Gastrointestinal Flashcards
Liver segments by portal and hepatic veins
Portal vein: superior/inferior
Middle hepatic vein: right/left
Left hepatic vein: 2,3/4
Right hepatic vein: 5,8/6,7
Hepatic segment vasculature
Central:
portal triad—> portal vein, hepatic artery, bile duct
Peripheral:
venous —>hepatic vein—>IVC
Caudate:
Direct to the IVC
Routine contrast enhanced CT usage
Portal venous phase(70s after injection)
Hepatic steatosis, cirrhosis
Most metastasis ( not hyper vascular)
Some breast Mets are iso in portal phase/detected on unenhanced
Arterial phase CT usage in liver
20-25 s after injection
Primary liver masses (hyper vascular)
Optimal view—> late arterial (35 s)
NAFLD categories
Steatosis
Steatohepatitis
Metabolic syndrome
NAFLD
Obesity
Insulin resistance
Dyslipidemia
Hepatic steatosis on CT
Un-enhanced:
Liver attenuated 10 HU less than spleen
Contrast enhanced: liver 25 HU less than spleen in pvp
Fatty liver on MRI
In and out of phase GRE MRI
complete signal loss on out of phase
In phase: water+fat
Out of phase:water-fat
Decreased signal on in phase MRI
Hepatic iron overload
Increases TE—> longer dephasing—> exaggerated T2*
Focal liver fat characteristics
No mass effect
Vessels run through it
Location:
Gallbladder fossa/ subcapsular/periportal/
Hyper echo on US and hypo on CT
Liver amyloidosis
Decreased attenuation on CT
Wilson disease on CT
Copper : basal ganglia/cornea/liver
Liver:
Hyper on CT—> multiple nodules—>hepatomegaly—>cirrhosis
Excess hepatic iron accumulation pathways
Within hepatocytes: hemochromatosis
Increased uptake in RES: kupffer cells/ hemosiderosis
Iron overload liver imaging
MRI: hypo compared to paraspinal muscle
Hemochromatosis vs Hemosiderosis
Hemochromatosis: spleen and bone marrow are spared
Involves pancreas,myocardium,skin,joint/ cause cirrhosis/ tx: phlebotomy
Hemosiderosis: spleen and bone marrow are involved/ no cirrhosis/ tx: iron chelator
Hypo-attenuated liver on CT
Fatty liver Hepatic amyloid ( rare)
Hyper attenuated liver on CT
>75 HU iron overload Medication: amiodarone, gold, methotrexate Copper overload Glycogen excess
Viral hepatitis imaging
Normal CT
Gallbladder wall thickening
Periportal edema
DDx for multiple tiny hypo hepatic lesions
Candidiasis (involves spleen/ rim enhanced/ immunocompromised)
Mets
Lymphoma
Biliary hamartoma
Caroli disease (dilatation of intrahepatic bile ducts/fibrocystic anomalies of the kidneys)
Causes of liver abscess
Diverticulitis Appendicitis Crohn Bowel surgery Ascending cholangitis ( less common)
E.Coli
Hepatic abscess on imaging
Mimics Mets
CT: ring enhanced
MRI: central hyper on T2/ irregular wall with late enhancement/ perilesional enhancement
Hepatic echinococcosis on imaging
CT: well defined hypo mass with floating membrane and peripheral calcification
US: hypoechoic mass with hyperechoic undulating membrane
Cirrhosis forms
Micronodular: metabolic causes
Macronodular: post viral
Cirrhosis on imaging
Early: preportal space expansion Caudate enlargement Caudate/right lobe>0.65 Empty gallbladder fossa sign
Secondary:
Portal HTN—> splenomegaly, portosystemic collaterals, varies
Gall bladder wall thickening
Gamna-Gandy bodies( splenic microhemorrhage)
Regenerative liver nodules on imaging
Supplied by portal vein/ non pre malignant
No enhancement on arterial phase
Low on T2
Contrast enhanced MRI: iso to liver parenchyma
Dysplastic liver nodule on imaging
Premalignant/ supplied by portal vein Mostly don’t enhance Hypo on T2 High grade: hyper on T2 Contrast enhanced: Low grade—> iso to liver High grade—> arterial enhancement
Siderotic liver nodule on imaging
Iron rich regenerative or dysplastic nodule
Hypo on T1 and T2*
Hyper on CT
HCC on CT and MRI
Encapsulate
Enhances on arterial and washes out on portal venous
Hyper on T2
10-20% of HCCs are hypoenhancing
Nodule in nodule appearance
Enhancing nodule in a dysplastic nodule
Early HCC
HCC invasion pattern
Port, portal veins, IVC and bile ducts
Mets to the liver are less locally invasive
HCC treatment
Hepatectomy
Transplant
Percutaneous ablation
Transcatheter embolization
Fibrolamellar carcinoma
HCC subtype
Young patient without cirrhosis
AFP not elevate
Better prognosis
Fibrolamellar carcinoma on imaging
Large, heterogenous Fibrotic central scar: hypo on T1 and T2 Focal nodular hyperplasia: T2 hyper with delayed enhancement Capsular retraction in 10% Do not have capsule Have pseudocapsule
Liver metastasis imaging
Mostly hypovascular
Seen on portal venous phase
Calcification: mucinous colorectal/ ovarian serous
MRI: hypo T1/hyper T2
Hyper vascular liver metastasis
Neuro endocrine tumors RCC Thyroid carcinoma Melanoma Sarcoma
Pseudocirrhosis
Multiple hepatic metastasis
Treated breast cancer
Can have capsular retraction
Hepatic lymphoma
Primary is rare
Usually secondary with splenomegaly and LAP
Epithelioid hemangioendothelioma
Vascular malignancy
Multiple round subcapsular masses that can be confluent
Can have halo or target
Capsular retraction
DDx for capsular retraction
Metastatic tumors Fibrolamellar HCC HCC epithelioid hemangioendothelioma Intrahepatic cholangiocarcinoma Confluent hepatic fibrosis: wedge shaped Cirrhosis Medial left/ anterior right
Focal nodular hyperplasia
Disorganized tissue
Not malignant
More in women
Not associated with OCP
FNH in imaging
Central scar (not true scar) is T2hyper ductules and venules, with delayed enhancement
Avid enhancement on arterial with quick wash out
Has kupffer cells (sulfur colloid study) and bile duct (HIDA scan)
Hepatic hemangioma
Benign
Hepatic artery at the periphery
More female
Uncommon in cirrhosis
Hepatic hemangioma
Nonenhancing center ( cystic degeneration)
Peripheral, discontinuous, progressive, nodular enhancement
SI is identical to aorta
Hyper on T2 with even subtle areas of even higher SI ( cystic degeneration)
On CT: hypo mass
Hepatic adenoma
Benign Hepatocyte Kupffer cells No bile ducts More in females With OCP High risk of hemorrhage Multiple: von Gierke disease
Hepatic adenoma on imaging
Might have pseudocapsule with late enhancement
Hyper on arterial
Microscopic fat on in and out phase
Internal hemorrhage: T1 hyper
Budd Chiari causes
Hepatic venous obstruction Hypercoag state Hematologic disease, pregnancy, OCP Malignancy, infection,trauma Congenital vein anomaly
Budd Chiari symptoms
Acute: hepatomegaly, ascites, abdominal pain
Lack of flow in hepatic vein Thrombus in IVC Collateral vessels Edematous periphery Caudate sparing Prominent regen nodules
Veno-occlusive disease
Destruction of post sinusoid all venules
Patent hepatic vein
In BM transplant due to chemo
Imaging: peripheral edema Narrow hepatic vein Hepatomegaly Hetero enhancement Caudate is not spared
Cardiac hepatopathy
Heart failure
Constrictive pericarditis
Right valvular disease
Imaging: enlarged vein and IVC
reflux of contrast from Right atrium into IVC
Mottled enhancement
Biliary hamartomas
Von Meyenburg complex
Incidental
Small cystic lesions
Embryologic failure
Smaller and more irregular than simple cysts
ADPLD
40% of ADPKD
Similar findings
Failure is rare
Imaging: innumerable no enhancing simple cyst
MDCT hepatic trauma
Grade1: superficial laceration,subcapsular hematoma<1cm
Grade 2: laceration, subcapsular/intraparenchymal hematoma>1 <3 cm
Grade3: >3cm
Grade 4: hematoma>10cm or destruction of one lobe
Grade 5: destruction of both lobes
Magnetic resonance cholangiopancreatography
Heavy T2 weighted
Increase contrast between biliary tract and surroundings
Fast spin echo sequences
Intermediate T2: evaluate extraluminal structures
Gad contrasts with biliary excretion
Gadoxetic acid disodium ( Eovist) Gadobenate dimeglumine (Multihance)
Require 20-45 minutes delay
T1 hyper biliary fluid
Choledochal cysts classification
Todani system:
Type1: CBD fusiform/ most common
Type2:extrahepatic saccular
Type3:intraduodenal
Type4:multiple segments
Type5:intrahepatic/ caroli/ associated with PKD
Caroli syndrome: disease+hepatic fibrosis
Imaging:central dot sign(portal vein and hepatic artery bridging bile ducts)
Increase risk of cholangiocarcinoma
Cholecystitis
Obstruction of GB neck or cystic duct Acute: Wall thickness >3cm Pericholecystic fluid GB hyperemia GB calculi
Acute cholecytitis complications
Gangrenous: asymmetric GB wall thickening/ intraluminal membrane
Acute perforation: high mortality/ bile peritonitis
Subacute:pericholecystic abscess
Chronic:cholecystoenteric fistula
Emphysematous: gas forming bacteria,in lumen or wall/ elderly diabetic
Porcelain GB
Peripherally calcified
Chronic cholecystitis
Increased carcinoma
Ascending cholangitis
Fever, abdominal pain, jaundice
Imaging: hyper and thickened wall of bile ducts+ CBD stone
Tx: AB and fluid then endoscopy
PSC
Destruction of bile ducts
Associated with UC, most male
Imaging: beaded, irregular CBD and intrahepatic ducts
Complications: cirrhosis, cholangiocarcinoma,recurrent biliary infection
PBC
Destruction of smaller bile ducts
Middle aged women, pruritus
Hepatic cirrhosis
AIDS cholangitis
Cryptosporidium and CMV
RUQ pain, fever, LFT
Imaging: identical to PSC, distinguished: papillary stenosis
Recurrent pyogenic cholangitis
Oriental cholangiohepatitis
Clonorchis sinesis
Pigment stone, biliary stasis, cholangitis
Southeast Asia
Recurrent jaundice and fever
Imaging: pnemobilia, lamellated bile duct filling defect, intra and extra bile dilation and strictures
Increased cholangiocarcinoma
Biliary cyst adenoma
Middle aged women
Benign
Abdominal pain, nausea, vomiting and obstructive jaundice
Imaging: large loculated cystic mass, with septation
Rarely turns into cystadenocarcinoma( large solid, thick calcification)
Cholangiocarcinoma
Hilar tumor: right and left biliary ducts/ Klatskin
Bile duct obstruction/intrahepatic dilation
Lobar atrophy
Risk factors for cholangiocarcinoma
Choledochal cyst PSC FAP Clonorchis Sinesis Thorium dioxide
Cholangiocarcinoma on imaging
Intrahepatic mass at confluence of central bile ducts
Bile duct dilation
Capsular retraction
Tumor fingers in bile ducts
Gallbladder carcinoma
Chronic cholecystitis
Gallstone
Porcelain gallbladder
Scirrhous infiltrating mass(most common)
Polyploid mass
Mural thickening
Direct invasion to liver
Poor prognosis
Gallbladder metastasis
Melanoma
Pancreatic neoplasm
Solid epithelial: Ductal Adenocarcinoma, Acinar cell carcinoma
Cystic: serous, mucinous,solid and papillary epithelial neoplasm, intraductal papillary mucinous neoplasm
Endocrine: insulinoma, gastrinoma, glucagonoma, VIPoma, Somatostatinoma
Ductal adenocarcinoma
80-90% of tumors
CT: unenhanced, late arterial phase, PVP
Late arterial: best phase
Pancreatic head
Imaging: hypo on CT and T1, ill defined, hypovascular,ductal obstruction and tail atrophy
Double duct sign: CBD and pancreatic duct
Pancreatic mass with no ductal dilation
Autoimmune pancreatitis Groove pancreatitis Cystic tumor Neuroendocrine tumor Duodenal GIST Peripancreatic LN Mets (RCC, Thyroid, melanoma) Lymphoma
Unresectable PDAC
Encasement of SMA
Extensive venous invasion
Mets
Resectable PDACs
No SMA or celiac or portal invasion
Limited duodenum, distal stomach, CBD
Limited venous
Acinar cell carcinoma
Rare, aggressive
Elderly males
Lipase hyper secretion syndrome: Sub Q fat necrosis, bone infarcts—> polyarthralgias, eosinophilia
Serous cystadenoma
Benign, elderly women
> 6 cysts <2 cm
Maybe solid on CT—> do MRI
Hyper vascular
No ductal dilation or tail atrophy
Central stellate calcification
Mucinous cystic neoplasm
Middle aged women Benign with malignant potential Resection <6 cysts >2 cm in body and tail Capsulated
Capsulated pancreatic tumors
SPEN
Mucinous cystic neoplasm
Solid and papillary epithelial neoplasm
Young women and children
Abdominal pain
Low malignancy
Imaging: large, heterogenous solid and cystic, hemorrhage, capsule
Intraductal papillary mucinous neoplasm
Elderly male Main pancreatic duct or sidebranch Main duct more malignancy Endoscopy: fish-mouth papilla Imaging: cystic in contiguity with duct Nodular or enhancing —> malignancy <1 cm annual follow up >3 , mural nodule, ductal dilation—> resection
Pancreatic endocrine tumors
Hyper vascular
Late arterial phase
Solid
Hyper vascular liver+ pancreatic mass—> Pancreatic endocrine tumors Mets
Insulinoma
Presents early
Whipped triad: hypoglycemia, symptoms, better with glucose
Gastrinoma
Zollinger- Ellison
If in MEN 1–> duodenum
Location: gastrinoma triangle/ junction of cystic duct and CBD, duodenum (inferior),pancreas neck(medial)
Can cause stomach carcinoid
Pancreatic duct anatomy
Main duct drains the tail(always)—>duct of Wirsung—> major papilla (ampulla of Vater)
CBD always meets Wirsung at major papilla
Santorini, superior, always goes to minor papilla
Sphincter of Oddi at ampule of Vater
Pancreas divisum
Failure of fusion of dorsal (main) and ventral duct(Wirsung)
Majority drains by Santorini
Pancreatitis, santorinicelr
Imaging: crossing sign: CBD crossing over main duct to join Wirsung
Annular pancreas
Failure of ventral bud rotation
Pancreas around duodenum
Neonate: double bubble sign
Adults: pancreatitis,PUD, duodenum obstruction
Common channel syndrome
Pancreaticobiliary maljunction
Usually: CBD and Wirsung are separate
Common channel syndrome: no septum, reflux between two systems
Cholangiocarcinoma
Pancreas in von Hippel Lindau
Serous cystadenoma
Pancreatic neuroendocrine tumors
Pancreas in cystic fibrosis
Childhood atrophy
Fatty atrophy or pancreatic cystosis
Pancreas in Schwachman Diamond
Fatty replacement
Exocrine insufficiency
Neutropenia
Bone dysplasia
Intrapancreatic accessory spleen
1-3 cm Well defined Pancreatic tail DDx: MRI Tc-99m sulfur colloid or Tc-99m RBC scintigraphy
Imaging of pancreatitis
Late arterial (40 s after injection)
CT is key
Not indicated in mild acute pancreatitis
Acute pancreatitis Balthazar classification
A: normal B: enlargement C: mild peripancreatic inflammation D: single fluid E: two or more fluid A,B,C: 0 mortality, 4 morbidity D, E: 14 mortality, 54 morbidity
Acute pancreatitis CT severity classification
0-4 for Balthazar A-E
0: 0 necrosis
2: <30
4: 30-50
6: >50
CTSI: 0-3: 3 mortality, 8 morbidity
7-10: 17 mortality, 92 morbidity
Pancreatitis pancreatic complications
Necrosis: focal or diffuse nonenhancing/ after 48-72 hours/ late arterial phase/ risk of infection
Fluid collection: peripancreatic
Pseudocyst: enzyme collection, fibrous wall, 4-6 weeks
Abscess: purulent, thicker, irregular wall, gas locales
Pancreatitis extrapancreatic complication
Pseudocyst: anywhere below diaphragm
Perihilar renal inflammation: venous compression, thrombosis
Bowel:transverse colon
Adjacent vascular inflammation:
Arterial bleeding—> splenic artery erosion
Pseudoaneurysm—> splenic artery
Venous thrombosis—> splenic vein—> portal HTN
Chronic pancreatitis
Long term alcohol, pancreas divisum
Calcification along pancreatic duct
Autoimmune pancreatitis
Lymphoplasmacytic infiltrate
Sjogren syndrome, IgG4
Imaging: diffuse, sussage shaped entire pancreas
Focal—> mimics mass
Tx: steroid
Groove pancreatitis
Focal pancreatitis
Between head, duodenum and CBD
Heavy drinker young man
Fibrosis in pancreaticoduodenal groove
Can cause: duodenal stenosis, cystic change of duodenal wall
Imaging: duodenal thickening, cystic changes on MRI
DDx: adenocarcinoma
Peritoneum
Single layer of mesothelial cells supported by subserosal fat, lymphatic cells and WBC
Most dependent
For women: pouch of Douglas
Men: retrovesical area
Mesentry
Blood vessels and lymphatic between peritoneal layers
True:connects to posterior abdominal wall
Small bowel—>jejunum and ileum/from ligament of Treitz (LUQ) to ileocecal junction( RLQ)
Transverse—>posterior transverse to posterior wall
Sigmoid—>sigmoid colon
Omentum: specialized, attach to stomach, not to posterior wall
Greater—>anterior abdomen/ stomach to anterior transverse colon
Lesser—>stomach to liver
Misty mesentry
Mesenteries are fatty fold—> normally not seen on CT
Fluid or inflammation —>mesenteric vasculature become in distinct
Mesenteric edema
Systemic: diffuse edema, CHF, low protein, third spacing
Intra abdominal: focal edema, vessel thrombosis, Budd Chiari, IVC obstruction
Bowel ischemia
Vascular insult
Imaging: bowel wall thickening, pneumatosis, mesenteric venous gas
Mesenteric inflammation
Most common: acute pancreatitis
Appendicitis, IBD, diverticulitis,
Local misty mesentery
Neoplastic infiltration
Misty mesenteric after tx limited to treated LN
Most common: NHL, bulky adenopathy
Pancreatic, colon, breast,GIST, mesothelioma
Carcinoid
Most common small bowel tumor
Distal ileum
Intraluminal—>mesentery(direct or lymphatic)
Imaging: enhancing mass with radiating linear bands into mesenteric fat (intense desmoplastic reaction by serotonin), calcification
Sclerosing mesenteric mass
Carcinoid
Desmoid tumor
Sclerosing mesenteritis
Desmoid tumor
Benign, locally aggressive
Fibrous tissue
Gardner syndrome( FAP)
CT: iso to muscle, central necrosis, strands of tissue radiating to mesenteric fat
Sclerosing mesenteritis
Fatty necrosis and fibrosis of mesenteric root
Mesenteric mass with striation of ST, calcification
Panniculitis
idiopathic inflammation
Acute abdominal pain
CT: diffuse misty mesentery, linear bands of ST
Mesenteric Mets
Gastric, ovarian, breast, lung,pancreatic,biliary, colon, melanoma
Mesenteric lymphoma: Sandwich sign
Peritoneal carcinomatosis
Disseminated metastasis
Omental caking
Mucinous adenocarcinoma
Pseudomyxoma peritoneal
Low grade/ copious mucus in peritoneal cavity
Mucin producing adenoma or adenocarcinoma
Appendix(20%), ovaries(30%) or colon
Involves entire peritoneal cavity
Recurrent mucinous ascites ( jelly belly)
CT: lobular ascites, higher attenuation than fluid
Advanced: scalloping of hepatic margin
Tx: surgery, hyperthermia intra peritoneal chemotherapy lovage
Splenule
Accessory spleen
Splenic Hilum
MRI: follows splenic tissue
Tc-99m sulfur colloid/ heat damaged Tc-99m RBC
Polysplenia syndrome
Visceral heterotaxia
Multiple Foci of splenic tissue on the same side as the stomach
Severe cardiac anomalies
Venous anomalies( interruption of IVC with azygos or hemiazygos, preduodenal portal vein)
Wandering spleen
Abnormal laxity
Presents as abdominal mass
Acute abdominal pain due to torsion
Hemangioma of spleen
Most common
Kasabach-Merritt: anemia, thrombocytopenia, consumptive coagulopathy)
Klippel-Trenaunay-Weber:cutaneous hemangioma, varicose vein, extremity hypertrophy
Associated with phleboliths
CT: pre—> iso/ hypo hyperenhancing
MR: T2–> hyper Peripheral/ homogenous enhancement
NM: Tc-99m RBC—> delayed images
Spleen hamartoma
Malformed red pulp
Tuberous sclerosis
CT: pre: iso/ hypo mass heterogenous enhancement
MR: T2: iso, heterogenous early enhancement—> homogeneous delayed enhancement
True splenic cyst
Epithelial lining
Increased CA 19-9, CA125 , CEA
Septation
Calcification uncommon
Post-traumatic pseudocyst
End result of hematoma
Imaging: well circumscribed, fluid density, no peripheral enhancement
Septation uncommon
Calcification common
Intrasplenic pancreatic pseudocyst
Post pancreatitis pseudocyst at tail extends into spleen
Like post traumatic
Can cause splenic rupture
Spleen lymphangioma
Childhood
Solitary or multiple
Multilocular cystic structure with thin septation
Post contrast—> septal enhancement
Spleen sarcoidosis
Multiple nodule with noncaseating granulomas
Splenomegaly, hepatomegaly, LAP
Multi nodular pattern: numerous hypo 1-3 cm lesions no enhancement
Imaging: hypo on all MR sequences
Better seen on T2 and early post -T1
DDx: lymphoma
Inflammatory pseudotumor in the spleen
Focal collection of immune cells and exudate
Fever and malaise
Imaging: well circumscribed, heterogenous enhancing
Pyogenic abscess in spleen
Immunocompromised
Solitary—> bacterial
Multi focal—>fungal
CT: irregular, enhancing wall
Gas—> bacteria
US—>wheel within a wheel, bull’s eye
Tx: drainage
Fungal abscess in spleen
Multiple <1cm
Immunocompromised
Candida, aspergillus, cryptococcal
CT: hypo
Pneumocystis jiroveci—> advanced AIDS, multi calcified lesions
Echinococcal cyst in spleen
Associated with other organs
True cyst
Imaging: internal undulating membrane and daughter cysts
Splenic lymphoma
Most common malignancy
Primary: rare, solitary, hypo, extends beyond capsule
Secondary:
Miliary masses, multiple small to moderate, one large,splenomegaly without mass
Best on post T1/involved portion will be hypo
US—> cystic Color—> internal flow
Splenic Mets
Low rate of Mets
Most common—> breast,lung,ovarian,melanoma
Ovarian and melanoma—> cystic
Calcification—> mucinous adenocarcinoma
Angiocarcinoma of spleen
Rare
Aggressive
20% 6month survival
Enlarged, heterogenous
Variable enhancement
Splenic infarct
Emboli(older)
Thrombosis(young with hematologic disease)
Wedge shaped peripheral region non enhancement
MR: acute—> T1 hyper. Chronic—> T2 hyper
Lack of enhancement of entire spleen—> torsion(wandering spleen)
Gamma Gandy bodies
Tiny foci of hemosiderin—> portal HTN
Hypo on all sequences
In phase—> blooming
Portal HTN
Splenomegaly Varices Recanalized umbilical vein Ascites Nodular liver contour
Gaucher disease
AR deficiency of glucocetebrosidase
Splenomegaly, multiple splenic nodules
Bone: Erlenmeyer flask deformity of distal femurs, femoral head AVN, H shaped vertebral bodies
Evaluating spleen trauma
Portal venous phase
Splenic hematoma
Most—> subcapsular
Hypo to enhanced spleen
Splenic laceration
Only on contrast enhanced
Linear or branching hypo
Splenic vessel injury
Active extravas—> area of hyper which increases in size on delayed phase
Pseudoaneurysm/AV fistula—> well circumscribed hyper but do not increase on delayed ( differentiate with splenic arteriography)
MDCT based splenic injury grading system
Grade 1: <1cm subcap Grade 2: >1 and <3 subcap Grade 3: splenic capsular, >3 cm lac Grade IVA: active extravas, vascular injury, shattered spleen Grade IVB: active intraperitoneal bleed
