GI Flashcards
Location
H pylori gastritis
usually antrum
Location
Zollinger-Ellison
Ulcerations in the stomach (jejunal ulcer is the buzzword).
Duodenal bulb is actually the most common location for ulcers in ZE. Remember ZE is
from gastrinoma - and might be a way to test MEN syndromes.
Location (stomach)
Crohns
Uncommon in the stomach, but when it is, it likes the antrum
Location
Menetrier’s
Usually in the Fundus (classically spares the antrum)
Location
Lymphoma
Crosses the Pylorus” - classically described as doing so, although in reality adenocarcinoma does it more.
FAP
100s of polyps - 100% risk of Colon CA (usually before 40)
Hyperplastic Stomach Polyps , Adenomatous Bowel Polyps
Adenomatous
Locally invasive desmoid tumors are common at surgicai ls■i*tes post
colectomy (these actually kill 10%ofFAPers)
HNPCC (Lynch)
As the name implies, this is not a disease of 100s of polyps. Instead it is DNA Mismatch Repair problem associated with lots of cancers.
Another difference between this and FAP is that the cancers of the colon are usually solitary (and right sided).
They also get lots of other cancers (endometrial being the second most common)
Gardner Syndrome
FAP + Desmoid Tumors, Osteomas, Papillary Thyroid Cancer
Turcots
FAP + Gliomas and Medulloblastomas
Peutz-Jeghers
Hamartoma Style!
Mucocutaneous Pigmentation (gross Dalmatian dog lips)
Small and Large Bowel CA, Pancreatic CA, and GYN CA
Cowden
Hamartoma Style!
BREAST CA, Thyroid CA,
Lhermitte-Duclos (posterior fossa noncancerous brain tumor)
Hamartoma Style!
Cronkhite-Canada
Hamartoma Style!
Stomach, Small Bowel, Colon,
Ectodermal Stuff (skin, hair, nails, yuck)
Juvenile Polyps
Hamartoma Style!
Increased risk for colorectal and gastric cancer (different than sporadic juvenile polyps -which are typically solitary and benign)
Stomach ulcer
Malignant
Width > depth
located within lumen
nodular irregular edges
folds adjacent to ulcer
aunt minnie: carmen meniscus sign
can be anywhere
Stomach Ulcers
benign
Depth>Width
Project beyond the expected lumen
sharp contour
folds radiate to ulcer
Aunt minnie: hamptons line
mostly on lesser curvature
GIST
overview
This is the most common mesenchymal tumor of the GI tract (70% in stomach, duodenum is second most common — colon is actually the least common). Think about this in an old person (it’s rare before age 40).
Gist
Tricks to know
• Lymph node enlargement is NOT a classic feature
• Malignant ones tend to be big angry mother fuckers (>10cm with ulceration - and possible perforation).
• If they do met - it is typically to the liver.
• Having said that, malignancy is rare with these.
They typically don’t met anywhere, which is why lymph node enlargement is uncommon.
• The association with Carney’s triad
• The association with NF-1
Carneys triad
“Carney’s Eat Garbage”
Chondroma (pulmonary)
Extra Adrenal Pheo
GIST
Gastric “Cancer” is either
Lymphoma (<5%) or Adenocarcinoma (95%)…. Rarely a malignant GIST.
Gastric adenocarcinoma
overview
is usually a disease of an old person (median age 70).
H. Pylori is the most tested risk factor.
Gastric adenocarcinoma
trivia to know
• Ulcerated carcinoma (or the “penetrating cancer”) has the
look of an advanced cancer
• Metastatic spread to the ovary is referred to as a Krukenberg Tumor.
• Gastroenterostomy performed for gastric ulcer disease
(old school - prior to PPIs) have a 2x - 6x- increased risk
for development of carcinoma within the gastric remnant.
• Step 1 trivia question: swollen left supraclavicular node = Virchow Node.
Gastric Adenocarcinoma
The look
Gastric Adenocarcinoma looks very different (usually) than a GIST.
GIST (arrow) is usually smoothly marginated and exophytic
Gastric
Adenocarcinoma is usually a large, ulcerated, heterogenous mass
Ulcer Trivia:
Duodenal Ulcers are 2-3x more common than Gastric Ulcers.
Gastric Ulcers - They have 5% chance o f being cancer.
Duodenal Ulcers - Are never cancer (on multiple choice)
Gastric Ulcers occurs from “altered mucosal resistance”, and favor the bulb
Duodenal Ulcers occur from….
Gastric Lymphoma
overview
can be primary (MALT), or secondary (systemic lymphoma). The stomach is the
most common extranodal site for non-Hodgkin lymphoma.
Gastric Lymphoma
even when extensive
rarely causes gastric outlet obstruction. It was classically described as “crossins
the pylorus ’’ , although since gastric carcinoma is like lOx more common, it is actually more likely to do that.
Gastric Lymphoma
looks like
Has multiple looks and can be big, little, ulcerative, polypoid, or look like target lesions. It can also look like Linitis Plastica
Gastric Lymphoma
Trivia
it can rupture with treatment
Gastric Cancer is “More Likely” Than Lymphoma to…
- More Likely to Cause Gastric Outlet Obstruction
- More Likely to be in the distal stomach
- More Likely to extend beyond the serosa and obliterate adjacent fat plains
- More Likely to be a focal mass (95% of primary gastric tumors are adenocarcinoma)
Mets to the Stomach: This is actually very rare.
Melanoma
Breast
Lung
Mets to the Stomach:
Melanoma
Melanoma is probably the most common culprit, when it does occur.
This obviously has a variable appearance but multiple button type soft tissue nodules is probably the most classic look.
Mets to the Stomach:
Breast and lung
these are
known for producing a particular look of diffuse infiltration and a contracted desmoplastic deformity resembling a stiff leather bottle.
This is the so called Linitis Plastica appearance
Chronic Aspirin Therapy
“Multiple gastric ulcers” is the buzzword. Obviously this is nonspecific, but some sources say it occurs in 80% of patient’s with chronic aspirin use.
As a point of trivia, aspirin does NOT cause duodenal ulcers.
If you see multiple duodenal ulcers (most duodenal ulcers are solitary) you should think
ZE
Areae Gastricae
This is a normal fine reticular pattern seen on double contrast. A favorite piece of trivia to ask is when does this “enlarge” ? The answer is that it enlarges in elderly and patient’s with H. Pylori. Also it can focally enlarge next to an ulcer. It becomes obliterated by cancer or atrophic gastritis.
Menetrier’s Disease
Rare and has a French sounding name, so it’s almost guaranteed to be on the test. It’s an idiopathic gastropathy, with rugal thickening that classically involves the fundus and spares the antrum. Bimodal age distribution (childhood form thought to be CMV related). They end up with low albumin, from loss into gastric lumen.
Menetrier’s Disease
Essential trivia
inolves the fundus and spares the antrum
Ram’s Horn Deformity (Pseudo Billroth I)
Tapering of the antrum causes the stomach to look like a Ram’s Horn. This is a differential case, and can be seen with Scarring via peptic ulcers, Granulomatous Disease (Crohns, Sarcoid, TB, Syphilis), or Scirrhous Carcinoma.
Ram’s Horn Deformity (Pseudo Billroth I)
Essentrial trivia
The stomach is the most common GI tract location for sarcoid.
Gatric volvulus
Organoaxial
the greater curvature flips over the lesser
curvature. This is seen in old ladies with paraesophageal hernias. It’s way more common.
Gastric volvulus
meseneroaxial
twisting over the mesentery. Can cause ischemia and needs to be fixed. Additionally this type causes obstruction. This type is more common in kids.
Gastric Diverticulum
The way they always ask this is by trying to get you to call it an adrenal mass (it’s most commonly in the posterior fundus).
Gamesmanship: Find the normal adrenal.
Gastric Varices
Gastric Varices: This gets mentioned in the pancreas section, but I just want to hammer home that test writers love to ask splenic vein thrombus causing isolated gastric varices.
Some sneaky ways they can ask this is by saying “pancreatic cancer” or “Pancreatitis” causes gastric varices. Which is true…. because they are associated with splenic vein thrombus. So, just watch out for that.
Bilroth 1
Pylorus is removed and the proximal stomach is sewed directly to the duodenum.
Done for Gastric CA, Pyloric Dysfunction, or Ulcers.
Less Post Op Gastritis (relative to Billroth 2)
Bilroth 2
Partial gastrectomy, but this time the
stomach is attached to the jejunum.
Done for Gastric CA, or Ulcers.
Risks:
• Dumping syndrome
• Afferent loop syndrome
• Increased risk of gastric CA 10-20 year after surgery
Roux-en-y
Stomach is divided to make a “pouch.” This gastric pouch is attached to the jejunum. The excluded stomach attaches to the duodenum as per normal. The jejunum is attached to the other jejunum to form the bottom of the Y.
can also be performed for gastric cancer as an alternative to Billroth if the primary lesion has directly invaded the duodenum or head of the pancreas.
Supposedly these have less reflux, and less risk of recurrent gastric CA.
They are at increased risk for gallstones, and they have all that internal hernia shit.
Dumping syndrome
group of symptoms; diarrhea, nausea, and lightheaded / tired after a meal, - caused by rapid gastric emptying (seen classically with Billroth 2 and early in the post op period after Roux-en Y).
Afferent Loop Syndrome
An uncommon complication post billroth 2. The most common cause is obstruction (adhesions, tumor, intestinal hernia) o f the afferent. The acute form may have a closed loop obstruction. The result o f this afferent obstruction is the build up of biliary, pancreatic, and intestinal secretions resulting in afferent limb dilation. The back pressure from all this back up dilates the gallbladder, and causes pancreatitis. A much less common cause is if the stomach preferentially drains into the afferent loop.
Jejunogastric Intussusception
This is a rare complication o f gastroenterostomy. The Jejunum herniates back into the stomach (usually the efferent limb) and can cause gastric obstruction. High mortality is present with the acute form.
Bile Reflex Gastritis:
Fold thickening and filling defects seen in the stomach after Billroth 1 or II are likely the result o f bile acid reflux.
Gastro-Gastric Fistula
This is seen in Roux-en-Y patients who gain weight years later. The anastomotic breakdown is a chronic process, and often is not painful.
Cancer after gastric surgery
With regard to these old peptic ulcer surgeries (Billroths), there is a 3-6 times increased risk o f getting adenocarcinoma in the gastric remnant (like 15 years after the surgery).
Dumping Syndrome 2
Different than the “dumping syndrome” associated with late night Taco Bell. This type o f dumping is related to rapid transit o f undigested food from the stomach. Tc Gastric Emptying study is an option to diagnose this. The therapy is typically conversion o f Billroth to Roux-en-Y (and avoiding delicious carbs).
Small bowel follow through
Steps
Step 1 evaluate the folds
Step 2a evaluate for loop seperation with t without tethering
step 2b if nodules are present evaluate the distribution and secondary findings to help narrow diff
step 3 trademark features
SBFT step 1
thin <3mm, straight folds with dilation
Mechanical Obstruction
Paralytic Ileus
Scleroderma
Sprue
SBFT step 1
thick straight folds >3mm
segmental distribution
Ischemia
Radiation
Hemorrhage
Adjacent Inflammation
SBFT step 1
thick straight folds >3 mm
diffuse distribution
Low Protein
Venous Congestion
Cirrhosis
SBFT step 1
thick folds with nodularity
segmental distribution
Crohns
Infection
Lymphoma
Mets
SBFT step 1
thick folds with nodularity diffuse distribution
Whipples Lymphoid Hyperplasia Lymphoma Mets Intestinal Lymphangiectasia
SBFT step 2a
loop seperation without tethering
• Ascites, • Wall Thickening (Crohns, Lymphoma), • Adenopathy • Mesenteric Tumors
SBFt step 2a
loope separation with tethering
Tethering looks like someone is pinching and pulling the loops towards the displacing mass.
• Carcinoid
SBFT Step 2b
sand like nodules
Diffuse nodules in the jejunum
whipples (tropheryma whipplei)
pseudo whipples (MAC)
SBFT Step 2b
uniform 2-4 mm nodules
Lymphoid Hyperplasia
SBFT Step 2b
nodules of larger or varying sizes
Cancer - th in k M e ts (M e la n om a )
SBFT Step 2b
cobblestoning
- Raised islands o f mucosa separated by linear streaks running perpendicular to the lumen o f the bowel.
- These streaks represent ulceration.
- This findings (especially when combined with areas o f stricture, and loop separation from fat proliferation) should make you think Crohns
SBFT Step 3
ribbon bowel
bowel is featureless, atrophic, and has fold thickening (ribbon-like).
Graft Vs Host
SBFT Step 3
hidebound bowel
Narrow separation of normal folds with mild bowel dilation.
Scleroderma
SBFT Step 3
Moulage sign (tube of wax)
Dilated jejunal loop with complete loss of
jejunal folds - opacified like a “tube o f wax”
Celiac
SBFT Step 3
Fold reversal
Jejunum loses folds to look more like the normal Ileum, Ileum
gains folds (in the right lower quadrant) to look
more like normal Jejunum
Celiac
SBFT Step 3
Freaking worm
Thread like defect in the barium column
ascaris suum (demon worm)
Small bowel path
The target sign
’ Single Target: GIST, Primary Adenocarcinoma, Lymphoma, Ectopic Pancreatic Rest, Met (Melanoma).
’Multiple Target: Lymphoma, Met (Melanoma)
Small bowel path
clover leaf sign
This is an Aunt Minnie for Healed Peptic Ulcer of the Duodenal Bulb.
Small bowel path
Whipples
Just like a stripper - it prefers white men in their 50s. The bug infdtrates the lamina propria with large macrophages infected by intracellular whipple bacilli leading to marked swelling of intestinal villi and thickened irregular mucosal folds primarily in duodenum and proximal jejunum.
Small bowel path
Buzzword for whipples
“sand like nodules” referring to diffuse micronodules in the jejunum.
Small bowel path
Pseudo whipples
MAI (instead of T. Whipplei). This is seen in AIDS patients with CD4<100. The imaging findings of nodules in the jejunum and retroperitoneal nodes are similar to Whipples (hence the name). The distinction between the two is not done with imaging but instead via an acid fast stain (MAC is positive).
Small bowel path
Intestinal lymphangiectasia
Lymphangiectasia results from obstruction to the flow of lymph from the small intestine into the mesentery. This results in dilation of the intestinal and serosal lymphatic channels. This can be primary from lymphatic hypoplasia, or secondary from obstruction of the thoracic duct (or any place in between).
Small bowel path
Graft vs Host
It occurs in patients after bone marrow transplant. It’s less common with modem anti-rejection drugs. Skin, Liver, and GI tract get hit. Small bowel is usually the most severely affected. Bowel is featureless, atrophic, and has fold thickening (ribbonlike).
Small bowel path
graft vs host buzzword
ribbon bowel
Small bowel path
SMA Syndrome
This is an obstruction of the 3rd portion of the duodenum by the SMA (it pinches the duodenum in the midline). It is seen in patients who have recently lost a lot of weight.
Small bowel path
Celiac sprue
Small bowel malabsorption of gluten
Small bowel path
Celiac sprue high yeild points
- Can cause malabsorption of iron, and lead to iron deficiency anemia.
- Associated with Idiopathic Pulmonary Hemosiderosis (Lane Hamilton Syndrome)
- Increased Risk of bowel wall lymphoma
- Gold standard is biopsy (surprisingly not barium)
- Dermatitis Herpetiformis - some skin thing (remember that from step 1)
Small bowel path
Celiac sprue findings on CT/Barium
- Fold Reversal is the Buzzword (Jejunum like Ileum, Ileum like Jejunum)
- Moulage Sign - dilated bowel with effaced folds (tube with wax poured in it)
- Cavitary Lymph Nodes (low density)
- Splenic Atrophy
Small bowel path
M e c k e l’s D iv erticu lum I D iv e rtic u litiss
This is a congenital true diverticulum of the distal ileum. A piece of total trivia is that it is a persistent piece of the omphalomesenteric duct.
Step 1 style, “rule of 2s” occurs in 2% of the population, has 2 types of heterotopic mucosa (gastric and pancreatic), located 2 feet from the IC valve, it’s usually 2 inches long (and 2 cm in diameter), and usually has symptoms before the child is 2. If it has gastric mucosa (the ones that bleed typically do) it will take up Tc-Pertechnetate just like the stomach (hence the Meckel’s scan).
Small bowel pathM e c k e l’s D iv erticu lum I D iv e rtic u litis
high yield trivia
Can get diverticulitis in the Meckels (mimic appendix)
GI Bleed from Gastric Mucosa (causes 30% of symptomatic cases)
Can be a lead point for intussusception (seen with inverted diverticulum)
Can cause Obstruction
Small bowel path
Duodenal In flam m a to ry Disease:
You can have fold thickening of the duodenum from adjacent inflammatory processes of the pancreas or gallbladder. You can also have thickening and fistula formation with Crohn’s (usually when the colon is the primary site). Primary duodenal Crohns can happen, but is super rare. Chronic dialysis patients may get severely thickened duodenal folds which can mimic the appearance of pancreatitis on barium.
Small bowel path
Jejunal diverticulosis
Less common than colonic diverticulosis, but does occur. They occur along the mesenteric border. Important association is bacterial overgrowth and malabsorption. They could show this with CT, but more likely will show it with barium (if they show it at all).
Small bowel path
Gallstone ileus
Not a true ileus, instead a mechanical obstruction secondary to the passage of a gallstone in the lumen of the bowel. Gallstones access the bowel by eroding through the duodenum (usually). As you can imagine, only elderly or weak patients (those unworthy of serving in the spartan infantry) are susceptible to this erosion.
Small bowel path riglers triad
pneumobilia, obstruction, and an ectopic location o f a gallstone. The classic trick is to try and get you to say that free air - the “Riglers Sign” - is part of the Riglers Triad (it isn’t) — mumble to yourself “nice try assholes.”
Direct signs of bowel trauma
Spilled oral contrast
active mesentric bleed
indirect signs of bowel trauma
fat stranding
fluid layering along the bowel
Shock Complex Features
• Thickened Enhancing Bowel Loops (small bowel involved more than larger bowel)
• On Non-Contrast, bowel loops may appear denser than the psoas
. Collapsed IVC
• HYPO-enhancement of solid organs (liver and spleen)
• Bilateral delayed nephrograms (persistence nephrograms)
• HYPER-enhancement of the adrenals
“Shock Bowel” “Hypovolemic Shock Complex”
This is typically seen with severe hypotension , although anything that gives you low volume - (cardiac arrest, septic shock, bacterial endocarditis, diabetic ketoacidosis, etc.. so on and so forth) can also cause it.
Bowel Trauma vs shock bowel findings
Focal vs Diffuse
Wall Thickening with High Attenuation Blood in the Submucosa vs Wall Thickening with Near Water Attenuation Edema
Mucosa enhances normally (or less than normal) vs Mucosa demonstrates intense enhancement
Secondary signs of injury (free air, leaked contrast, mesenteric hematoma, etc… etc… so on and so forth). vs
Other signs of shock (bright adrenals, flat IVC, etc…)
Small bowel cancer
Adenocarcinoma
Most common in the proximal small bowel (usually duodenum). Increased incidence with celiac disease and regional enteritis. Focal circumferential bowel wall thickening in proximal small bowel is characteristic on CT. The duodenal web does NOT increase the risk.
Small bowel cancer
adenocarcinoma gamesmanship
Adenocarcinoma is more likely to obstruct relative to lymphoma.
Small bowel cancer
Lymphoma
It’s usually the non-Hodgkin flavor. Patients with celiac, Crohns, AIDS, and SLE are higher risk. It can look like anything (infiltrative, polypoid, multiple nodules etc….)
The Hodgkin subtype is more likely to cause a desmoplastic reaction..
Small bowel cancer
lymphoma key triia
do not obstruct even with massive circum involvement
Small bowel cancer
trivia
favors the ileum
Small bowel cancer
gamesmanship
obstruction is rare
Small bowel cancer
Carcinoid
aunt minnie
a mass + desmoplastic stranding. “Starburst” appearance of the mesenteric mass with calcifications.
Small bowel cancer
carcinoid
This tumor most commonly occurs in young adults. The primary tumor is often not seen. That calcified crap you are seeing is the desmoplastic reaction. Liver mets are often hyper vascular. Step 1 style, you don’t get carcinoid syndrome (flushing, diarrhea) until you met to the liver.
The appendix, has the best prognosis of all G1 primary sites. Systemic serotonin degrades the heart valves (right sided), and classically causes tricuspid regurgitation.
MIBG or Octreotide scans can assist with diagnosis
Small bowel cancer
carcinoid most common primary location
distal ileum
Small bowel cancer
Mets
This is usually melanoma (which hits the small bowel in 50% of fatal cases). You can also get hematogenous seeding of the small bowel with breast, lung, and Kaposi sarcoma. Melanoma will classically have multiple targets.
Most common type of abdominalhernia
inguinal M>F (7:1)
femoral hernia
Likely to obstruct. Seen in old ladies. They are medial to the femoral vein, and posterior to the inguinal ligament (usually on the right).
Obturator hernia
Another old lady hernia. Often seen in patients with increased intra-abdominal pressure (Ascites, COPD - chronic cougher). Usually asymptomatic - but can strangulate.
Direct inguinal hernia
Less common
Medial to inferior epigastric artery
Defect in Hesselbach’s Triangle
NOT covered by internal spermatic fascia
Indirect inguinal hernia
More Common
Lateral to inferior epigastric artery
Failure of processus vaginalis to close
Covered by internal spermatic fascia
Lumbar Hernia
Can be superior (Grynfeltt-Lesshaft) through the superior lumbar triangle, or inferior (Petit) through the inferior lumbar triangle. Superior is more common than inferior. Otherwise, they are very similar and usually discussed together. Causes are congenital or acquired (post-surgery).
Spigelian Hernia
The question is probably the location along the Semilunar line ( “S ” fo r “S ”) through the transversus abdominis aponeurosis close to the level of the arcuate line.
Littre hernia
hernia with a meckedl diverticulum in it
amyand hernia
hernia with the appendix in it
Richter hernia
Contains only one wall of bowel and therefore does not obstruct. This are actually at higher risk for strangulation.
Hernias Post laparoscopic Roux-en-Y Gastric Bypass
Factors that promote internal hernia after gastric bypass
(1) Laproscopic over Open - supposedly creates fewer adhesion, so you have more mobility
(2) Degree of weight loss ; more weight loss = less protective, space occupying mesenteric fat.
Hernias Post laparoscopic Roux-en-Y Gastric Bypass
There are 3 potential sites
(1) At the defect in the transverse mesocolon, through which the Roux-Loop Passes (if it’s done in the retrocolic position).
(2) At the mesenteric defect at the enteroenterostomy
(3) Behind the Roux limb mesentery placed in a retrocolic or antecolic position (retrocolic Petersen and antecolic Petersen type). ** This is the one they will likely ask because it has an eponym with it.
Internal Hernias
overviews
The most common manifestation is closed loop obstruction (often with strangulation). There are 9 different subtypes, of which I refuse to cover. I will touch on the most common, and the general concept.
Internal Hernias
General concept
This is a herniation of viscera through the peritoneum or mesentery. The herniation takes place through a known anatomic foramina or recess, or one that has been created post operatively.
Internal Hernias
Paraduodenal
overview
This is by far the most common type of internal hernia. They can
occur in 5 different areas, but it’s much simpler to think of them as left or right. Actually, 75%
of the time they are on the left.
Paraduiodenal leftsided hernia
The exact location is the duodenojejunal junction (“fossa of Landzert”). Here is the trick; the herniated small bowel can become trapped in a “sac of bowel” between the pancreas and stomach to the left of the ligament of Treitz. The sac characteristically
contains the IMV and the left colic artery.
Paraduodenal right sided hernia
located just behind the SMA and just below the transverse segment of
the duodenum, at the “Fossa of Waldeyer.” The classic setting for right-sided PDHs is nonrotated small bowel, with normally rotated large bowel.
Crohns disease
overview
Typically seen in a young adult (15-30), but has a second smaller peak later 60-70. Discontinuous involvement of the entire GI tract (mouth -> asshole). Stomach, usually involves antrum (Ram’s Horn Deformity). Duodenal involvement is rare, and NEVER occurs without antral involvement. Small bowel is involved 80% o f the time, with the terminal ileum almost always involved (Marked Narrowing = String Sign). After
surgery the “neo-terminal ileum” will frequently be involved. The colon involvement is usually right sided, and often spares the rectum / sigmoid. Complications include fistulae, abscess, gallstones, fatty liver, and sacroiliitis.
Crohns disease
squaring of the folds
An early manifestation from obstructive lymphedema
Crohns disease
skip lesions
Discontinuous involvement o f the bowel
Crohns disease
proud loops
Separation of the loops caused by infiltration o f the mesentery, increase in mesenteric fat and enlarged lymph nodes
Crohns disease
cobblestoning
Irregular appearance to bowel wall caused by longitudinal and
transverse ulcers separated by areas o f edema
Crohns disease
pseudopolyps
Islands of hyperplastic mucosa
Crohns disease
Filiform
Post-inflammatory polyps - long and worm-like
Crohns disease
pseudodiverticula
Found on anti-mesenteric side. From bulging area of normal wall opposite side o f scarring from disease
Crohns disease
string-sign
Marked narrowing of terminal ileum from a combination of edema, spasm, and fibrosis
IBD trivia associating
increased risk of melanoma
UC overview
Just like Crohns, it typically occurs in a “young adult” (age 15-40), with a second peak at 60-70. Favors the male gender. It involves the rectum 95% of the time, and has etrograde progression. Terminal ileum is involved 5-10% of the time via backwash ileitis (wide open appearance). It is continuous and does not “skip” like Crohns. It is associated with Colon Cancer, Primary Sclerosing Cholangitis, and Arthritis (similar to Ankylosing Spondylitis).
UC Barium
On Barium, it is said that the colon is ahaustral, with a diffuse granular appearing mucosa. “Lead Pipe” is the buzzword (shortened from fibrosis).
UC key clinical point
UC has an increased risk of cancer (probably higher than Crohns), and it doesn’t classically have enlarged lymph nodes (like Crohns does), so if you see a big lymph node in an UC patient (especially one with long standing disease), you have to think that it might be cancer.
More common in crohns vs UC
Gallstones
PSC
Hepatic Abscess
Pancreatities
Gallstones Crohns
PSC UC
Hepatic Abscess Crohns
Pancreatities Crohns
Cronhs this vs that
Slightly less common in the USA Discontinuous “Skips” Terminal Ileum - String Sign Ileocecal Valve “Stenosed” Mesenteric Fat Increased "creepingfat” Lymph nodes are usually enlarged Makes Fistulae
UC this vs that
Slightly more common in the USA Continuous Rectum Ileocecal Valve “Open” Perirectal fat Increased Lymph nodes are NOT usually enlarged Doesn’t Usually Make Fistulae
Toxic Megacolon
Ulcerative colitis, and to a lesser degree Crohns, is the primary cause. C-Diff can also cause it. Gaseous dilation distends the transverse colon (on upright fdms), and the right and left colon on supine films. Lack of haustra and pseudopolyps are also seen. Some people say the presence of normal hausta excludes the diagnosis. Don’t do a barium enema because of the risk of perforation. Another piece of trivia is that peritonitis can occur without perforation.
Behcets
Ulcers of the penis and mouth. Can also affect GI tract (and looks like Crohns) - most commonly affects the ileocecal region. It is also a cause of pulmonary artery aneurysms (test writers like to ask that).
Diverticulosis/Dviverticulitis
Some trivia worth knowing is that diverticulosis actually bleeds more than diverticulitis. Right-sided is less common (but is seen in young Asians). Fistula fonnation is actually most common with diverticulitis, and can occur to anything around it (another piece of bowel, the bladder, etc..).
Epiploic appendagitis
Epiploic appendages along the serosal surface of the colon can torse, most commonly on the left. There is not typically concentric bowel wall thickening (unlike diverticulitis).
Omental infarction is typically a larger mass with a more oval shape and central low density. It
is more common on the right (ROI - right omental infarct). Both entities are self-limiting.
Appendicitis
steps
The classic pathways are: obstmction (fecalith or reactive lymphoid tissue) -> mucinous fluid builds up increasing pressure -> venous supply is compressed -> necrosis starts -> wall breaks down -> bacteria get into wall -> inflammation causes vague pain (umbilicus) -> inflamed appendix gets larger and touches parietal peritoneum (pain shifts to RLQ).
appendix mucocele
Mucinous cystadenomas are the most common mucinous tumor of the appendix. They produce mucin and can really dilate up and get big. They look similar to cystadenocarcinomas and can perforate leading to pseudomyxoma peritonei. On ultrasound the presence of an “onion sign” - layering within a cystic mass - is a suggestive feature of a
mucocele.
Omental infarction
Omental infarction is typically a larger mass with a more oval shape and central low density. It is more common on the right (ROI - right omental infarct). Both entities are self-limiting.
Appenix ages
It occurs in an adolescent or young adult (or any age).
appendix ct
The measurement of 6 mm was originally described with data from ultrasound compression, but people still generally use it for CT as well. Secondary signs of inflammation are probably more reliable for CT.
appendix gamesmanship
In pregnancy MRI without contrast is the test of choice
sigmoid colonic volvulus
Most common adult form. Seen in the nursing home patient (chronic constipation is a predisposing factor). This is the “Grandma” volvulus. Buzzword is coffee bean sign (or inverted 3 sign). Another less common buzzword is Frimann Dahl’s sign - which refers
to 3 dense lines converging towards the site o f obstruction. Points to the RUQ. Recurrence rate after decompression = 50%.
cecal colonic volvulus
Seen in a younger person (20-40). Associated with people with a “ long mesentery.” More often points to the LUQ. Much less common than sigmoid.
Cecal bascule colonic volvulus
Anterior folding o f the cecum, without twisting. A lot o f surgical text books dispute this thing even being real (they think it’s a focal ileus). The finding is supposedly dilation o f the cecum in an ectopic position in the middle abdomen, without a mesenteric twist.
Colonic Pseudo-Obstruction
(Colonic Ileus, Ogilvie Syndrome): Usually seen after serious medical conditions and in nursing home patients. It can persist for years, or progress to bowel necrosis and perforation. The classic look is marked diffuse dilation o f the large bowel, without a discrete transition point.
Diversion colitis
Bacterial overgrowth in a blind loop through which stool does not pass (any surgery that does this).
Colitis cystica
superficial
The superficial kind consists of cysts that are small in the entire colon. It’s associated with vitamin deficiencies and tropical sprue. Can also be seen in terminal leukemia, uremia, thyroid toxicosis, and mercury poisoning.
Colitis cystica
deep
These cysts may be large and are seen in the pelvic colon and rectum.
Rectal cavernous hemangioma
Obviously very rare. Just know it’s associated with a few syndromes; Klippel-Trenaunay-Weber, and Blue Rubber Bleb. They might show is. you a ton of phleboliths down there.
Gossypiboma
It’s a retained cotton product or surgical sponge and it can elicit an inflammatory response.
Entamoeba Histolytica
Parasite that causes bloody diarrhea. Can cause liver abscess, spleen abscess, or even brain abscess. Within the colon it is one of the causes of toxic megacolon. They are typically “flask-shaped ulcers” on endoscopy.
It affects the cecum and ascending colon most commonly and unlike many other GI infections, spares the terminal ileum.
Entamoeba histolytica
barium
the buzzword is “conedcecum” referring to a change in the normal bulbous appearance of the cecum, to that of a cone.
Colonic TB
Typically involves the terminal ileum, and is another cause of the “coned cecum”
appearance. Causes both ulcers and areas of nanowing. Two other signs: (1) Fleischner sign - enlarged gaping IC valve, and (2) Stierlin sign - narrowing of the Tl.
Infections tht like the duodenum and proximal small bowel
Giardia
strongyloides
infections that like the TI
TB
Yersinia
This vs that sigmoid vs cecal
sigmoid - old person, points to the RUQ
cecal - younger person, points to the LUIQ
colonic CMV
Seen in patients who are immunosuppressed. Causes deep ulcerations - which can lead to perforation. Step 1 question = Cowdry Type A intranuclear inclusion bodies
C-DIFF
Classically seen after antibiotic therapy, the toxin leads to a super high WBC count. CT findings of the “accordion sign” with contrast trapped inside mucosal folds is always described in review books and is fair game for multiple choice. The barium findings include thumb printing, ulceration, and irregularity. Of course it can cause toxic megacolon as mentioned on the prior page.
Neutropenic Colitis (Typhlitis):
Infection limited to the cecum occurring in severe neutropenia.
Colon Cancer
adenocarcinoma
overview
Common cause of cancer death (#2 overall). Cancers on the right tend to
bleed (present with bloody stools, anemia). Cancers on the left tend to obstruct. Apple core is a buzzword.
Colon Cancer
adenocarcinoma
gamesmanship
Large bowel intussusception in adult = Malignancy
Colon Cancer
adenocarcinoma
gamesmanship 2
Colon likes to Met to the Liver. Liver Mets will classically be T1 Dark, T2 Mildly Bright (“evil grey”), heterogenous non-progressive in enhancement, sometimes target.
Colon Cancer
squamos cell carcinoma
occasionally in the anus (HPV)
Rectal Cancer Trivia
- Nearly always (98%) adenocarcinoma
- If the path says Squamous - the cause was HPV (use your imagination on how it got there).
- Lower rectal cancer (0-5 cm from the anorectal angle), have the highest recurrence rate.
- MR1 is used to stage - and you really only need T2 weight imaging - contrast doesn’t matter
- Stage T3 - called when tumor breaks out of the rectum and into the perirectal fat. This is the critical stage that changes management (they will get chemo/rads prior to surgery).
nodes in perirectal fat are abnormal when
> 5mm
High rectal cancer
- Treated with Low Anterior Resection (LAR)
- These patients will maintenance fecal
continence post op
Low rectal cancer
- Treated with Abdomino- Perineal Resection (APR)
- These poor bastards will end up with colostomies
Rectal Cancer surgery
classically determined by the position of the tumor relative to the butthole.
Most people will use the number “5 cm” above the anorectal angle to delineate “high” vs “low.”
Both surgical approaches are performed with a total mesorectal excision (tumor, nodes, and blood supply).
Colon lipomas
Second most common tumor in the colon
Colon adenomas
The most common benign tumor of the colon and rectum. The villous adenoma has the largest risk fo r malignancy.
McKittrick-Wheelock Syndrome:
This is a villous adenoma that causes a mucous diarrhea leading to severe fluid and electrolyte depletion.
The clinical scenario would be something like “80 year old lady with diarrhea, hyponatremia, hypokalemia, hypochloremia… and this” and they show you a mass in the rectum / bowel.
Pseudomyxoma Peritonei
This is a gelatinous ascites that results from either
(a) ruptured mucocele (usually appendix), or intraperitoneal spread of a mucinous neoplasm (ovary, colon, appendix, and pancreas). It’s usually the appendix (least common is the pancreas).
The buzzword is “scalloped appearance of the liver.” Recurrent bowel obstructions are common
Peritoneal carcinomatosis
The main thing to know regarding peritoneal implants is that the natural flow of ascites dictates the locat ion of implants. This is why the retrovesical space is the most common spot, since it’s the most dependent part of the peritoneal cavity.
Omental seeding/caking
The omental surface can get implanted by cancer and become thick (like a mass). The catch-phrase is “posterior displacement of the bowel from the anterior abdominal wall.”
Primary peritoneal mesothelioma
This is super rare. People think about mesothelioma involving the pleura (and it does 75% of the time), but the other 25% of the time it involves the peritoneal surface. The thing to know is that it occurs 30-40 years after the initial asbestosis exposure.
Cystic peritoneal mesothelioma
This is the even more rare benign mesothelioma, that is NOT associated with prior asbestos exposure. It usually involves a women of childbearing
age (30s).
Mesenteric Lymphoma
This is usually non-Hodgkin lymphoma, which supposedly involves the mesentery 50% of the time. The buzzword is “sandwich sign.” The typical appearance is a lobulated confluent soft tissue mass encasing the mesenteric vessels “sandwiching them.”
Barium peritonitis
This is why you use water soluble contrast anytime you are worried about leak. The pathology is an attack of the peritoneal barium by the leukocytes which creates a monster inflammatory reaction (often with massive ascites and sometimes hypovolemia and resulting shock). If no “real doctor” is available, you should give IV fluids to reduce the risk of hypovolemic shock. The long tenn sequela of barium peritonitis is the development of granulomas and adhesions (causing obstructions and an eventual lawsuit).
Barium intravasation
This is super rare, but can happen. If barium ends up in the systemic circulation it kills via pulmonary embolism about 50% of the time. Risk is increased in patients with inflammatory bowel or diverticulitis (altered mucosa).
Liver bare area
The liver is covered by visceral peritoneum except at the porta hepatis, bare area, and the gallbladder fossa. An injury to the “bare area” can result in a retroperitoneal bleed.
Couinaud system
testable trivia
- Right Hepatic Vein Divides 7/8, and 6/5
- Middle Hepatic Vein Divides 4a/8, 4b/5
- Left Hepatic Vein / Fissure for the Ligamentum Teres (falciform) divides 4a/2, 4b/3
- The Portal Vein Divides the Liver into Upper and Lower Segments
- The Caudate Lobe (Segment 1) is unique in that it drains directly to the IVC.
Cantlies line
divides the liver into a functional left and right hepatic lobes.
This line runs from the IVC to the middle of the gallbladder fossa.
Caudate Lobe
The caudate lobe (segment 1) has a direct connection to the IVC through it’s own hepatic veins, which do not communicate with the primary hepatic veins.
Additionally, the caudate is supplied by branches o f both the right and left portal veins - which matters because the caudate may be spared or hypertrophied as the result o f various pathologies such as Budd Chiari, etc…
Liver trivia 1
Along the same lines of anatomy explaining pathology, the intra-hepatic course of the right portal vein is longer than the left, which is why it is more susceptible to fibrosis (this is why the right liver shrinks, and the left liver grows in cirrhotic morphology).
Liver trivia 2
Most common vascular variant = Replaced right hepatic (origin from the SMA)
Liver trivia 3
Most common biliary variant = Right posterior segmental into the left hepatic duct.
Liver Normal MRI Signal Characteristics
I like to think of the spleen as a bag o f water/blood (T2 bright, T1 dark). The pancreas is the “brightest T1 structure in the body” because it has enzymes. The liver also has enzymes and is similar to the pancreas (T1 Brighter, T2 darker), just not as bright as the pancreas
Liver fetal circulation
Placenta > Umbilical Vein > Liver > IVC
Placenta > Umbilical vein > Ductus Venosus (remnant of ligamentum venosum) > IVC
Liver us trivia
Pancreas should be more echogenic than liver
classic liver ultrasound anatomy
pic 1 Pancreas
Anterior to posterior
Pancreas Splenic vein SMA LRV to the IVC on the pts right Aorta Vert Body
classic liver ultrasound anatomy
pic 2 porta hepatis
Anterior to posterior
CBD
RHA
PV
Liver pic three porta hepatis mickey mouse
Left ear Bile duct
Right hear hepatic artery
Head portal vein
Another consequences of the Longer Right Portal Vein Course is that Hepatic Abscess (often from ascending hematogenous sources) nearly always (75%+) involves
right hepatic lobe
Cirrhosis most common cause
us
world
etoh
schistosomiasis
portal htn measurements
portal vein pressure 6-8 mmhg above hepatic veins
variceal bleeding and ascites around >12mmhg
prehepatic causes of portal htn
portal vein thrombosis
tumor compression
hepatic causes of portal htn
cirrhosis
schistosomiasis
posthepatic causes of portal htn
budd chiari
prehepatic portal htn collateral
form above the diaphragm
THAD overview
These Transient Hepatic Attenuation Differences are typically seen in the arterial / early portal phase - NOT on the equilibrium / delayed phases (hence the word “transient”). The easiest way to think about them is that they are focal “arterial buffer responses.” In other words, in that tiny little spot right there the liver feels like there isn’t enough portal flow, so it responses by increasing the arterial flow.
Causes of THAD
Cirrhosis
Clot
Mass
Abscess/Infection
THAD
Cirrhosis
A bunch o f scar / fibrosis deforms the hepatic sinusoids compressing the tiny little portal veins (think about arteries and veins in the neck or groin - pressure will compress the vein first) - people call this “shunting.” This is most typical in the subcapsular region.
THAD
Clot
Venous blood flow could be compromised from a clot in a portal vein branch (these enhancement patterns are typically larger, wedge shaped, and extend towards the periphery).
THAD
MAss
(B9 or Malignant): This can occur from two primary mechanisms. 1 - You could have the direct mass effect from the mass smashing the veins. 2 - The tumor could be recruiting /up-regulating arterial flow (VEGF etc…).
THAD
Abscess/Infection
Also probably a mixed mechanism. Some direct mass effect, but also
some element o f “hyperemia” - causing a “siphon effect.” For clarity we aren’t just talking liver abscess here, cholecystitis can also have this region effect.
parasitizing the portosystemic decompressive apparatus
So the artery does something else, it opens up tiny little connections to the portal system. The enlargement o f these tiny communications has been referred to as “parasitizing the portosystemic decompressive apparatus.”
Portal hypertensive colopathy
With increased resistance in the liver to the portal circulation, you also start to have colonic venous stasis (worse on the right). This can lead to “Portal Hypertensive Colopathy, ” which is basically an edematous bowel that mimics colitis.
Portal hypertensive colopathy
why worse on the right
The short answer is that collateral pathways develop more on the left (splenorenal shunt, short gastrics, esophageal varices), and decompress that side.
Portal hypertensive gastropathy
same things as portal hypertensive colopathy but in the stomach
causing a thickened gastric wall on CT, as welt as cause upper GI bleeding in the absence of varices.
HCC overview
This is how multi-focal HCC starts. Regenerative nodules -> Dysplastic nodules (increased size and ccilularity) -> HCC. As this process takes place, the nodule changes from preferring to drink portal blood to only wanting to drink arterial blood. This helps explain why HCC has arterial enhancement and rapid washout. The transformation also follows a progression from T2 dark (regenerative) -> T2 bright (HCC).
HCC transformation buzzword
“nodule within nodule ’’ where a central bright T2 nodule has a T2 dark border. This is concerning for transformation to HCC.
Regenerative nodules
Contains iron
T1 dark T2 dark
does not enhance
Dysplastic nodules
Contains fat, glycoprotein
T1 bright T2 Dark
Usually does no enhance
HCC nodules
T2 bright
does enhance
OATP
As hepatocytes become cancer they lose function in this transporter and become dark on the delayed phase. The exception (highly testable) is the well differentiated HCC which retains OATP function and is therefore bright on the 20 min delayed Eovist sequence.
Hepatic contrast phase timing
arterial phase 25-30 seconds
portal venous phase 70 seconds
liver late arterial phase
This (“Late A rterial”) is the most critical phase for HCC evaluation. You can recognize this timing as contrast in the hepatic artery and portal vein (but none in the hepatic veins).
Liver window
Center 100
width 200
MR Contrast Hepatobiliary Considerations
How they work
Gadolinium (which is super toxic) is bound to some type of chelation agent to keep it from killing the patient. The shape and function of the chelation agent determine the class and brand name. The paramagnetic qualities of gadolinium cause a local shortening of the T1 relaxation time on neighboring molecules (remember short T1 time = bright image).
MR Contrast Hepatobiliary Considerations
Types of agents
I want you to think about MR1 contrast in two main flavors:
(1) Extracellular
(2) Hepatocyte Specific.
MR Contrast Hepatobiliary Considerations
Etracellular
These are nonspecific agents that are best thought of as Iodine contrast for
CT. They stay outside the cell and are blood flow dependent (just like CT contrast). The
imaging features in lesions will be the same as CT - although the reason they look bright is
obviously different - CT contrast increases the density (attenuation), MR contrast shortens the
T1 time locally - which makes T1 brighter. The classic imaging set up is a late hepatic arterial
phase (15-30 seconds), portal venous phase (70 seconds), and a hepatic venous or interstitial
phase (90 seconds - 5 mins) - just like CT.
MAgnevist
MR Contrast Hepatobiliary Considerations
Hepatocyte specific
Certain chelates are excreted via the bile salt pathway. In other
words, they are taken up by normal hepatocytes and excreted into the bile. This gives you great
contrast between normal hepatocytes and things that aren’t normal hepatocytes (cancer). The 20
min delay is the imaging sequence that should give you a homogenous bright liver (dark holes
are things that don’t contain normal liver cells / couldn’t drink the contrast). The problem is that
it’s pretty non-specific with a handful of benign things still taking it up (classical example is
FNH), and at least one bad thing taking it up (well-differentiated HCC). Plus, a handful of
benign things won’t take it up (cysts, etc..). There are at least three good reasons to use this
kind of agent: (1) it’s great for proving an FNH is an FNH - as most lesions won’t hold onto the
Gd at 20 mins, (2) it’s great for looking for bile leaks, and (3) once you’ve established a
baseline MRI (characterized all those benign lesions) it’s excellent for picking up new mets
(findings black holes on a white background is easy).
Eovist
Is Eovist a pure Hepatocyte Specific Agent
Nope - It also acts like a non-specific extracellular agent early on (although less intense). About 55% is excreted into the bile - and gives a nice intense look at 20 mins.
What about Gd-BOPTA (Multihance)
This is mostly an extra-cellular agent, but has a small amount (5%) of biliary excretion. The implication is that you can use Multihance to look for a bile leak you just have to wait longer (45mins-3 hours) for the Gd to accumulate.
What about Manganese instead o f Gd
This is the old school way to do biliary imaging. It works the same as Gd - by causing T1 shortening.
Luver Hemangioma
This is the most common benign liver neoplasm. Favors women 5:1. They may enlarge with pregnancy. On US will be bright (unless it’s in a fatty liver, than can be relatively dark). On US, flow can be seen in vessels adjacent to the lesion but NOT in the lesion. On CT and MR1 tends to match the aorta in signal and have “peripheral nodular
discontinuous enhancement”. Should totally fill in by 15 mins. Atypical hemangioma can have the “reverse target sign.”
Liver Hemangioma
Trivia
A hemangioma can change its sonographic appearance during the course of a single examination. No other hepatic lesion is known to do this.
Hemangioma ultrasound pearls
Need to core for biopsy, FNA does not get enough tissue (only blood)
Hyperechoic (65%)
Enhanced thru transmission is common
NO Doppler flow inside the lesion itself
Atypical appearance - hyperechoic periphery, with hypoechoic center (reverse target)
Calcifications are extremely rare
FNH
This is the second most common benign liver neoplasm. Believed to start in utero as an AVM. It is NOT related to OCP use. It is composed of normal hepatocytes, abnormally arranged ducts, and Kupffer cells (reticuloendothelial cells). May show spoke wheel on US Doppler. On CT, should be“homogenous” on arterial phase. Can have a central scar. Scar will demonstrate delayed enhancement (like scars do).
Sulfur Colloid is always the multiple choice test question (reality is that it’s only hot 30-40%). Unlike hepatic adenomas, they are not related to the use of birth control pills, although as a point of confusing trivia and possibly poor multiple choice test question writing, birth control pills may promote their growth.
Focal Nodular Hyperplasia (FNH):
Trivia
You have to hit the scar, otherwise path results will say normal hepatocytes.
FNH stealth
a “Stealth” lesion on MRI - T1 and T2 isointense.
Hepatic adenoma
Usually a solitary lesion seen in a female on OCPs. Alternatively could be seen in a man on anabolic steroids. When it’s multiple you should think about glycogen storage disease (von Gierke) or liver adenomatosis. No imaging methods can reliably differentiate hepatic adenoma from hepatocellular carcinoma. Rarely, they may degenerate into HCC after a long period of stability. They often regress after OCPs are stopped. Their propensity to bleed sometimes makes them a surgical lesion if they won’t regress.
Hepatic adenoma
gamesmanship
Signal Drop Out with in and out of phase can be used to show fat
Hepatic adenoma
Trivia
Q: Most common location for hepatic adenoma (75%)
A: Right Lobe liver
Hepatic adenoma
management
You stop the OCPs and re-image, they should get smaller. Smaller than 5cm, watch them. Larger than 5cm they often resect because (1) they can bleed and (2) they can rarely turn into cancer.
HCC
Occurs typically in the setting of cirrhosis and chronic liver disease; Hep B, Hep C, hemochromatosis, glycogen storage disease, Alpha 1 antitrypsin. AFP elevated in 80-95%. Will often invade the portal vein, although invasion of the hepatic vein is considered a more “specific finding.’’
HCC
Doubling time
the classic Multiple Choice Question. This is actually incredibly stupid to ask because there arc 3 described patterns of growth (slow, fast, and medium). To make it an even worse question, different papers say different stuff. Some say: Short is 150 days, Medium to 150-300, and Long is >300. I guess the answer is 300 - because it’s in the middle. Others define medium at around 100 days. A paper in Radiology {May 2008 Radiology, 247, 311-330) says 18-605 days. The real answer would be to say follow up in 3-4.5 months.
HCC
Other random trivia
HCCs like to explode and cause spontaneous hepatic bleeds.
this vs that
FNH vs Fibrolamellar HCC
FNH FL HCC
T2 Bright T2 Dark (usually)
Enhances on Delays Does NOT enhance
Mass is Sulfur Colloid Avid (sometimes)
Mass is Gallium Avid
this vs that
HCC vs FL HCC
HCC FL HCC Cirrhosis No Cirrhosis Older (50s-60s) Young (30s) Rarely Calcifies Calcifies Sometimes Elevated AFP Normal AFP
Cholangiocarcinoma
overview
Where HCC is a cancer of the hepatocyte, cholangiocarcinoma is a cancer of the bile duct. Cholangiocarcinoma believes in nothing Lebowski. It fucks you up, it takes the money (prognosis is poor).
Cholangiocarcinoma
gamesmanship
Gamesmanship - They could tell you the dude has ulcerative colitis, as a way to infer that he also has PSC.
Cholangiocarcinoma
buzzword
“Painless Jaundice.” (just like pancreatic head CA)
Cholangiocarcinoma
who gets it
The most classic multiple choice scenario would be an 80 year old man, with primary sclerosing cholangitis - PSC (main risk factor in the West), recurrent pyogenic “oriental” cholangitis (main risk factor in the
East), Caroli Disease, Hepatitis, HIV, history of cholangitis, and fucking Liver Worms (Clonorchis). Oh who also had a semi-voluntary cerebral angiogram
performed by a Nazi with a cleft asshole (in 1930s Germany, Thorotrast was the preferred angiographic contrast agent).
Cholangiocarcinoma
what does ti look like
It is variable and the described subtypes overlap. The easiest way to conceptualize this thing is as a scar generating cancer. Fibrosis (scar) is the main thing you are seeing - either primarily as a mass that enhances on delayed imaging (just like scar in the heart), or secondarily through the desmoplastic pulling of the scar (example capsular retraction and ductal dilation). The dilation of ducts is most likely to be shown as unilateral and
peripheral, although if the lesion is central the entire system can obstruct.
cCholangiocarcinoma
classic features
Delayed Enhancement
Peripheral Biliary Dilation
Liver Capsular Retraction
NO tumor capsule
Klatskin tumor
Cholangiocarcinoma that occurs at the bifurcation of the right and left hepatic ducts. It’s usually small but still causes biliary obstruction (“shouldering / abrupt tapering” on MRCP). These things are mean as cat shit. It is a “named” subtype, so that increases the likelihood of it showing up on a multiple choice exam.
Cholangiocarcinoma
staging pearls
- Proximal extent of involvement is a key factor for surgical candidacy (more = bad).
- Atrophy of a lobe implies biliary +/- vascular involvement o f that lobe (imaging often underestimates disease burden).
- Typically combinations of bilateral involvement (veins on the right, ducts on the left - vice versa, etc.. etc… etc… ) is bad news.
this vs that
Cholangiocarcinoma vs hcc
HCC = Invades the Portal Vein
Cholangiocarcinoma = Encases the
Portal Vein
ABD tumor markers
-Cholangio: CEA and Ca19-9 elevated
Pancreatic Ca19-9 elevated
Colon CA: CEA elevated
Hepatic Angiosarcoma
This used to be the go to for thorotrast questions. Even though everyone who got thorotrast died 30 years ago, a few dinosaurs writing multiple choice test questions still might ask it. Hepatic Angiosarcoma is very rare, although technically the most common primary sarcoma o f the liver. It is associated with toxic exposure - arsenic use (latent period is about 25years), Polyvinyl chloride exposure, Radiation, and yes… thorotrast.
Hepatic angiosarcoma addt trivia
Can see in hemochromatosis and NF patients
biliary cystadenoma
Uncommon benign cystic neoplasm o f the liver. Usually seen in middle aged women. Can sometimes present with pain, or even jaundice. They can be unilocular or multilocular and there are no reliable methods for distinguishing from biliary cystadenocarcinoma (which is unfortunate).
Mets to the Liver
If you see rnets in the liver, first think colon. Calcified mets are
usually the result o f a mucinous neoplasm (colon, ovary, pancreas).
Mets to the Liver
US
Hyperechoic mets are often hypervascular (renal, melanoma, carcinoid, choriocarcinoma, thyroid, islet cell). Hypoechoic mets are often hypovascular (colon, lung, pancreas).
Mets to the Liver
too small to characterize
even in the setting of breast cancer (with no definite hepatic mets) tiny hypodensities have famously been shown to be benign 90-95% o f the time.
Liver lymphoma
Hodgkins lymphoma involves the liver 60% o f the time (Non Hodgkins is around 50%), and may be hypoechoic.
Kaposi sarcoma liver
Seen in patients with AIDS. Causes diffuse periportal hypoechoic infiltration. Looks similar to biliary duct dilation.
Hemangioma
Ultrasound
Hyperechoic with increased through transmission
Hemangioma
CT
Peripheral
Nodular
Discontinuous
Hemangioma
MR
T2 Bright
Hemangioma
Trivia 1
Rare in
Cirrhotics
Hemangioma
Trivia 2
Kasabach- Merritt; the sequestration of platelets from giant cavernous hemangioma
FNH
Ultrasound
Spoke
Wheel
FNH
CT
Homogenous
Arterial
Enhancement
FNH
MR
“Stealth
Lesion -
Iso on T1
and T2”
FNH
Trivia 1
Central
Scar
FNH
Trivia 2
Bright on
Delayed
Eovist
(Gd-EOBDTPA)
Hepatic Adenoma
Ultrasound
Variable
Hepatic Adenoma
CT
Variable
Hepatic Adenoma
MR
Fat
Containing
on In/Out
Phase```
Hepatic Adenoma
Trivia 1
OCP use,
Glycogen
Storage
Disease
Hepatic Adenoma
Trivia 2
Can
explode
and bleed
Hepatic angiomyolipoma
Ultrasound
Hyperechoic
Hepatic angiomyolipoma
CT
gross fat
Hepatic angiomyolipoma
MR
t1 and t2 bright
Hepatic angiomyolipoma
Trivia 1
Unlike renal AML, 50% don’t have fat
Hepatic angiomyolipoma
Trivia 2
Tuberous sclerosis
Congenital liver
cystic kidney disease
Patient’s with AD polycystic kidney disease will also have cysts in the liver. This is in contrast to the AR form in which the liver tends to have fibrosis.
Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu)
Autosomal dominant disorder characterized by multiple AVMs in the liver and lungs. It leads to cirrhosis and a massively dilated hepatic artery.
Hereditary Hemorrhagic Telangiectasia (Osler-Weber-Rendu)
trivia
The lung AVMs set you up for brain abscess.
Liver infections where?
Most common in the right hepatic lobe bc of the longer R port vein
Liver infection buzzwords
viral hepatitis
starry sky (US)
Liver infection buzzwords
pyogenic abscess
double target (CT)
Liver infection buzzwords
Candida
Bulls eye (US)
Liver infection buzzwords
amoebic abscess
Extra hepatic extension
Liver infection buzzwords
Hydatid diesease
Water lily Ct sand storm US?
Liver infection buzzwords
Schistosomiasis
tortois shell
Liver infections
Viral
Hepatitis which is chronic in B and C, and acute with the rest. A point of trivia is that HCC in the setting of hepatitis can occur in the acute form of Hep B (as well as chronic). Obviously, chronic hep C
increases risk for HCC. On ultrasound the “starry sky” appearance can be seen. Although, this is non-specific and basically just the result of liver edema making the fat surrounding the portal triads look brighter than normal.
Liver infections
Pyogenic overview
These can mimic cysts. For the purpose of multiple choice, a single abscess is Klebsiella, and multiple are E. Coli. The presence of gas is highly suggestive of pyogenic abscess.
Liver infections
double targert
pyogenic
sign with central low density, rim enhancement, surrounded by more low density is the classic sign of a liver abscess on CT.
Liver infections
next step amebic abscess
A special situation (potentially testable) is the amebic abscess in the left lobe. Those needs to be emergently drained (they can rupture into the pericardium).
Fitz-Hugh-Curtis Syndrome
Overview
This syndrome is seen exclusively in women of questionable moral standard (“free spirits”). It manifests on multiple choice exams in the setting of known pelvic inflammatory disease (Gonococcal salpingitis and/or Chlamydia infection), with right upper quadrant pain
Fitz-Hugh-Curtis Syndrome
imaging
The classic imaging features are enhancement of the anterior liver capsule, perihepatic ascites, and peritoneal septations. They could show you a tubo-ovarian abscess in the pelvis to cue you in on the excessively promiscuous behaviors this young lady has been engaging in.
Fatty liver
overview
Very common in America. Can be focal (next to gallbladder or ligamentum teres), can be diffuse, or can be diffuse with sparing. You can call it a few different ways.
Fatty liver
CT
If it’s a non-contrast study, 40 HU is a slam dunk. If it’s contrasted, some people say you can NEVER call it. Others say it’s ok if (a) it’s a good portal venous phase (b) the HU is less than 100, and (c) it’s 25 H.U. less than the spleen.
Fatty liver
US
If the liver is brighter than the right kidney you can call it. Hepatosteatosis is a fat liver. NASH (hepatitis from a fat liver) has abnormal LFTs.
Fatty liver
MRI
Two standard deviation difference between in and out of phase imaging. Remember the drop out is on the out of phase images (india ink ones - done at T.E 2.2 ms - assuming 1.5T).
Fatty liver
Stuffery
This signal drop out assumes there is more water than fat in the liver. As such, the degree of signal loss is maximum when the fat infiltration is 50% (exactly 1:1 signal loss). When the percentage of fat grows larger than 50% you will actually see a less significant signal loss on out of phase imaging, relative to that maximum 50%.
Fatty liver
What causes it
McDonalds, Burger King, and Taco Bell. Additional causes include chemotherapy (breast cancer), steroids, cystic fibrosis.
Hemochromatosis
overview
Iron overload. They can show this two main ways:
(1) The first is just liver and spleen being T 1 and T2 dark.
(2) The second (and more likely) way this will be shown is in and out of phase changes the opposite of those seen in hepatic steatosis. Low signal on in phase, and high signal on out of phase (“Iron on In-phase”)
Hemochromatosis innout
Watch out now — this is the opposite of the fat drop out
- *FAT - Drop out on OUT of phase (india ink one - T.E. 2.2 ms) - 1.5 T
- *IRON - Drop out on IN phase (non india ink one - T.E. 4.4 ms) - 1.5 T
Hemochromatosis
primary
the inherited type, caused by more GI uptake, with resulting iron overload. The key point is the pancreas is involved and the spleen is spared.
Hemochromatosis
secondary
the result of either chronic inflammation or multiple transfusions. The body reacts by trying the “Eat the Iron,” with the reticuloendothelial system. The key point is the pancreas is spared and the spleen is not.
This vs that
hemochromatosis primary vs secondary
Primary Secondary
genetic elev absorption acquired trans
liver and panc liver and spleen
heart, thyroid, pituitary
Budd Chiari Syndrome overview
Classic multiple choice scenario is a pregnant woman, but can occur in any situation where you are hypercoagulable (most common cause is idiopathic). The
result of hepatic vein thrombosis.
Budd Chiari Syndrome
imaging findings
The characteristic findings of Budd-Chiari syndrome include hepatic venous outflow obstruction, intrahepatic and systemic collateral veins, and large regenerative (hyperplastic)
nodules in a dysmorphic liver. The caudate lobe is often massively enlarged (spared from separate drainage into the IVC). In the acute phase, the liver will show the classic “flip-flop pattern ’’ on portal phase with low attenuation centrally, and high peripherally. The liver has been described as “nutmeg” with an inhomogeneous mottled appearance, and delayed enhancement of the periphery of the liver.
who gets a nutmeg liver
- Budd Chiari
- Hepatic Veno-occlusive disease
- Right Heart Failure (Hepatic Congestion)
- Constrictive Pericarditis
Budd Chiari Syndrome
arterial
Central Enhancement
Peripheral Minimal
Budd Chiari Syndrome
portal v
Central Washout
Peripheral Enhancement
Budd Chiari Syndrome
renerative nodules
Regenerative (hyperplastic) nodules can be difficult to distinguish from multifocal hepatocellular carcinoma. They are bright on T1 and typically dark or iso on T2. Multiple big (>10cm) and small (<4cm) nodules in the setting of Budd-Chiari suggest a benign process. T2 dark also helps (HCC is usually T2 bright).
Budd Chiari Syndrome presentation
Presentation can be acute or chronic. Acute from thrombus into the hepatic vein or IVC. These guys will present with rapid onset ascites. Chronic from fibrosis of the intrahepatic veins, presumably from inflammation.
who gets massive caudate lobe hypertrophy
- Budd Chiari
- Primary Sclerosing Cholangitis
- Primary Biliary Cirrhosis
Hepatic Veno-occlusive Disease
This is a form of Budd Chiari that occurs from occlusion of the small hepatic venules. It is endemic in Jamaica (from Alkaloid bush tea). In the US it’s typically the result of XRT and chemotherapy. The main hepatic veins and IVC will be patent, but portal waveforms will be abnormal (slow, reversed, or to-and fro).
Passive Congestion
overview
Passive hepatic congestion is caused by stasis of blood within the liver due to compromise o f hepatic drainage. It is a common complication of congestive heart failure and constrictive pericarditis. It is essentially the result o f elevated CVP transmitted from the right atrium to the hepatic veins.
Passive Congestion:
Findings
Refluxed contrast into the hepatic veins
Increased portal venous pulsatility
Nutmeg liver
Portal Vein Thrombosis
Occurs in hypercoaguable states (cancer, dehydration,e tc .. .)• Can lead to cavernous transformation, with the development of a bunch of serpiginous vessels in the porta hepatis which may reconstitute the right and left portal
veins. This takes like 12 months to happen (it proves portal vein is chronically occluded).
Pseudo Cirrhosis
Treated breast cancer mets to the liver can cause contour changes that mimic cirrhosis. Specifically, multifocal liver retraction and enlargement o f the caudate has been described. Why this is specific for breast cancer is not currently known, as other mets to the liver don’t produce this reaction.
Cryptogenic Cirrhosis
Essentially cirrhosis o f unknown cause. Most o f these cases are probably the result of nonalcoholic fatty liver disease.
Liver transplant
overview
The liver has great ability to regenerate and may double in size in as little as 3 weeks, making it ideal for partial donation. Hepatitis C is the most common disease requiring transplantation (followed by EtOH liver disease and cryptogenic cirrhosis). In adults, right lobes (segments 5-8) are most commonly implants. This is the opposite o f pediatric transplants, which usually donates segments 2-3. The modem surgery has four connections (IVC, artery, portal vein, CBD).
Liver transplant
contraindications
Contraindications include, extrahepatic malignancy, advanced cardiac disease, advanced pulmonary disease, or active substance abuse. Portal HTN is NOT a true contraindication although it does increase the difficulty o f the surgery and increase mortality.
Liver transplant
normal us
Normal Doppler should have a RAPID systolic upstroke
* Diastolic -> Systolic in less than 80msec (0.08 seconds)
Resistive Index is Normally between 0.5 - 0.7
Hepatic Artery Peak Velocity should be < 200 cm/sec
Liver transplant
syndrome of impending thrombus
3-10 days post transplant (1st) Initial Normal Waveform (2nd) No diastolic flow (3rd) Dampening Systolic flow Tardus Parvus R1 < 0.5 (4th) Loss o f Hepatic Waveform
Liver transplant
vessels
As mentioned before, the normal liver gets 70% blood flow from the portal vein, making it the key player. In the transplanted liver, the hepatic artery is the king and is the primary source of blood flow for the bile ducts (which undergo necrosis with hepatic artery failure). Hepatic artery thrombosis comes in two flavors: early (< 15 days), and later (years). The late form is associated with chronic rejection and sepsis
Liver transplant
trivia
Tardus Parvus is more likely secondary to stenosis than thrombosis
Portal venous gaus vs pneumobilia
These are the two patterns of branching air in the liver. The classic way to distinguish between the two is Central (Pneumobilia) vs Peripheral (PVG). The way to remember this is that bile is draining out of the liver into the bowel - so it is flowing towards the porta-hepatis and should be central. Portal blood, on the other hand, is being pumped into the liver - so it will be traveling towards the periphery. The potential trivia question is
how peripheral is peripheral — and that is 2cm. Within 2cm of the liver capsule = portal venous gas. Other things to remember - gas in the bile is usually related to a prior procedure (anything that fucks with the sphincter of Oddi). Gas in the portal system can be from lots of stuff (benign things like COPD or bad things - the most classic being bowel necrosis -look for pneumatosis*).
Jaundice
You always think about common duct stone, but the most common etiology is actually from a benign stricture (post traumatic from surgery or biliary intervention).
Bacterial Cholangitis
Hepatic abscess can develop secondary to cholangitis, usually as the result of stasis (so think stones). The triad of jaundice, fever, and right upper quadrant pain is the step 1 question.
PSC overview
Chronic cholestatic liver disease of unknown etiology characterized by progressive inflammation which leads to multifocal strictures of the intra and /or
extrahepatic bile ducts. The disease often results in cirrhosis, and is strongly associated with cholangiocarcinoma. The buzzword for the cirrhotic pattern is “central regenerative hypertrophy”. It is associated with inflammatory bowel disease (Ulcerative Colitis 80%, Crohn’s 20%). It is an indication for transplant, with a post transplant recurrence of about 20%.
PSC Buzzwords
‘“Withered Tree” - The appearance on MRCP, from abrupt narrowing of the branches
‘“Beaded Appearance” - Strictures + Focal Dilations
Dilated intrahepatic bile ducts are very rare in all forms of cirrhosis except
PSC
AIDS Cholangiopathy
Infection of the biliary epithelium (classically Cryptosporidium) can cause ductal disease in patients with AIDS. The appearance mimics PSC with intrahepatic and/or extrahepatic multifocal strictures.
The classic association/finding is papillary stenosis (which occurs 60% of the time).
This vs that
AIDS cholangioapathy
Focal Strictures of the extrahepatic duct > 2cm
Absent saccular deformities o f the ducts
Associated Papillary Stenosis
This vs that
PSC
Extrahepatic strictures rarely > 5mm
Has saccular deformities o f the ducts
Oriental Cholangitis
overview
Recurrent pyogenic cholangitis): Common in Southeast Asia (hence the culturally insensitive name). They always show it as dilated ducts that are full of pigmented stones.
Oriental Cholangitis
buzzword
“straight rigid intrahepatic ducts.”
Oriental Cholangitis location
cuase
The cause o f the disease is not known, but it may be associated with clonorchiasis, ascariasis, and nutritional
deficiency. These guys don’t do as well with endoscopic decompression and often need surgical decompression.
Remember this is a major risk factor for cholangiocarcinoma in the East.
Oriental Cholangitis location
The anatomically longer, flatter left biliary system
tends to make the disease burden left dominant (the opposite o f hematogenous processes which favor the right lobe).
Primary Biliary Cirrhosis
An autoimmune disease that results in the destruction of small & medium bile ducts (intra not extra). It primarily affects middle-aged women, who are often asymptomatic. In the early disease, normal bile ducts help distinguish it from PSC. In later stages, there is irregular dilation o f the intrahepatic ducts, with normal extrahepatic ducts. There is increased risk of HCC. If caught early it has an excellent prognosis and responds to medical therapy with ursodeoxycholic acid. The step 1 trivia is “antimitochondrial antibodies (AMA)” which are present 95% o f the time.
Long Common Channel
An anatomic variant in which the common bile and pancreatic duct fuse prematurely at the level o f the pancreatic head (prior to the sphincter o f Oddi complex).
The testable consequence is the increased incidence o f pancreatitis - as reflux o f enzymes is more common.
There is also an association with Type 1 choledochocysts.
Choledocchal cysts
types
type 1 is focal dilation o f the CBD
Type 2 and 3 are super rare. Type 2 is
basically a diverticulum o f the bile duct.
Type 3 is a “choledochocele.”
Type 4 is both intra and extra.
Type 5 is Caroli’s, and is intrahepatic only
Choledocchal cysts
high yield trivia
type 1 is focal dilation o f the CBD and is by fa r the most common.
Carolis overview
AR disease associated with polycystic kidney disease and medullary sponse kidney. The hallmark is intrahepatic duct dilation, that is large and saccular. Buzzword is “central dot sign” which
corresponds to the portal vein surrounded by dilated bile ducts
Carolis
compications
Cholangiocarcinoma
- Cirrhosis
- Cholangitis
- Intraductal Stones
Carolis gamesmanship
If they give you imaging o f dilated biliary ducts and a history of repeated cholangitis, think choledocal cyst. These things get stones in them and can be recurrently infected.
Ductal High Yield Summary
Carolis
-Communicates with the ducts
-Type 5 Cyst
-Central Dot Sign (on CT, MR, US)
-Associated with Polycystic Kidney,
Medullary Sponge Kidney
Cholangiocarcinoma
Ductal High Yield Summary
PSC
-40 year old Male with U.C.
-Withering Tree
-Beading
-Mild Dilation
-Strongly Associated with Ulcerative
Colitis & Cholangiocarcinoma
Ductal High Yield Summary
Oriental cholangioheatitis (recurrent pyogenic)
-Associations with clonorchiasis, ascariasis -Lots of Stones -Favors the left ductal system - Strongly Associated with Cholangiocarcinoma
Ductal High Yield Summary
AIDS cholangiopathy
-Related to Cryptosporidium or cytomegalovirus. -Segmental Strictures (looks like PSC) -Ducts look like PSC + Papillary Stenosis - Associated with Cholangiocarcinoma
Cholangiocarcinoma VS B9 Strictures
CA Strictures tends to be long, with “shouldering.’
B9 strictures tend to be abrupt and short.
Duct path association
If you can’t remember what
the association is, and it’s
ductal pathology, always
guess Cholangiocarcinoma.``
Normal Gallbladder
The normal gallbladder is found inferior to the interlobar fissure between the right and left lobe. The size varies depending on the last meal, but is supposed to be < 4 x < 10cm. The
wall thickness should be < 3mm. The lumen should be anechoic.
Gallbladder
phyrgian cap
A phrygian cap is seen when the GB folds on itself. It means nothing.
Gallbladder
intrahepatic gallbladder
Variations in gallbladder location are rare, but the intrahepatic gallbladder is probably the most frequently recognized variant. Most are found right above the interlobar fissure.
Gallbladder
duplicated
it can happen
Gallbladder duct of luschka
An accessory cystic duct. This can cause a big problem (persistent bile leak) after cholecystectomy. There are several subtypes which is not likely to be tested.
GB Wall Thickening (> 3mm):
Very non-specific. Can occur from biliary (Cholecystitis, AIDS, PSC…) or non-biliary causes (hepatitis, heart failure, cirrhosis, etc….).
Gallstones
Gallstones are found in 10% o f asymptomatic patients/ Most (75%) are cholesterol, the other 25% are pigmented. They cast shadows.
Reasons a gallstone might not cast a shadow
- It’s not a stone
- It’s a stone, but < 3mm in size
- The sonographer is an amateur (Bush league psyche-out stuff. Laughable, man)
Gallbladder shadowing
(1) Gallbladder full of stones
* Clean shadowing.
(2) Porcelain Gallbladder
* Variable shadowing
(3) Emphysematous Cholecystitis
* Dirty shadowing.
Mirrizzi syndrome
This occurs when the common hepatic duct is obstructed secondary to an impacted cystic duct stone. The stone can eventually erode into the CHD or GI tract.
Mirrizzi syndrome
key point
increased co-incidence o f gallbladder CA (5x more risk) with Mirizzi.
Mirrizzi syndrome
trivia
Mirizzi occurs more in people with a low cystic duct insertion (normal variant), allowing for a more parallel course and closer proximity to the CHD.
Clinically Meaningless THIS vs THAT:
Gallbladder Adenomyomatosis VS Cholesterolosis
overview
Nothing makes an Academic Radiologist happier than spending time deploying intense focused concentration targeted at distinguishing between two very similar appearing completely benign (often incidental) processes. They believe this “adds value” and will save them from the eventual avalanche of reimbursement cuts with subsequent AI
takeover.
Clinically Meaningless THIS vs THAT:
Gallbladder Adenomyomatosis VS Cholesterolosis
classic example
Adenomyomatosis vs Gallbladder Cholesterolosis. These things are actually different - and even though it makes zero difference clinically, this is just the kind of thing people who write questions love to write questions about.
Clinically Meaningless THIS vs THAT:
Gallbladder Adenomyomatosis VS Cholesterolosis
adenomyomatosis
You have hypertrophied mucosa and muscularis propria, with the cholesterol crystals deposited in an intraluminal location (within Rokitansky-Aschoff sinuses).
Clinically Meaningless THIS vs THAT:
Gallbladder Adenomyomatosis VS Cholesterolosis
cholesterolosis
Cholesterol and triglyceride deposition is within the substance of the lamina propria, and associated with formation o f cholesterol polyps.
Adenomyomatosis
imaging
manifest from the unique acoustic signature as comet-tail artifact (highly specific for adenomyomatosis).
Adenomyomatosis
3 types
Generalized (diffuse), Segmental (annular), and Fundal (localized or adenomyoma). The Localized form can’t be differentiated from GB cancer.
Adenomyomatosis
gamesmanship
Don’t be tricked into selecting “Adenomyosis” as a distractor. That shit is in the uterus. Remember the larger word is in the smaller organ. Or, you can think about the two Ms in MyoMat - turned inward sorta looks like a gallbladder.
Porcelain gallbladder
- Extensive wall calcification.
- The key point is increased risk o f GB Cancer.
- These are surgically removed.
Gallbladder polyps benign
< 5mm
* these are nearly always cholesterol polyps
Pedunculated
Multiple
Comet Tail Artifact on Ultrasound (seen in cholesterol polyps)
Gallbladder polyps malignat
> 1cm
*between 5mm-10mm usually get followed for growth
Sessile
Solitary
Enhancement on CT/MRI greater than the adjacent gallbladder wall. Flow on Doppler.
Gallbladder polyps overview
These can be cholesterol (by far the most common), or non cholesterol (adenomas, papillomas). Cholesterol polpys aren’t real polyps, but instead are essentially enlarged papillary fronds full o f lipid filled macrophages, that are attached to the wall by a stalk.
The non-cholesterol subtypes are almost always solitary and are typically larger. The larger polyps may have Doppler flow. They are NOT mobile and do NOT shadow. Once they get to be 1 cm, people start taking them out.
Gallbladder cancer classic vignette
elderly women with nonspecific RUQ pain, weight loss, anorexia and a long standing history o f gallstones, PSC, or large gallbladder polyps.
Gallbladder cancer risk factors
- Mirizzi syndrome has a well described increased risk o f GB cancer
- Other risk factors include smoldering inflammatory processes (PSC, Chronic Cholecystitis, Porcelain Gallbladder), and large polyps (“large” = bigger than 1cm)
Gallbladder cancer presentation
Unless the cancer is in the fundus (which can cause biliary obstruction) they often present late and have horrible outcomes with 80% found with direct tumor invasion o f the liver or portal nodes at the time of diagnosis.
Duplex
means color
spectral
means color with a waveform
Concept of arterial resistance
Some organs require continuous flow (brain), whereas others do not (muscles). The body is
smart enough to understand this, and will make alterations in resistance / flow to preserve energy.
When an organ needs to be “on,” its arteriolar bed dilates, and the waveform becomes low
resistance. This allows the organ to be appropriately perfused. When an organ goes to “power
save” mode, its arterioles constrict, the waveform switches to high resistance, and blood flow is
diverted to other more vital organs.
Continuous diastolic flow
low resistance
RI
To help quantify this low resistance high
resistance thing, we use this “Resistive
Index (RI)” - which is defined as V1-V2 /
VI.
RI = PSV - EDV / PSV
Tardus
Refers to a slowed systolic upstroke. This can be measured by acceleration time, the time from end diastole to the first systolic peak. An acceleration time > 0.07 sec correlates with >50% stenosis of the renal artery
parvus
Refers to decreased systolic velocity. This can be measured by calculating the acceleration index, the change in velocity from end diastole to the first systolic peak.
Upstream
Blood that has NOT yet passed through the stenosis
Downstream
Blood that has passed through the area o f stenosis
Stenosis direct sign
The direct signs are those found at the stenosis itself and they include elevated
peak systolic velocity and spectral broadening (immediate post stenotic).
Stenosis indirect sign
The indirect signs are going to be tardus parvus (downstream) - with time to
peak (systolic acceleration) > 70msec. The RI downstream will be low (< 0.5) because the
liver is starved for blood. The Rl upstream will be elevated (> 0.7) because that blood needs
to overcome the area o f stenosis.
Hepatic vein flow
Flow in the hepatic veins is complex, with alternating forward and backward flow. The bulk
of the flow should be forward “antegrade” (liver -> heart). Things that mess with the
waveform are going to be pressure changes in the right heart which are transmitted to the
hepatic veins (CHF, Tricuspid Regurg) or compression o f the veins directly (cirrhosis).
Anything that increases right atrial
pressure (atrial contraction) will
cause the wave to slope upward.
“A” represents atrial contraction.
Anything that decreases right atrial
pressure will cause the wave to
slope downward.
Abnormal Flepatic Vein
Waveforms can manifest in one o f three main
categories:
1) More Pulsatile
(2) Less Pulsatile
(3) Absent = Budd Chiari
Tricuspid regurg vs right sided chf on hepatic vein us
- Tricuspid Regurg - D deeper than S
* Right Heart Failure - S deeper than D
Portal vein us
Flow in the portal vein should always be towards the liver (antegrade). You can see some
normal cardiac variability from hepatic venous pulsatility transmitted through the hepatic
sinusoids. Velocity in the normal portal vein is between 20-40 cm/s. The waveform should be a
gentle undulation , always remaining above the baseline.
portal vein us patterns
(1) Normal
(2) Pulsatile
(3) Reversed
Causes o f Portal Vein Pulsatility
Right-sided CHF, Tricuspid Regurg, Cirrhosis with Vascular
AP shunting.
Causes o f Portal Vein Reversed ¥\ow
The big one is Portal HTN (any cause).
Portal vein absent flow
This could be considered a fourth pattern. It’s seen in thrombosis, tumor invasion,
and stagnant flow from terrible portal HTN.
Portal vein slow flow
Velocities less than 15 cm/s. Portal HTN is the most common cause. Additional
causes are grouped by location:
- Pre - Portal Vein Thrombosis
- Intra - Cirrhosis (any cause)
- Post - Right-sided Heart Failure, Tricuspid Regurg, Budd-Chiari
Liver doppler trivia
An ultra-common quiz question is to ask “what should the
Doppler angle be?” Now even though ultrasound physics
is covered in more detail in the dedicated section o f the War
Machine this is a high yield enough point to warrant
repetition. The answer is “less than 60. ”
Why? Doppler strength follows the cosine o f the angle. For
example, Cos 90 = 0, Cos 60 = 0.5, Cos 0 = 1.0 - the
doppler strength follows the Cos.
Pancreas anatomy
The pancreas is a retroperitoneal structure (the tail may be intraperitoneal).
Pancreas Classic US Trivia
The Pancreatic Echogenicity should be
GREATER than the normal liver.
Pancrease CF
The pancreas is involved in 85-90% of CF patients. Inspissated secretions cause proximal duct obstruction leading to the two main changes in CF:
(1) Fibrosis (decreased T1 and T2 signal)
(2) Fatty replacement (increased T l) - the more common of the two
Patients with CF, who are diagnosed as adults, tend to have more pancreas problems than those diagnosed as children. Just remember that those with residual pancreatic exocrine function tend to have bouts of recurrent acute pancreatitis (they keep getting clogged up with thick secretions). Small (1-3 mm) pancreatic cysts are common.
Pancreas high yield trivia
• Complete fa tty replacement is the most common imaging finding in adult CF
• Markedly enlarged with fatty replacement has been termed lipomatous pseudohypertrophy of the pancreas.
*This is a buzzword.
• Fibrosing Colonopathy: Wall thickening of the proximal colon as a complication of enzyme replacement therapy.
Shwachman-Diamond Syndrome
The 2nd most common cause of pancreatic insufficiency in kids (CF #1). Basically, it’s a kid with diarrhea, short stature (metaphyseal chondroplasia), and eczema. Will also cause lipomatous pseudohypertrophy o f the pancreas.
Pancreatic lipomatosis
Most common pathologic condition involving the pancreas. The most common cause in childhood is CF (in adults it’s Burger King).
Additional causes worth knowing are Cushing Syndrome, Chronic Steroid Use, Hyperlipidemia, and Shwachman-Diamond Syndrome.
Pancreatic agensis does not have a
duct
Dorsal Pancreatic Agenesis
All you need to know is that (1) this sets you up for diabetes (most o f your beta cells are in the tail), and (2) it’s associated with polysplenia.
Annular Pancreas
Essentially an embryologic screw up (failure o f ventral bud to rotate with the duodenum), that results in encasement o f the duodenum. Results in a rare cause o f duodenal obstruction (10%), that typically presents as duodenal obstruction in children and pancreatitis in adults. Can also be associated with other vague symptoms (postprandial fullness, “symptoms of peptic ulcer disease”, etc…).
Annular pancreas adults vs kids
Remember in adults this can present with pancreatitis (the ones that present earlier - in kids - are the ones that obstruct).
Annular pancreas imaging
look for an annular duct encircling the descending duodenum.
Pancreatic Trauma
overview
The pancreas sits in front o f the vertebral body, so it’s susceptible to getting smashed in blunt trauma. Basically, the only thing that matters is integrity of the duct. If the duct is damaged, they need to go to the OR. The most common delayed complication is pancreatic fistula (10-20%), followed by abscess formation. Signs of injury can be subtle, and may include focal pancreatic enlargement or adjacent stranding/fluid.
Pancreatic Trauma
imaging pearls
• Remember it can be subtle with just focal enlargement of the pancreas
• If you see low attenuation fluid separating two portions o f the enhancing pancreatic
parenchyma this is a laceration, NOT contusion.
• The presence o f fluid surrounding the pancreas is not specific, it could be from injury or
just aggressive hydration — on the test they will have to show you the liver and IVC to
prove it’s aggressive fluid resuscitation.
Pancreatic trauma high yield
Traumatic Pancreatitis in a kid too young to ride a bike = NAT.
Suspected pancreatic duct injury?
Next Step - MRCP or ERCP
Acute pancreatitis
Etiology
By far the most common causes are gallstones and EtOH which combined makeup 80% o f the cases in the real world. However, for the purpose o f multiple choice tests, a bite from the native scorpion o f the island of Trinidad and Tobago is more likely to be the etiology. Additional causes include ERCP (which usually results in a mild course), medications (classically valproic acid), trauma (the most common cause in a child), pancreatic cancer, infectious (post viral in children), hypercalcemia, hyperlipidemia, autoimmune pancreatitis, pancreatic divisum, groove (para-duodenal) pancreatitis, tropic
pancreatitis, and parasite induced.
Acute pancreatitis
clinical outcomes
Prognosis can be estimated with the “Balthazar Score.” Essentially, you can think about pancreatitis as “mild” (no necrosis) or “severe” (having necrosis). Patients with necrosis don’t start doing terrible until they get infected, then the mortality is like 50-70%
Acute pancreatitis
key point
Outcomes are directly correlated with the degree o f pancreatic necrosis
Acute pancreatitis
severe pancreatitis
Severe acute pancreatitis has a biphasic course. With the first two weeks being a proinflammatory phase. This is a sterile
response in which infection rarely occurs. The third and fourth weeks transition to an anti-inflammatory period in which the
risk of translocated intestinal flora and thesubsequent development o f infection
increases.
Acute pancreatitis
words??
No necrosis < 4 week > acute peripancreatic fluid collection
No necrosis > 4 weeks > pseudocyst
Necrosis < 4 weeks > acute necrotic collection
Necrosis > 4 weeks > Walled off necrosis
Acute pancreatitis
Vascular compications
- Splenic Vein and Portal Vein Thrombosis
O Isolated gastric varices can be seen secondary to splenic vein occlusion - Pseudo-aneurysm o f the GDA and Splenic Artery
Acute pancreatitis
nonvascular compications
- Abscess, Infection, etc… as discussed
- Gas, as a characteristic sign of an infected fluid collection, is detected in only 20% of cases o f pancreatic abscesses.
Acute pancreatitis
random imaging pearl
On Ultrasound, an inflamed pancreas will be hypoechoic (edematous) when compared to the liver (opposite o f normal).
Pancreatic Divisum
anatomy
There are two ducts, a major (Wirsung), and a minor (Santorini). Under “normal” conditions the major duct will drain in the inferior of the two duodenal papilla (major papilla). The minor duct will drain into the superior of the two duodenal papilla (minor papilla). The way I remember this is that “Santorini drains Superior”, and “Santorini is Small,” i.e. the minor duct.
Pancreatic Divisum
overview
Pancreatic Divisum is the most common anatomic variant of the human pancreas, and occurs when the main portion of the pancreas is drained by the minor or accessory papilla. The clinical relevance is an increased risk of pancreatitis.
Chronic Pancreatitis
Overview
CP represents the end result o f prolonged inflammatory change leading to irreversible fibrosis of the gland. Acute pancreatitis and chronic pancreatitis are thought o f as different disease processes, and most cases of acute pancreatitis do not result in chronic disease. So, acute doesn’t have to lead to chronic (and usually doesn’t), but chronic can still have recurrent acute.
Chronic pancreatitis
Etiology
Same as acute pancreatitis, the most common causes are chronic alcohol abuse and cholelithiasis which together result in about 90% of the cases. (EtOH is #1)
Chronic pancreatitis
imaging findings
early
- Loss o f T1 signal (pancreas is normally the brightest T1 structure in the body)
- Delayed Enhancement
- Dilated Side Branches
Chronic pancreatitis
imaging findings late
- Commonly small, uniformly atrophic - but can have focal enlargement
- Pseudocyst formation (30%)
- Dilation and beading of the pancreatic duct with calcifications
- most characteristic finding o f CP.
This vs that CP vs Cancer
CP
Dilatation is irregular
duct is <50% of the AP gland diameter
This vs that CP vs Cancer
Cancer
Dilation is uniform
duct is >50% of the AP gland diameter
Chronic pancreatitis complication
Pancreatic cancer (20 years o f CP = 6% risk o f Cancer) is the most crucial complication in CP and is the biggest diagnostic challenge because focal enlargement o f the gland induced by a fibrotic inflammatory pseudotumor may be indistinguishable from pancreatic carcinoma.
Autoimmune pancreatitis
Associated with elevated IgG4
Absence of Attack Symptoms
Responds to steroids
Sausage Shaped Pancreas, capsule like delayed rim enhancement around gland (like a scar). No duct dilation. No calcifications.
Groove pancreatitis
Looks like a pancreatic head
Cancer - but with little or no biliary obstruction.
Less likely to cause obstructive
jaundice (relative to pancreatic CA)
Duodenal stenosis and /or strictures of the CBD in 50% of the cases
Soft tissue within the pancreaticoduodenal groove, with or without delayed enhancement
Tropic pancreatitis
Young Age at onset, associated with malnutrition
Increased risk of adenocarcinoma
Multiple large calculi within a dilated pancreatic duct
Hereditary Pancreatitis
Young Age at Onset
Increased risk of adenocarcinoma
SPINK-1 gene
Similar to Tropic Pancreatitis
Ascaris Induced
Most commonly implicated parasite in pancreatitis
Worm may be seen within the bile ducts
1 Say Autoimmune Pancreatitis
you say IGG4
I Say IgG4
Autoimmune Pancreatitis Retroperitoneal Fibrosis Sclerosing Cholangitis Inflammatory Pseudotumor Riedel’s Thyroiditis
THIS vs THAT:
Autoimmune Pancreatitis vs Chronic Pancreatitis
Autoimmune Pancreatitis Chronic Pancreatitis
No ductal dilation Ductal Dilation
No calcifications Ductal Calcifications
Pancreatic pseudocyst
When you see a cystic lesion in the pancreas, by far the most common cause is going to be an inflammatory pseudocyst, either from acute pancreatitis or chronic pancreatitis.
Pancreatic simple cyst
True epithelial lined cysts are rare, and tend to occur with syndromes such as VHL, Polycystic Kidney Disease, and Cystic Fibrosis.
Pancreas serous cystadenoma
demographics
(Grandma). The former term “microcystic adenoma” helps me think o f a little old lady, which is appropriate for a lesion primarily found in elderly ladies. The lesion is benign
Pancreas serous cystadenoma
imaging
classically described as a heterogeneous, mixed-density lesion made up o f multiple small cysts, which resembles a sponge. They are more commonly (70%) located in the pancreatic head (mucinous is almost always in the body or tail). An additional key distinction is that it does NOT communicate with the pancreatic duct (IPMNs do). About 20% of the time they will have the classic central scar, with or without central calcifications (mucinous calcifications are peripheral).
Rarely, they can be unilocular. When you see a unilocular cyst with a lobulated contour located in the head o f the pancreas, you should think about this more rare unilocular macrocystic serous cystadenoma subtype.
Pancreas serous cystadenoma
trivia
Serous Cystadenoma is associated with Von Hippel Lindau
Pancreas serous cystadenoma
Memory aid
“GRANDMA Serous is the HEAD o f the household”
Pancreas mucinous cystic neoplasm
demographics
Mother. This pre-malignant lesion is “always” found in women, usually in their 50s. All are considered pre-malignant and need to come out.
Pancreas mucinous cystic neoplasm
imaging
They are found in the body and tail (serous was more common in the head). There is generally no communication with the pancreatic duct (IPMNs will communicate). Peripheral calcifications are seen in about 25% o f cases (serous was more central). They are typically unilocular. When mutlilocular, individual cystic spaces tend to be larger than 2 cm in diameter (serous spaces are typically smaller than 2 cm).
Pancreas mucinous cystic neoplasm
memory aid
Mucinous in the mother
Solid Pseudopapillary Tumor of the Pancreas
Demographics
(Daughter): Very rare, low grade malignant tumor that occurs almost exclusively in young (30s) females (usually Asian or Black).
Solid Pseudopapillary Tumor of the Pancreas
imaging findings
It is typically large at presentation, has a predilection for the tail, and has a “thick capsule.” Similar to a hemangioma it may demonstrate progressive fill-in o f the solid
portions.
IPMN - intraductal Papillary Mucinous Neoplasm
Overview
These guys are mucin producing
tumors that arise from the duct epithelium. They can be either side branch, main branch, or both.
IPMN - intraductal Papillary Mucinous Neoplasm
side branch
“The pulmonary nodule of the pancreas”
common and usually meaningless
typically appear as a small cystic mass, often in the head or uncinate process
if large amounts of mucin are produced it may result in main duct enlargement
lesions less than 3 cm are usually benign
IPMN - intraductal Papillary Mucinous Neoplasm
main branch
produces diffuse dilation of the main duct
atrophy of the gland and dystrophic calcs may be seen (mimicking chronic pancreatitis
have a much higher%of malignancy compared to side branch
all main ducts are considered malignany and resection should be considered
IPMN - intraductal Papillary Mucinous Neoplasm
Features concerning for malignancy
main duct >10mm (some sources say 1.5 cm)
enhancing nodules
solid hypovascular mass
Main Branch IPMN summary
- “The Bad One”
- Has malignant potential
Solid Pseudopapillary summary
- Daughter Lesion
- Solid with Cystic parts, enhances like a hemangioma
- Capsule
Side Branch IPMN summary
- “Common One”
- Has much less malignant potential
- Often in head /uncinate
- Communicates with duct
Serous cystic summary
- Grandma Lesion
- Benign
- Microcystic, with central calcifications
Mucinous cystic summary
- Mother Lesion
- Premalignant
- Body / Tail - 95%
- Unilocular with thick wall septations
Solid Pancreatic lesions
overview
Pancreatic Cancer basically comes in two flavors. (1) Ductal Adenocarcinoma - which is hypovascular and (2) Islet Cell / Neuroendocrine which is hypervascular.
Ductal Adenocarcinoma
overview
In the setting of a multiple choice test, the finding o f an enlarged gallbladder with painless jaundice is highly suspicious for pancreatic adenocarcinoma, especially when combined with migratory thrombophlebitis (Trousseau’s syndrome). The peak incidence is in the 7th or 8th decade. The strongest risk factor is smoking.
Ductal Adenocarcinoma
imaging findings
Approximately two-thirds o f these cancers arise from the pancreatic head. On ultrasound, obstruction o f both the common bile duct and the pancreatic duct is referred to as the “double duct sign”. On CT, the findings are typically a hypo-enhancing mass which is poorly demarcated and low attenuation compared to the more brightly enhancing background parenchyma. The optimal timing is on a pancreatic phase (40 seconds).
Ductal Adenocarcinoma
staging
The key to staging is assessment o f the SMA and celiac axis, which if involved make the patient’s cancer unresectable. Involvement o f the GDA is ok, because it comes out with the Whipple.
Ductal Adenocarcinoma
trivia
• Tumor Marker = CA 19-9 # Hereditary Syndromes with Pancreatic CA: O HNPCC, BRCA Mutation, Ataxia-Telangiectasia, Peutz-Jeghers * Small Bowel Follow Through: Reverse impression on the duodenum “Frostburg’s Inverted 3 Sign” or a “Wide Duodenal Sweep.” They would have to actually find a case o f the inverted 3 to show it, but could ask it in words. The ‘Wide Duodenal Sweep ” could actually be shown.
Periampullary Tumor
overview
Defined as originating within 2cm of the major papilla. It can be difficult to differentiate from a conventional pancreatic adenocarcinoma as both obstruct the bile duct, and present as a mass in the pancreatic head. Basically, all you need to know about them is they can try and treat them with a Whipple and they have a better prognosis than pancreatic adenocarcinoma.
Periampullary tumore
trivia
There is an increased incidence o f ampullary carcinoma in Gardner’s Syndrome.
Islet cell/neuroendocrine pancreatic tumors
overview
Neuroendocrine tumors are uncommon
tumors of the pancreas. Typically
hypervascular, with brisk enhancement during arterial or pancreatic phase. They can be thought of as non-functional or functional, and then subsequently further divided based on the hormone they make. They can be associated with both MEN 1 and Von Hippel Lindau.
Islet cell/neuroendocrine pancreatic tumors
Insulinoma
The most common type (about 75%). They are almost always benign (90%), solitary, and small (< 2cm).
Islet cell/neuroendocrine pancreatic tumors
gastrinoma
The second most common type overall, but most common type associated with MEN 1. They are malignant like 30-60%. They can cause increased gastric acid output and ulcer formation - Zollinger-Ellison syndrome.
Islet cell/neuroendocrine pancreatic tumors
non-functional
The 3rd most common type, usually malignant (80%), and are usually large and metastatic at the time of diagnosis.
Islet cell/neuroendocrine pancreatic tumors
I say nonfunctional
you say large with calcification
gastrinoma
buzzword
Jejunal Ulcer = Zollinger-Ellison
Gastrinoma triangle
The anatomical region where most (90%) of gastrinomas arise.
Boundaries
• Superior: Junction of the cystic and common bile ducts
• Inferior: Start of the third portion of the duodenum
• Medial: Start of the body of the pancreas
Intrapancreatic Accessory Spleen
Overview
It is possible to have a pancreatic mass that is actually just a piece of spleen. The typical scenario is that of post traumatic splenosis. Look for the question stem to say something like “history o f trauma. ” Another hint may be the absence of a normal spleen.
Intrapancreatic Accessory Spleen
Imaging Findings
- Follows spleen on all image sequences (dark on Tl, and bright on T2 - relative to the liver).
- It will restrict diffusion (just like the spleen).
- The classic give away, and most likely way it will be shown is as a tiger striped mass on arterial phase (tiger striped like the spleen on arterial phase).
Intrapancreatic Accessory Spleen
trivia
Nuclear medicine tests - (1) Heat Treated RBCs, and (2) Sulfur Colloid can be used to prove the mass is spleen (they both take up tracer— just like a spleen).
The Whipple Procedure
overview
The standard Whipple procedure involves resection of the pancreatic head, duodenum, gastric antrum, and almost always the gallbladder. A jejunal loop is brought up to the right upper quadrant for gastrojejunal, choledochojejunal or hepaticojejunal, and pancreatojejunal anastomosis.
The Whipple Procedure
alternative
An alternative method used by some surgeons is to perform a pancreatoduodenectomy and preserve the pylorus when possible. There is debate in the surgery literature with regard to which method should be the standard. In this pylorus-preserving pancreatoduodenectomy, the stomach is left intact and the proximal duodenum is used for a duodenojejunal anastomosis.
The Whipple Procedure
complications
Delayed gastric emptying (needfor NG tube longer than 1- day) and pancreatic fistula (amylase through the surgical drain >50 ml fo r longer than 7-10 days), are both clinical diagnoses and are the most common complications after pancreatoduodenectomy. Wound infection is the third most common complication, occurring in 5%-20% of patients.
Pancreas transplant
overview
Pancreas transplant (usually with a renal transplant) is an established therapy for severe type 1 diabetes - which is often complicated by renal failure. The vascular anatomy regarding this transplant is quite complicated and beyond the scope of this text. Just know that the pancreas transplant receives arterial inflow from two sources: the donor SMA, (which supplies the head via the inferior pancreaticoduodenal artery) and the donor splenic artery, (which supplies the body and tail). The venous drainage is via both the donor portal vein and the recipient SMV. Exocrine drainage is via the bowel (in older transplants via the bladder).
Pancreas transplant
graft failure
The number one cause of graft failure is acute rejection. The number two cause of graft failure is donor splenic vein thrombosis. Donor splenic vein thrombosis usually occurs within the first 6 weeks of transplant. Venous thrombosis is much more common than arterial thrombosis in the transplant pancreas, especially when compared to other transplants because the vessels are smaller and the clot frequently forms within and propagates from the tied-off stump vessels.
Both venous thrombosis and acute rejection can appear as reversed diastolic flow. Arterial thrombosis is also less of a problem because of the dual supply to the pancreas (via the Y graft). A point of trivia is that the resistive indices are not of value in the pancreas, because the organ lacks a capsule. The graft is also susceptible to pancreatitis, which is common < 4 weeks after transplant and usually mild. Increased rates of pancreatitis were seen with the older bladder drained subtype.
Pancreas transplant
shrinking transplant
is a buzzword for chronic rejection, where the graft progressively gets smaller in size.
Spleen normal trivia
By the age of 15 the spleen reaches its normal adult size. The spleen contains both “red pulp” and “white pulp” which contribute to its tiger striped appearance during arterial phase imaging. The red pulp is filled with blood (a lot o f blood), and can contain up to one liter of blood at any time. The spleen is usually about 20 HU less dense than the liver, and slightly more echogenic than the liver (equal to the left kidney). The splenic artery (which usually arises from the celiac trunk) is essentially an end vessel, with minimal collaterals. Occlusion o f the splenic artery will therefore result in splenic infarction. Pathology involving the spleen can be categorized as either congenital, acquired (as the sequela o f trauma or portal hypertension), or related to a “mass.” A general rule is that most things in the spleen are benign with exception o f lymphoma or the rare primary angiosarcoma.
Normal Spleen on MRI:
Bright on T2, relative to the liver
Dark on T1 relative to the liver
Like a lymph node it restricts diffusion
Accessory spleens
These are very common; we see them all the time. Some random trivia that might be testable includes the fact that sulfur colloid could be used to differentiate a splcnule from an enlarged pathologic lymph node. Additionally, in the scenario where a patient is post splenectomy for something like ITP or autoimmune hemolytic anemia, an accessory spleen could hypertrophy and present as a mass. Hypertrophy of an accessory spleen can also result in a recurrence of the original hematologic disease process.
Wandering Spleen
A normal spleen that “wanders” off and is in an unexpected location. Because of the laxity in the peritoneal ligaments holding the spleen, a wandering spleen is associated with abnormalities of intestinal rotation. The other key piece of trivia is that unusual locations set the spleen up for torsion and subsequent infarction. A chronic partial torsion can actually lead to splenomegaly or gastric varices.
Splenic Traums
The spleen is the most common solid organ injured in trauma. This combined with the fact that the spleen contains a unit or so of blood means splenic trauma can be life threatening. Remember the trauma scan is done in portal venous phase (70 second), otherwise you’d have to tell if that is the normal tiger-striped arterial-phase spleen or it is lacerated.
Splenosis
This occurs post trauma where a smashed spleen implants and then recruits blood supply. The implants are usually multiple and grow into spherical nodules typically in the peritoneal cavity of the upper abdomen (but can be anywhere). It’s more common than you think and has been reported in 40-60% of trauma. Again, Tc Sulfur colloid (or heat-treated RBC) can confirm that the implants are spleen and not ovarian mets or some other terrible thing.
Spleen Gamn Gandy Bodies (siderotic nodule)
These are small foci of hemorrhage in the splenic parenchyma that are usually associated with portal hypertension. They are T2 dark.
Gradient is the most sensitive sequence.
Spleen sarcoidosis
Sarcoid is a disease o f unknown etiology that results in noncaseating granulomas which form in various tissues o f the body (complete discussion in the chest section o f this text). The spleen is involved in 50% - 80% o f patients. Splenomegaly is usually the only sign. However, aggregates o f granulomatous splenic tissue in some patients may appear on CT as numerous discrete l-2cm hypodense nodules. Rarely, it can cause a massive splenomegaly and possibly rupture. Don’t forget that the gastric antrum is the most common site in the GI tract.
Spleen
Peliosis
This is a rare condition characterized by multiple blood filled cyst-like spaces in a solid organ (usually the liver - peliosis hepatitis). When you see it in the spleen it is usually also in the liver (isolated spleen is extremely rare). The etiology is not known, but for the purpose of multiple choice tests it occurs in women on OCPs, men on anabolic steroids, people with AIDS, renal transplant patients (up to 20%), and patients with Hodgkin lymphoma. It’s usually asymptomatic but can explode spontaneously.
Splenic artery aneurysm
the most common visceral arterial aneurysm.
Pseudoaneurysm can occur in the setting of trauma and pancreatitis. The incidence is higher in women o f child bearing age who have had two or more pregnancies (4x more likely to get them, 3x more likely to rupture). It’s usually saccular and in the mid-to-distal artery. They usually fix them when they get around 2-3cm.
Colossal fu c k up to avoid: Don’t call them a hypervascular pancreatic islet cell mass and biopsy them.
Splenic vein thrombosis
frequently occurs as the result o f pancreatitis. Can also occur in the setting o f diverticulitis or Crohn’s. Can lead to isolated gastric varices.
Splenic infarction
can occur from a number of conditions. On a multiple choice test the answer is sickle cell. The imaging features are classically a wedge-shaped, peripheral, low attenuation defect.
Splenic infections
Most common radiologically detected splenic infection is histoplasmosis (with multiple round calcifications). Splenic TB can have a similar appearance (but much less common in the US). Another possible cause of calcified granuloma in the spleen in brucellosis, but these are usually solitary and 2 cm or larger. They may have a low density center, encircled by calcification giving the lesion a “bull’s eye” appearance.
In the immunocompetent patient, splenic abscess is usually due to an aerobic organism. Salmonella is the classic bug - which develops in the setting of underlying splenic damage (trauma or sickle cell). In immunocompromised patients, unusual organisms such as fungi, TB, MAI, and PCP can occur and usually present as multiple micro-abscesses. Occasionally, fungal infections may show a “bulls-eye” appearance on ultrasound.
Small spleen
ddx
sickle cell
post radiation
post thorostras
malabsorption syndromes (uc>crohns)
Big spleen ddx
passive congestion (heart failure, portal HTN, Splenic vein thrombosis)
lymphoma
leukemia
gauchers
Feltys syndrome
abnormality o f granulocytes, with a triad of:
(1) Splenomegaly, (2) Rheumatoid Arthritis, (3) Neutropenia
Splenic post traumatic cysts
(pseudocysts) are the most common cystic lesion in the spleen. They can occur secondary to infarction, infection, hemorrhage, or extension from a pancreatic pseudocyst. As a point o f trivia they are “pseudo” cysts because they have no epithelial lining. They may have a thick wall or prominent calcifications peripherally.
Splenic epidermoid cysts
second most common cystic lesion in the spleen. They are congenital in origin. As a point o f absolutely worthless trivia, they are “true” cysts and have an epithelial lining. They typically grow slowly and are usually around 10cm at the time o f discovery. They can cause symptoms if they are large enough. They are solitary 80% o f the time, and have peripheral calcifications 25% o f the time.
Hydatid or echinococcal cysts
third most common cystic lesion in the spleen. They are caused by the parasite Echinococcus Granulosus. Hydatid cysts consist o f a spherical “mother cyst” that usually contains smaller “daughter cysts.” Internal septations and debris are often referred to as “hydatid sand.” The “water lily sign” is seen when there is detachment o f the endocyst membrane resulting in floating membranes within the pericysts (looks like a water lily). This was classically described on CXR in pulmonary echinococcal disease.
Splenic hemangiom
most common benign neoplasm in the spleen. This dude is usually smooth and well marginated demonstrating contrast uptake and delayed washout. The classic peripheral nodular discontinuous enhancement seen in hepatic lesions may not occur, especially if the tumor is smaller than 2 cm.
Splenic lymphangiomas
rare entities in the spleen but can occur. Most occur in childhood. They may be solitary or multiple, although most occur in a subcapsular location. Diffuse lymphangiomas may occur (lymphangiomatosis).
Splenic hamartomas
rare in the spleen, but can occur. Typically this is an incidental finding. Most are hypodense or isodense and show moderate heterogeneous enhancement. They can be hyperdense if there is hemosiderin deposition.
Spleen littoral cell angiomas
zebra that shows up occasionally in books and possibly on multiple choice tests. Clinical hypersplenism is almost always present. Usually presents as multiple small foci which are hypoattenuating on late portal phase. MR shows hemosiderin : 5 ; : (low T1 & T2).
Malignant Masses of the Spleen
overview
Most things that occur in the spleen are benign. Other than lymphoma (discussed below) it is highly unlikely that you will encounter a primary malignancy of the spleen (but i f you do i t ’s likely to be vascular). For the purposes o f academic discussion (and possible multiple choice trivia), angiosarcoma is the most common.
Splenic angiosarcoma
It is aggressive and has a poor prognosis. On CT it can manifest as a poorly defined area o f heterogeneity or low density in an enlarged spleen. They can contain necrosis and get big enough to rupture (spontaneous rupture occurs like 30% o f the time). Contrast enhancement is usually poor. Yes, these can occur from prior thorotrast exposure.
Splenic lymphoma
is the most common malignant tumor o f the spleen, and is usually seen as a manifestation of systemic disease. Splenomegaly is the most common finding (and maybe the only finding in low-grade disease). Although both Hodgkins and Non-Hodgkins types can involve the spleen, Flodgkins type and high-grade lymphomas can show discrete nodules o f tumor. With regard to imaging, they are low density on CT, T1 dark, and are PET hot.
Spleen mets
Metastatic Disease to the spleen is rare. When it does occur, it occurs via common things (Breast, Lung, Melanoma).
Trivia: Melanoma is the most common primary neoplasm to met to the spleen.
