammation
