Liver, Gallbladder, Pancreas Flashcards
Rate limiting step for bilirubin conjugation
2-3-UDP-glucoronyltransferase
Painless posthepatic jaundice is most often going to be . . .
. . . cancer or strictures
1000 foot interpretation of localization of process based on bilirubin
Unconjugated predominant: Prehepatic
Mixed: Intrahepatic
Conjugated predominant: Post-hepatic
Presentation of painless obstructive jaundice
- Indolent process that happens over long periods of time (stricture or cancer)
- Gall bladder and biliary tree have time to adjust: GB will become very large and thin walled, biliary tree will become huge.
- No inflammation, no leukocytosis, no Murphy’s sign
- Courvoisier’s sign: Palpable distended gallbladder
- Bilirubin levels will be way higher than in gallstone disease. Stools may be gray.
- Dx: RUQ-US, MRCP (best test), CT to detect cancer
- Tx: Endoscopic US w/ biopsy or ERCP w/ biopsy. Then stent for stricture, resect for cancer.
Classic presentation of malignant obstruction of the bile tree
- Indolent progression of jaundice, gray stools, weight loss
Distended gallbladder that is palpable, but non-painful
Some sort of obstructive jaundice (stricture, cancer)
What are you looking for on CT in a patient with obstructive jaundice?
-
Pancreatic cancer
- Dx with endoscopic US + biopsy. Tx with Whipple procedure.
-
Biliary cancer (likely cholangiocarcinoma, if pigmented melanona)
- Remember PSC is risk factor for cholangiocarcinoma
- Dx with ERCP + biopsy. Tx with resection.
-
Unrevealing US
- Likely to indicate pathology at ampulla of Vater
- FOBT + and negative colonoscopy -> duodenal cancer
- Dx: ERCP + biopsy. Tx with resection.
Obstructive jaundice + migratory thrombophlebitis
Pancreatic cancer
Treatment for biliary tree strictures
Stenting
UNLESS, they have PSC. This is because these patients will eventually need transplant, and if you stent them it will be harder to do the transplant. In these cases, use ursodeoxcholic acid instead.
Sphincter of Odi dysfunction
- Presents following cholecystectomy
- Causes RUQ or epigastric pain, cholestasis, sometimes pancreatitis
- Dx and Tx with ERCP
- Post-ERCP complications: pancreatitis, cholangitis, cholicky pain, cholestasis due to post-operative swelling at the ampulla of Vater. Tx with supportive care.
Standard antibiotics prior to surgery for cholecystitis
- Ceftriaxone
- Flagyl
B-SAFE mnemonic for gallbladder surgery
- Landmarks to identify prior to beginning the procedure
- Bile duct
- Sulcus of Rouviere
- Left hepatic Artery pulsations
- Umbilical Fissure
- Duodenum (Enterics)
In-detail biliary tree anatomy
ERCP and EDGE
Done in patients with history of Roux en Y gastric bypass who develop gallstone disease
EDGE is done in two parts: Make a hole, then come back in 2 weeks to do ERCP
Five F’s of mixed cholesterol cholelithiasis
- Fat
- Female
- Forty
- Fertile
- First Americans (Native Americans)
Green bile stones vs black bile stones
Green: Mixed cholesterol, most common
Black: Bilirubin stones, from hemolysis
Treatment for uncomplicated cholelithiasis (w/o cholecystitis)
- Tx:
- Elective cholecystectomy for good surgical candidates
- Ursodeoxycholic acid for poor surgical candidates
In the context of gallstone disease, whenever you have an obstruction. . .
. . . everything proximal will be inflamed
Dx and Tx for cholecystitis
- Start w/ RUQ US. If positive, you are done, proceed w/ management.
-
If above negative, do a HIDA scan. If positive, proceed w/ management.
- Note: HIDA scan in cholecystitis will fill the right and left hepatic ducts, but not the obstructed portion of the cystic duct or gall bladder.
- Tx: NPO, IV fluids, IV abx, urgent cholecystectomy (w/in 72-96 hours to prevent perforation)
- In a non-surgical candidate, percutaneous cholecystostomy.
Labs in choledocolithiasis
- Bile stasis markers: Bilirubin, GGT
- Hepatocellular injury markers: AST, ALT
-
Pancreas injury markers: Lipase, pancreatic amylase
- Not all of them will always be present. Bilirubin and GGT will be elevated, but liver markers and pancreas markers may or may not be.
Dx and Tx for choledocolithiasis
- Start w/ RUQ US. If positive, you are done, proceed w/ management.
- If above negative, do an MRCP. If positive, proceed w/ management.
- Note: For cholecystitis, you do HIDA. For choledoco, you do MRCP.
- Tx: NPO, IV fluids, IV abx. Urgent ERCP is definitive therapy. But, you can also go straight to cholecystectomy. Either way, the eventually need a cholecystectomy.
- F/u: “Ball-Valve” effect. While working up, pain gets better, bilirubin goes down. But then the next day, pain is back and bilirubin is up again. This is the effect of the stone moving back and forth. It is possible to pass a stone spontaneously in real life, but you have to be careful not to be fooled by this. However, this will never be the case on the test.
Dx and Tx for cholangitis (aka ascending cholangitis)
- Etiology: Infection of static fluid in choledocolithiasis by gut flora
- Dx:
- Charcot’s triad (RUQ pain, jaundice, fever). Indicates choledocolithiasis.
- Reynold’s Pentad (RUQ pain, jaundice, fever, hypotension, AMS). Indicates cholangitis.
- RUQ US is the first and only test. If positive, diagnosis is done, proceed to surgery without further testing (no MRCP, no HIDA).
- Tx: NPO, IV fluids, Abx. Follow w/ EMERGENT ERCP. Then, urgent cholecystectomy.
- Note: Give abx on the way to the endo suite.
Abx in gallstone disease
- You want to cover gram negatives and anaerobes
- Cipro + metronidazole
- Amp + Gent + metronidazole
- Pip-Tazo will be on there, and it will be the wrong answer. You may see it done in the hospital. It is convenient. But, it is a poor choice for antibiotic stewardship, even though it technically covers what you want. It over-covers.
Differentiating pancreatic pseudocyst vs abscess on CT
Pseudocyst: Tender abdomen, smooth, round, cystic structure. Usually not febrile, but can produce febrile peritonitis and sepsis if it ruptures.
Abscess: Fever, tender abdomen, complex/multiloculated cavity.
Following one episode of varix rupture, the next step is to. . .
. . . schedule an elective prophylactic varix ligation for the remaining varices in 1-2 weeks
Then, confirm their absence in 3-6 months with EGD.
In the meantime, the patient should be on propranolol.
When to do pancreaticoduodenectomy (Whipple) vs duodenum-preserving pancreatic head resection for pancreatic cancer
- Whipple: Treatment of choice for nonmetastatic pancreatic head carcinoma
- Duodenum-preserving: Performed for small islet cell tumors (neuroendocrine syndromes) or for chronic pancreatitis
Chylous ascites (triglycerides > 200) w/ lymphocytes most likely etiology
In a patient with no history of Tb risk factors: Intraperitoneal lymphoma
In a patient with a history of Tb risk factors: Tb
May rarely be due to lymphatic injury or lymphatic hyperplasia.
Best laboratory prognostic factor for acute pancreatitis
Hematocrit
The volume loss in pancreatitis is so substantial that it hemoconcentrates the blood. Changes in hematocrit over time can tell you how severe the fluid loss is.
What do you do with a pancreatic pseudocyst?
- Asymptomatic small pseudocysts: Observation and re-imaging in 6 weeks
- Symptomatic small (< 6 cm) pseudocysts: CT-guided percutaneous drainage
- Complicated pseudocyst (necrotic, infected, large): Laporoscopic surgical drainage
In the management of esophageal varices: Octrotide is used ___, propranolol is used ___.
Octrotide is used acutely, propranolol is used prophylactically.
Before you do an EGD to band esophageal varices, you should give two things:
- Octreotide
- Ceftriaxone
Most accepted indications for transjugular intrahepatic porto-systemic shunt (TIPS)
- Recurrent variceal hemorrhage
- Acute variceal hemorrhage refractory to pharmacologic and endoscopic therapy
Post-surgical pancreatic fistula
- Presents w/ NAGMA due to loss of bicarbonate rich pancreatic fluids a few days after surgery involving the pancreas
- Tx:
- Conservative treatment: Octreotide, TPN
- If above fails, stenting of the pancreatic duct
Nontender enlargement of the gallbladder
Pancreatic head malignancy
Key features of pancreatic head malignancy / pancreatic adenocarcinoma
- Nontender enlarged gallbladder
- Jaundice
- Dark urine / Pale stools
- Weight loss
- Dull pancreatitis-type pain
- Migratory thrombophlebitis
Percutaneous cholecystostomy
- Image-guided placement of drainage catheter into gallbladder lumen
- Indications:
- poor surgical candidate / high-risk patients with acute calculous or acalculous cholecystitis
- unexplained sepsis in critically ill patients (diagnostic for cholecystitis as etiology of sepsis if clinical improvement after cholecystostomy)
- access to or drainage of biliary tree following failed ERCP and PTC
Single most important risk factor for pancreatic cancer
Smoking
Common presentation and first steps in hepatorenal syndrome
- Presentation: Gradual loss of kidney function, oliguria, unremarkable urine sediment, FENa < 1%, and BUN/Cr ratio > 20
- Since Cr is so elevated, a typical picture is something like Cr 3.5 and BUN 74
- Tx: Octreotide, midodrine, IV albumin. Goal is to keep MAP > 65 mmHg and improve perfusion to kidneys. Only cure is liver transplant.
Any patient with ongoing hematemesis AND altered mental status (ie, the typical esophageal variceal rupture patient) should get ___ before anything else.
Any patient with ongoing hematemesis AND altered mental status (ie, the typical esophageal variceal rupture patient) should get intubated before anything else.
They are at high risk of aspiration and need airway protection.
Serum AST:ALT > 1
Suggestive of chronic alcohol use
Next best step in management after a patient presents with a picture of acute pancreatitis, positive lipase, and is started on IV fluids
RUQ ultrasound
Even if the history fits well with alcohol, triglycerides, or calcium, you have to rule out gallstone disease. It is just the most important etiology of pancreatitis.
3 most common etiologies of chronic hepatitis in the US
- Chronic viral
- Alcoholic
- NAFLD/hepatic steatosis
You have diagnosed a cirrhotic patient with SBP. What are the next steps?
-
First, paracentesis
- Diagnostic and therapeutic
- Confirm SBP by analysis
- Then, once you have your PMN > 250 read, administer ceftriaxone
Postcholecystectomy syndrome
- Persistent or new abdominal symptoms following gallbladder removal (~2 weeks)
- Etiology unclear, thought to involve Sphincter of Oddi dysfunction
- Symptoms include RUQ or epigastric pain, dyspepsia, nausea, vomiting, flatulence, bloating, and diarrhea
- Dx/Tx: ERCP with sphincterotomy. If diagnosis is unclear, ERCP with Sphincter of Oddi manometry can be performed for definitive Dx prior to sphincterotomy.
Management of acalculous cholecystitis
- Supportive measures:
- Fluids
- Broad spectrum antibiotics (piperacillin-tazobactam)
- Surgery:
- If need for temporizing measure or poor surgical candidate: immediate gallbladder drainage/decompression with percutaneous cholecystostomy, followed by urgent cholecystectomy
- If stable, early elective cholecystectomy
When do you give Abx for acute cholecystitis?
- ALWAYS
- Following Abx, Lap Chole in 2-3 days
Biliary cysts
- most commonly seen in patients of Asian descent
- Appear as saccular or fusiform dilations of the biliary tree or as dilated masses that communicate with the biliary tree
- Can result in cholestatic jaundice and, if left untreated, increases the risk of cholangitis and cholangiocarcinoma
- Dx: Imaging (RUQ US)
- Tx: Surgical excision of the cyst, followed by the creation of a biliary-enteric anastomosis with a Roux-en-Y hepaticojejunostomy
Caroli disease
- Heritable disease causing multiple saccular dilations within the intrahepatic bile ducts
- Causes cholestatic jaundice
- Symptoms typically onset in adulthood
Mirizzi syndrome
- Common hepatic duct obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder
- Results in cholestatic jaundice and dilation of the gall bladder and extrahepatic bile ducts on ultrasound
- Treat w/ cholecystectomy (including cystic duct), NOT ERCP
Alagille syndrome
- a genetic condition that is characterized by intrahepatic biliary duct aplasia or hypoplasia
- Autosomal dominant inheritance, mutation in JAG1
- Hepatic features: Cholestasis, jaundice, pruritis, cirrhosis at young age
- Facial dysmorphism: Triangular face, deep set eyes, broad nasal bridge
- Also other pictured features
- Dx: Liver biopsy shows decreased number of bile ducts. Genetic testing reveals JAG1 mutation.
- Tx: Ursodeoxycholic acid usually required. Full treatment plan depends on organs involved and extent of involvement.
___ should be suspected in critically ill and postoperative patients who develop unexplained jaundice, sepsis, fever, and leukocytosis
Acalculous cholecystitis (AC) should be suspected in critically ill and postoperative patients who develop unexplained jaundice, sepsis, fever, and leukocytosis
PBC vs PSC vs AIH
Absolute contraindications to organ donation
- Malignancy that is incurable or metastatic
- Sepsis
- Transmissible spongiform encephalopathies (Creutzfeld-Jakob)
- Cardiac arrest that occurred before brain death
- Note that HIV, hepatitis viruses, and CMV are NOT on this list.
Two mechanisms of acute allograft rejection
-
Acute cellular rejetion
- May occur any time within 6 months of transplant, even in the first week – however hyperacute is first 48 hours
- Mediated by T cells
- C4d staining will be negative
-
Acute humoral rejection
- May occur any time within 6 months of transplant, even in the first week – however hyperacute is first 48 hours
- Mediated by host anti-HLA antibodies formed either before or after transplantation
- C4d staining will be positive
Mechanism of hyperacute graft rejection
- Circulating antibodies against ABO antigens, or sometimes class I MHC
- This triggers complement activation, thrombosis of graft vessels, and ultimately graft infarction
Timeline for graft rejection
- < 48 hours: Hyperacute (preformed ABO or MHC-I antibodies)
- 48 hours - 6 months: Acute (humoral or cellular, can tell apart by C4d staining on biopsy)
- >6 months: Chronic (often preceded by episode of acute rejection, chronic inflammation, arteriosclerosis, scarring, microscopic vessel obstruction)
The best initial step in the treatment of patients with biopsy-confirmed acute renal allograft rejection
- Short course of high-dose intravenous methylprednisone (aka pulse steroid therapy)
Where is the stone in acute cholecystitis due to stones?
In the cystic duct
Not the gallbladder neck – the cystic duct
Management of acalculous cholecystitis
Typically with percutaneous cholecystostomy rather than cholecystectomy.
Very sick patients, in ICU
Patholoy from gallbladder removal comes back with gallbladder cancer. Next steps?
- Staging CT
- Even if staging is negative, go back and resect gallbladder fossa (liver around GB), cystic duct margin, lymph nodes
If your chole patient comes back feeling not so great, what do you NEED to rule out?
Bile leak
A HIDA scan or MRCP may help you identify it. Some may be treated with stent, some may need repeat surgery.
From where does the infection originate in acute cholecystitis?
In the setting of cystic duct obstruction, lymphatic channels act as conduits for bacteria to accumulate in the gallbladder
Common organisms are E. coli, Klebsiella, Proteus, and S. faecalis
Two biggest risk factors for acalculous cholecystits
- Poor perfusion
-
No oral diet
- This is why there is a predeliction for ICU patients!
Chronic cholecystitis tends to __ over time
Chronic cholecystitis tends to become less painful over time
However, we still want to take that gallbladder out since it has an increased risk for malignancy.
The types of gallstone
Pneumobilia may represent. . .
. . . bacterial metabolism (as in ascending cholangitis) OR fistulization (as in gallstone ileus)
It should always be interpreted in the context of the clinical picture (cholangitis vs SBO)
Diagnosis of biliary dyskinesia
- Mimics symptomatic cholelithiasis / biliary colic, however on ultrasound there are no stones!
- Due to dysfunctional gallbladder contraction in response to CCK
- The diagnostic test is CCK-stimulated HIDA scan
- Should demonstrate inadequate emptying to confirm diagnosis (EF<1/3)
- CCK should reproduce symptoms
- Treatment: CCBs and nitrates may help relax spasms. Ursodeoxycholic acid may help if there is “microlithiasis” present.
- Unfortunately, even with cholecystectomy the outcomes are not as good. 1/3 complete resolution, 1/3 some improvement, 1/3 no improvement at all.
Symptoms of cholecystoduodenal fistula vs cholecystocolonic fistula
Cholecystoduodenal fistula: SBO
Cholecystocolonic fistula: Acute cholecystitis or ascending cholangitis and/or diarrhea that burns
Bonus: Cholecystoduodenal fistula + PPI may present like cholecystocolonic with infections!
Diagnose with HIDA scan or colecystogram (if you have a tube!). If it’s duodenal, it has to be a HIDA.
Absolute contraindications to pancreatic cancer resection
- Involvement of the superior mesenteric artery (SMA)
- NOT the superior mesenteric vein
- Presence of distant metastases
- Presence of intraperitoneal metastases
Chemotherapeutics for pancreatic cancer
- Gemcitabine (classically)
- Folfox
- Folfiri
Major heritable risk factors for pancreatic cancer
- Lynch syndrome
- BRCA2
Use of CA19-9
- Tumor marker for pancreatic adenocarcinomas
- Limitations:
- Elevated in biliary obstruction from other causes
- Elevated in blood Lewis-antigen negative status
Palliative options for pancreatic cancer
- In the context of obstructive jaundice, stent placement or surgical bypass of biliary tree and duodenum (cholecystojejunostomy)
- In the context of duodenal obstruction, gastrojejunostomy
- In the context of severe pain, percutaneous celiac plexus block or nerve ablation
Pancreatic mucinous cystic neoplasms
- Wide variety of tumors, some benign some malignant
- All have mucin-secreting epithelial cells lining exocrine ducts
- Hormonally stimulated – almost exclusively occurs in women
- Fluid analysis: Low amylase, high CEA, positive mucin stain
- Cytology: Clusters or sheets of mucin-containing cells
Intraductal papillary mucinous neoplasm (IPMN)
- Mucous producing neoplasm originating in a pancreatic duct
- IPMN arising from the main duct (not a side branch) has a 30-50% probability of harboring pancreatic ductal adenocarcinoma
- Occurs in those >60-70 years of age, equally in M and F
- Differntiate origin by MRCP
- Often discovered as incidental cystic masses on CT
- May produce abdominal pain or pancreatitis
- Side-duct IPMN may be observed, but main duct IPMN requires intervention
- Fluid analysis: High amylase, high CEA, positive mucin staining
- Cytology: Tall, columnar mucin-containing cells
Serous cystic neoplasms of the pancreas
- Predilection for pancreatic head
- No potential for malignant tranformation
- Surgical resection is indicated only when lesions are symptomatic or in cases of diagnostic uncertainty
- Fluid analyses: Low amylase, low CEA, negative for mucin
- Cytology: Scant glycogen rich cells
Pancreatic pseudocyst fluid analysis and cytology
- Fluid analysis: Very high amylase, low CEA, negative mucin stain
- Cytology: Inflammatory cells
Most patients with pancreatic ductal carcinoma have __ at the time of diagnosis
Most patients with pancreatic ductal carcinoma have non-resectable disease at the time of diagnosis
In general, the Whipple procedure is reserved for. . .
. . . resectable malignancies near the Ampulla of Vater.
It offers a ~15% cure rate for these patients. This is their best shot in an otherwise abysmal prognosis.
Best method for assessing involvement of the superior mesenteric vessels in pancreatic cancer
Endoscopic ultrasound
Types of focal liver lesion
- Hemangioma (benign)
- Focal nodular hyperplasia (benign)
- Hepatic adenoma (potentially malignant)
- Hepatocellular carcinoma (malignant)
- Cholangiocarcinoma (malignant)
- Metastasis from distant site (malignant)
Liver hemangioma
- Most common benign liver tumor
- Typically asymptomatic, may cause vague abdominal pain, nausea, loss of apetite
- “Light bulb sign” is classical. Marked hyperintensity of the lesion relative to the surroundings with early filling of the rim and late filling of the central mass.
- Biopsy is contraindicated – highly vascular
- Surgical resection or embolization may be indicated for palliation of symptoms
Kasabach-Merritt syndrome
- Associated with highly vascularized liver tumors, most commonly hemangiomas
- Describes a consumptive process of tumors resulting in thrombocytopenia, low clotting factors, and low fibrinogen
Focal nodular hyperplasia
- Benign liver tumor common in women in their 40’s-50’s
- Mostly asymptomatic
- “Central scar” appearance on CT
- May require biopsy to differentiate from hepatic adenoma
Nodular regenerative hyperplasia
- Focal regeneration in the liver
- Thought to be related to obstructed blood flow in liver regions resulting in injury and subsequent regeneration
- Common in those over age 80
- No treatment necessary
Triple phase CT scan
CT scan with IV contrast that acquires images at 30 seconds (arterial), 60 seconds (portal-venous), and 90 seconds (equilibrium)
Alows for better characterization of liver lesions
CT scan has a reduced detection rate of hepatocellular carcinomas in patients with . . .
. . . cirrhotic livers
Cirrhosis makes it difficult to visualize the interior of the liver as well as you would otherwise
Management of a new diagnosis of hepatic adenoma
- If on an OCP or taking anabolic steroids, STOP these medications
- If < 5 cm in size, risk of rupture and malignant transformation is low. These can be safely observed and managed expectantly.
- Pregnancy is not contraindicated for women with <5 cm adenomas
- If > 5 cm in size, patient should be considered for tumor resection or ablation to reduce bleeding and malignant transformation risks
Major risk factors for hepatocellular carcinoma
- Untreated hepatitis B virus (most important of all)
-
Cirrhosis:
- Fatty liver
- Alcohol use disorder
- Chronic untreated hepatitis C virus
- Other etiologies of cirrhosis (less than the above three)
Subtypes of hepatic adenoma
-
Inflammatory:
- High risk for bleeding, low risk for malignant transformation
-
HNF-1 mutated:
- No risk for bleeding or malignant transformation – benign
-
Beta-catenin activated:
- High risk for malignant transformation when > 5 cm in size
Differentiating FNH from hepatic adenomas
Best test for this is radiolabeled sulfur colloid scintigraphy
This isotope is taken up by Kupffer cells in FNH, but not by adenomas.
This can be super helpful as the demographics affected by FNH and hepatic adenomas (middle aged, pre-menopausal women) are the same.
In general, in the workup of a solid liver mass, the first thing to do is ___ to rule out ___.
In general, in the workup of a solid liver mass, the first thing to do is triphasic CT to rule out hemangioma.
If there is no lightbulb sign, you proceed with biopsy of the mass.
Fluid resuscitation for pancreatitis
- Bolus: 20 mL/kg LR
- Infusion: 3 mL/kg/hr
- Interval assessment of vitals, labs, urine output q6h
- If BUN does not drop after 6 hours, re-bolus
- If BUN does drop, reduce infusion to 1.5mL/kg/hr
PaO2/FiO2
Managing nutrition for a patient with pancreatitis
At first, just give some dextrose along with your LR and keep NPO
Once the patient is stable, you can initiate intragatric feeding
Oral or enteral feeding is associated with reduced complication rates of acute pancreatitis.
Progression of peripancreatic disease in severe acute pancreatitis
- Pancreatic and peripancreatic necrosis may occur in the first few days
- This may be associated with peripancreatic fluid collections which are not walled off by a fibrous capsule (as a pseudocyst would be)
- The above undergo liquefactive necrosis, producing “pancreatic phlegmon”
- With resolution of pancreatitis, phlegmon breaks down and the inflammatory response produces a fibrous capsule where it once was
- This capsule may then give rise to one or more pseudocysts
When pseudocysts are infected, you can treat with ___.
When pancreatic phlegmon is infected, you may need ___.
When pseudocysts are infected, you can treat with percutaneous drainage.
When pancreatic phlegmon is infected, you may need surgical drainage and/or debridement.
A necrotic pancreas may be. . .
. . . infected
This can lead to an acute worsening in clinical picture. Antibiotics are required.
Unfortunately, prophylactic antibiotics have not been demonstrated to be of any therapeutic value.
When should surgical debridement be performed in patients with pancreatic necrosis?
At least 30 days following disease onset
This is associated with better outcomes than early surgical intervention
Etiologies of drug-induced pancreatitis
Thiazides
ACE inhibitors
Most common malignancy presenting with bloody ascites
Hepatocellular carcinoma
CEA and CA19-9 are elevated in. . .
. . . pancreatic cancer AND cholangiocarcinoma
While hepatic hemangiomas are full of blood, ___ are the liver lesions most associated with spotaneous, life-threatening hemorrhage
While hepatic hemangiomas are full of blood, hepatic adenomas are the liver lesions most associated with spotaneous, life-threatening hemorrhage
