The gall bladder and bile ducts

Haneen Omar Abu Hani

Anatomy

• The gallbladder lies on the underside of the liver at the junction of the right and left lobes of the liver.

• It is intraperitoneal, pear-shaped sac, 7.5–12cm long, with a normal capacity of about 25–30mL.

• The anatomical divisions are a fundus, a body and a neck that terminates in a narrow infundibulum.

• The mucous membrane contains indentations of the mucosa, called the crypts of Luschka.

• The mucosa of the cystic duct is arranged in spiral folds known as the valves of Heister and the wall is surrounded by a sphincteric structure called the sphincter of Lütkens.

Calot’s triangle

(Hepatobiliary triangle):

space bordered by :

1-Cystic duct inferiorly

2-Common hepatic duct

medially

3-Cystic artery superiorly

Contents: Calot’s node

It is an important surgical

landmark as the cystic artery

usually can be found within

it.

The Biliary Tree

The biliary tree is a series of gastrointestinal ducts allowing newly synthesised bile from the liver to be concentrated and stored in the gallbladder (prior to release into the duodenum).

Bile is initially secreted from hepatocytes and drains from both lobes of the liver via canaliculi, intralobular ducts and collecting ducts into the left and right hepatic ducts. These ducts amalgamate to form the common hepatic duct, which runs alongside the hepatic vein.

As the common hepatic duct descends, it is joined by the cystic duct – which allows bile to flow in and out of the gallbladder for storage and release. At this point, the common hepatic duct and cystic duct combine to form the common bile duct.

The common bile duct descends and passes posteriorly to the first part of the duodenum and head of the pancreas. Here, it is joined by the main pancreatic duct, forming the hepatopancreatic ampulla (commonly known as the ampulla of Vater) – which then empties into the 2nd part of the duodenum via the major duodenal papilla. This papilla is regulated by a muscular valve, the sphincter of Oddi.

Functions of the gallbladder:

It is a reservoir for bile.

Concentration of bile by active absorption of water, sodium chloride and bicarbonate via the mucous membrane of the gallbladder. It becomes concentrated 5–10 times.

secretion of mucus – approximately 20mL is produced per day.

a mucocoele may develop as a result of ongoing mucus secretion by the gallbladder mucosa.

Surgical physiology • Bile is produced by the liver and stored in the gallbladder,

from which it is released into the duodenum.

• As it leaves the liver it is composed of 97% water, bile salts,

phospholipids, cholesterol and bilirubin.

• The liver excretes bile at a rate estimated to be approximately 40mL/hour.

• About 95% of bile salts are reabsorbed in the terminal ileum (enterohepatic circulation).

The arterial supply to the gallbladder is via the cystic artery – a branch of the right hepatic artery (which itself is derived from the common hepatic artery, one of the three major branches of the coeliac trunk).

Venous drainage of the neck of the gallbladder is via the cystic veins, which drain directly into the portal vein. Venous drainage of the fundus and body of the gallbladder flows into the hepatic sinusoids.

The gallbladder receives parasympathetic (vagus nerve), sympathetic and sensory innervation (coeliac plexus).

The lymphatic vessels of the gallbladder (subserosal and submucosal) drain into cystic lymph nodes of Lund, situated at the junction of the cystic and common hepatic ducts, then emptying into the hepatic lymph nodes, and ultimately, the coeliac lymph nodes.

The subserosal lymphatic vessels of the gallbladder also connect with the subcapsular lymph channels of the liver, and this accounts for the frequent spread of carcinoma of the gallbladder to the liver.

Cholelithiasis

- Cholelithiasis refers to the presence of abnormal concretions (gallstones) in the gallbladder.

- Gallstones are the most common biliary pathology. It is estimated that gallstones affect 10–15% of the population in Western societies.

- They are asymptomatic in the majority of cases (>80%).

- Approximately 1–2% of asymptomatic patients will develop symptoms requiring surgery per year, making cholecystectomy one of the most common operations performed by general surgeons

• Gallstones form as a result of supersaturation of the bile.

• There are three main types of gallstones: Cholesterol stones – composed purely of cholesterol, from excess cholesterol production

There is a well recognised link between poor diet, obesity, and cholesterol stones

Pigment stones – composed purely of bile pigments, from excess bile pigments production, There are two types: black and brown.

Black stones are largely composed of an insoluble bilirubin pigment polymer mixed with calcium phosphate and calcium bicarbonate. The incidence is 20–30% & it rises with age. They are associated with haemolysis & cirrhosis.

Brown pigment stones contain calcium bilirubinate, calcium palmitate and calcium stearate, as well as cholesterol. They are rare.

Mixed stones – comprised of both cholesterol and bile pigments.

• In the USA and Europe 80% are cholesterol or mixed stones, whereas in Asia 80% are pigment stones.

Risk Factors

Classically the common risk factors for gallstone disease are colloquially described as the “5 F’s”: Fat, Female, Fertile, Forty, and Family history.

Other recognised risk factors include pregnancy and oral contraceptives*, haemolytic anaemia (specifically for pigment stones), and malabsorption such as: previous ileal resection; (which diminishes the enterohepatic circulation, will deplete the bile acid pool and result in

cholesterol supersaturation) or Crohn’s disease.

*Oestrogen causes more cholesterol to be secreted into bile

Clinical Features

• 80% of patients are asymptomatic, being detected incidentally as imaging is performed for other symptoms.

• Biliary colic is typically present in 10–25% of patients.

Gallstone found incidentally on an ultrasound scan in an asymptomatic patient

Biliary Colic Biliary colic occurs when the gallbladder neck becomes impacted by a

gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain.

The pain is typically sudden, dull, and colicky in nature which ebbs and flows. It is often focused in the right upper quadrant although it may radiate to the epigastrium,chest and/or back. The pain may be precipitated by the consumption of fatty foods* and the patient often complains of nausea / vomiting. In general, once pain relief has been started, symptoms often settle quickly.

Other symptoms include dyspepsia, flatulence, food intolerance

*Fatty acids stimulate the duodenum endocrine cells to release cholecystokinin (CCK), which in turn stimulates contraction of the gallbladder.

Cholecystitis

Acute cholecystitis refers to the acute inflammation of the gallbladder, which is typically due to cystic duct obstruction by a gallstone (acute calculous cholecystitis).

Acalculous cholecystitis is less common and is seen predominantly in critically ill patients and those recovering from major surgery, trauma and burns.

Etiology

Acute calculous cholecystitis: most common form, 90%

Cause: obstructing cholelithiasis

Pathophysiology

- Cholelithiasis → passage of gallstones into the cystic duct → cystic duct obstruction → distention and inflammation of the gallbladder

- Secondary bacterial infection may also be present (E. coli, Klebsiella, Enterobacter, Enterococcus spp. most common) but is not necessary for the development of cholecystitis.

Acalculous cholecystitis: 5–10% of acute cholecystitis Acute and chronic inflammation of the gallbladder can occur in the absence of stones The diagnosis is often missed and the mortality rate is high. Treatment is drainage

Clinical features

Patients with acute cholecystitis will report:

- Constant pain in the RUQ or epigastrium

• Typically more severe and prolonged (> 6 hours) than in biliary colic

• Postprandial

• Radiation to the right scapula (due to referred pain from phrenic nerve irritation)

- Signs of inflammation, such as fever or lethargy.

- positive Murphy’s sign

- guarding (may suggest a gallbladder perforation) and for features of sepsis.

Boas’ sign: referred right

subscapular pain

Acute cholecystitis should always be suspected in a patient with a history of gallstones who presents

with RUQ pain, fever, and leukocytosis

Murphy’s Sign

Sudden pausing during inspiration upon deep palpation of the RUQ due to pain.

*Murphy sign may be falsely negative in patients > 60 years

*This can be achieved more accurately with an ultrasound, namely the sonographic Murphy sign.

Differential Diagnosis There are a wide variety of pathologies that can present with RUQ pain. However, differentials to consider include:

1. gastro-oesophageal reflux disease

2. peptic ulcer disease

3. acute pancreatitis, or

4. Inflammatory bowel disease.

# Dr note: acute pyelonephritis is more common differential than perforated peptic ulcer.

Investigations

1. Laboratory Test

Certain blood tests can help in the initial evaluation of suspected cases:

FBC and CRP – assess for the presence of any inflammatory response, which will be raised in cholecystitis

LFTs – biliary colic and acute cholecystitis are likely to show a raised ALP (indicating ductal occlusion), yet ALT and bilirubin should remain within normal limits (unless a Mirizzi syndrome, discussed later on)

Amylase (or lipase) – to check for any evidence of pancreatitis

A urinalysis, including a pregnancy test if relevant, should be performed to exclude any renal or tubo-ovarian pathology.

2. Imaging

A trans-abdominal ultrasound is one of the most sensitive modalities for visualising gallstone disease and is typically used first line to investigate suspected gallstone pathology.

Characteristic findings:

• Gallbladder wall thickening > 3–5 mm

• Gallbladder distension (8–10 x 4 cm)

• Gallbladder wall edema (double-wall sign): The innermost and outermost layers appear hyperechoic; edematous tissue appears as a hypoechoic layer in between.

• Sonographic Murphy sign

• Pericholecystic free fluid

• Presence of gallstones and/or biliary sludge (the start of gallstone formation)

• In emphysematous cholecystitis, mural air appears as hyperechoic shadows within the gallbladder wall.

If results from US scans are inconclusive, further imaging options are available. The gold standard investigation* for gallstones is Magnetic Resonance Cholangiopancreatography (MRCP), largely replacing ERCP for diagnostic purposes (Fig. 3). MRCP can show potential defects in the biliary tree caused by gallstone disease, with a sensitivity approaching 100%.

*Any patient with symptoms suggestive of gallstones with inconclusive US (or CT scans) should undergo a MRCP

Hepatoiminodiacetic acid scintigraphy (HIDA scan):

• Indications: preferred confirmatory test for suspected uncomplicated acute cholecystitis if ultrasound findings are inconclusive.

• It can differentiate between acute and chronic cholecystitis.

Management

Biliary Colic

Patients with biliary colic should be prescribed analgesia (regular paracetamol +/- NSAIDs +/- opiates analgesia).

The patient should be advised about lifestyle factors that may help control symptoms (and help with future surgery), such as a low fat diet, weight loss, and increasing exercise.

Following first presentation of biliary colic, there is a high chance of symptom recurrence or the development of complications of gallstones, therefore an elective laparoscopic cholecystectomy* is warranted and should be offered within 6 weeks of first presentation.

*The laparoscopic route is preferred for cholecystectomy but is not always possible

Management Acute cholecystitis: patients with should be started on appropriate intravenous antibiotics (such as co-amoxiclav +/- metronidazole). Concurrent analgesia and antiemetics should also be prescribed.

A laparoscopic cholecystectomy is indicated within 1 week of presentation, as per NICE guidance, however this ideally should be done within 72hrs of presentation for a likely simpler procedure*.

For those not fit for surgery and not responding to antibiotics, a percutaneous cholecystostomy can be performed to drain the infection (although as the gallstones remain in-situ, the risk of recurring disease remains).

*In high-risk patients with severe cholecystitis, a temporizing gallbladder drainage procedure (e.g., percutaneous cholecystostomy) should be performed and elective interval cholecystectomy scheduled after the resolution of acute symptoms.

Any patient readmitted with RUQ pain post-cholecystectomy, it is important to exclude a retained CBD stone post-operatively. US abdomen scan may be useful, yet if this is unremarkable, then further investigation via MRCP imaging is warranted.

Complications

Mirizzi Syndrome

A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.

This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy.

Figure 5 – Mirizzi syndrome causes by a stone lodged in Hartmann’s pouch, compressing the common hepatic duct

Gallbladder Empyema • It occurs when the gallbladder becomes filled

with pus.

• Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis.

• They are associated with significant morbidity and mortality.

• The condition is diagnosed by either US scan or CT scan. Treatment is via laparoscopic cholecystectomy* (may require intra-operative drainage if tense gallbladder) or percutaneous cholecystostomy (if unsuitable for surgery).

*There is a higher rate of conversion to open cholecystectomy with emypema than with uncomplicated acute cholecystitis

Chronic Cholecystitis

• Patients with chronic cholecystitis will typically have a history of recurrent or untreated cholecystitis, which has led to a persistent inflammation of the gallbladder wall.

• Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting.

• It can be diagnosed typically by CT imaging (or often noted on histology post-cholecystectomy). Management in uncomplicated cases is via elective cholecystectomy.

• Its main complications are gallbladder carcinoma and biliary-enteric fistula.

Bouveret’s Syndrome and Gallstone Ileus Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel, termed a cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum)

As a consequence, bowel obstruction can occur:

Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstruction

Gallstone Ileus*– a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction

*The term ileus is misleading, as it is actually a bowel obstruction

Figure 7 – A Cholecystoduodenal Fistula, resulting in a gallstone entering the small bowel

Emphysematous cholecystitis (EC)

a rare but life-threatening form of acute cholecystitis characterized by air within the gallbladder wall that is caused by gas-forming bacteria (e.g., Clostridium spp., E.coli)

It is most commonly seen in elderly diabetic men (esp. 50–70 years of age)

It is often results in perforation of gallbladder.

Clinical features: Similar to acute calculous cholecystitis: fever, RUQ pain, referred pain , Symptoms progress rapidly. Associated with early gangrene and gallbladder perforation

Diagnostics

Imaging: The characteristic feature of EC on imaging is air within the gallbladder wall or lumen

RUQ ultrasound : hyperechoic air shadows within the gallbladder wall, and within bile in the gallbladder lumen

Abdominal x-ray : radiolucent rim outlining the gallbladder (pear-shaped radiolucency)

If gas is present in:

- Biliary tree > Think of fistula. - In gallbladder wall >think of

emphysematous GB.

Xanthogranulomatous cholecystitis

A rare inflammatory disease of the gallbladder characterized by a focal or diffuse destructive inflammatory process that leads to formation and accumulation of xanthoma cells.

➢ Its importance lies in the fact that it is a benign condition that may be confused with carcinoma of the gallbladder.

Choledocholithiasis

Choledocholithiasis

It refers to the presence of gallstones in the common bile duct.

Etiology Secondary choledocholithiasis (most common): cholelithiasis → passage of gallstones into the common bile duct → common bile duct obstruction → spasm of the biliary tracts

Risk factor: a history of cholelithiasis

Primary choledocholithiasis (less common): conditions predisposing to bile stasis → intraductal stone formation

Risk factors:

- Cystic fibrosis

- Prolonged total parenteral nutrition

Postcholecystectomy choledocholithiasis

Residual choledocholithiasis: CBD stones missed during cholecystectomy; typically becomes symptomatic within 2 years of surgery

Recurrent choledocholithiasis: CBD stones that developed after cholecystectomy, typically detected after 2 years of surgery

Risk factors for recurrent stones: periampullary duodenal diverticulum, dilated CBD, CBD stricture, chronic cholangitis, sickle cell anemia, and rapid weight loss (e.g., after bariatric surgery)

Clinical features

• RUQ pain

- More severe and prolonged (may last > 6 hours) than in cholelithiasis

- Postprandial

- May radiate to the epigastrium, right shoulder, and back (referred pain)

• Nausea, vomiting, anorexia

• Signs of extrahepatic cholestasis (e.g., jaundice, pale stool, dark urine, pruritus) may be present

• Features of complications

Diagnosis

Laboratory studies

• LFTs

Characteristic findings: evidence of cholestasis, i.e., ↑ ALP, ↑ GGT, ↑ total and ↑ direct bilirubin

*Tests to rule out related biliary comorbidities

• CBC: Leukocytosis is seen in cholecystitis or cholangitis.

• Amylase, lipase: elevated in biliary pancreatitis

Imaging 1.Transabdominal RUQ ultrasound

Indications: preferred first-line imaging modality in patients presenting with RUQ pain and/or jaundice

*Supportive findings

• Dilated common bile duct (CBD): Normal CBD diameter varies according to patient age and whether the gallbladder is intact or has been surgically removed.

Gallbladder in situ, age < 50 years: CBD diameter > 6 mm

Gallbladder in situ, age > 50 years: CBD diameter > 8 mm

Postcholecystectomy patients: CBD diameter > 10 mm

• Intrahepatic biliary dilatation may be seen.

• Visualization of an occluding CBD stone

• Stone(s) within the gallbladder

2. CT abdomen with IV contrast: not routinely recommended

Confirmatory imaging and further management

1. Endoscopic retrograde cholangiopancreatography (ERCP)

Contraindication (for urgent ERCP): acute biliary pancreatitis without evidence of cholangitis or biliary obstruction.

Characteristic findings

- Smooth-walled, well-defined, intraluminal filling defect(s) within the CBD, which may be dilated.

- Dilation of the intrahepatic biliary tree

- Cholelithiasis: mobile filling defect(s) within the gallbladder lumen

2. Magnetic resonance cholangiopancreatography (MRCP)

Differential diagnosis

* Differential diagnosis of jaundice with dilated biliary duct

- Biliary stricture

- Pancreatic carcinoma (head of pancreas)

- Cholangiocarcinoma

- Mirizzi syndrome

- Extrinsic compression of the bile duct (e.g., lymphadenopathy at the porta hepatis)

Treatment

* Treatment is recommended in all patients with choledocholithiasis, even if asymptomatic. The mainstay of treatment is the removal of the obstruction.

Approach

1. Provide supportive therapy for patients with acute symptoms; analgesics, spasmolytics, and antiemetics.

2. NPO in patients with acute pain

3. Identify and manage any complications (e.g., acute pancreatitis, cholangitis, cholecystitis).

4. Removal of choledocholithiasis; endoscopically (ERCP) or surgically (LCBDE; Laparoscopic bile duct exploration).

5. Elective cholecystectomy to prevent recurrence

Complications

1. Gallstone ileus: mechanical bowel obstruction due to obstructive gallstones

* Pathophysiology: gallbladder perforation or Mirizzi syndrome → biliary-enteric fistula formation (most commonly cholecystoenteric fistula) between the inflamed gallbladder and bowel → gallstones passing down into bowel lumen

* Sites of obstruction

- Terminal ileum, at ileocecal valve (most common)

- Gastric pylorus or duodenum

* Symptoms depend on the site of obstruction.

- Distal bowel obstruction: features of mechanical bowel obstruction (abdominal pain and distention, nausea, vomiting)

- Gastroduodenal obstruction (rare): features of gastric outlet obstruction (Bouveret syndrome).

* Diagnosis is based on the Rigler triad: imaging findings of small bowel obstruction, gallstone (most commonly in iliac fossa), and pneumobilia.

* Treatment

- Initial supportive therapy

- NPO, IV fluid resuscitation, analgesics, antiemetics, nasogastric tube insertion

- Empiric antibiotic therapy for intra-abdominal infections

- Enterolithotomy: emergency surgery to remove the obstructing stone

- Consider cholecystectomy and closure of the biliary-enteric fistula.

Complications

2. Gallstone pancreatitis

3. Acute cholangitis

4. Acute cholecystitis

5. Biliary stricture

6. Pyogenic liver abscess

Cholangitis

Introduction

Cholangitis refers to infection of the biliary tract. It is associated with high morbidity and mortality when left untreated, and therefore is an important condition to recognise and manage.

It is caused by a combination of biliary outflow obstruction* and biliary infection. During an obstruction, stasis of fluid allows the bacterial colonisation of the biliary tree to become pathological.

*In patients without outflow obstruction, a bacterial colonisation is unlikely to cause cholangitis

Causes

Any condition which causes occlusion of the biliary tree has the potential to cause cholangitis.

The most common causes are gallstones, ERCP (iatrogenic), and cholangiocarcinoma. Rarer causes include pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy, and parasitic infections.

The most common infective organisms implicated in cholangitis are Escherichia Coli (27%), Klebsiella species (16%), and Enterococcus (15%).

Clinical Features The common presenting symptoms of cholangitis are right upper quadrant pain, fever,and jaundice (when bilirubin >50 μmol/L). The patient may also complain of pruritus (itching), as a result of bile accumulation, and pale stool with dark urine, from the obstructive jaundice.

The patient’s past medical history may include gallstones, recent biliary tract instrumentation (i.e. ERCP/cholecystectomy), or previous cholangitis. Medication including oral contraceptive pill and fibrates can increase the risk, and a lipid-rich diet may be indicative of gallstones (as a potential underlying cause).

On examination, patients may have pyrexia (in 90% of cases), rigors, jaundice, right upper quadrant tenderness, confusion, hypotension, and tachycardia may be present.

Two common eponymous syndromes associated with cholangitis are:

Charcots Triad: Jaundice, Fever, and RUQ Pain

Reynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and Confusion

Figure –The clinical features of Charcot’s Triad: Jaundice, Fever, and Abdominal Pain

Differential Diagnosis

Cholangitis is not a complete diagnosis, as there is nearly always an underlying cause that should be identified and treated.

The clinical features of cholangitis are very similar to other biliary pathologies. A biliary colic will present with a colicky RUQ pain yet without fever, leucocytosis, or jaundice. Cholecystitis will present with RUQ pain and fever yet jaundice will be absent.

Investigations

Laboratory Tests

FBC (leucocytosis is found in the vast majority of patients) and LFTs (showing a raised ALP ± GGT with a raised bilirubin).

Blood cultures should always be taken in suspected cases, despite only being positive in 20% of cases. The best opportunity to obtain a positive blood culture is early, before the start of broad spectrum antibiotics.

Imaging

An ultrasound scan of the biliary tract will show: • bile duct dilation. The common bile duct is usually less

than 6mm in size (it may be greater in the elderly and those who have had previous cholecystectomy), so any diameter larger than this suggests dilatation.

• It may also demonstrate the presence an underlying cause (e.g. gallstones).

The gold standard investigation for cholangitis is ERCP, as it is both diagnostic and therapeutic. Many endoscopists may require an MRCP prior to intervention, however to obtain detailed imaging of the biliary system prior to scoping. Figure 3 – ERCP showing an obstruction in the biliary tree, resulting in cholangitis.

Management

Immediate Management

Patients with cholangitis may present with sepsis, so should be managed promptly, appropriately and often in a higher level of care.

- IV access

- sufficient fluid resuscitation,

- routine bloods, and blood cultures taken early,

- with broad spectrum IV antibiotic therapy instigated (e.g. co-amoxiclav + metronidazole).

Definitive Management

Endoscopic biliary decompression: it is the definitive management of cholangitis is via, removing the cause of the blocked biliary tree. For patients who are deteriorating, this may need to be done earlier than those who are responding well to antibiotic therapy.

ERCP, with or without a sphincterotomy and stenting, should clear any obstruction.

It is important to remember that there are significant complications of ERCP, including repeated cholangitis, pancreatitis (in 3-5% of patients), bleeding (more common when a sphincterotomy is performed), and perforation (a rare complication yet requires urgent surgical intervention if present)

Percutaneous transhepatic cholangiograpy (PTC) is the second line intervention, in patients who may be too sick to tolerate ERCP

In the long-term, patients may require a cholecystectomy if gallstones were the underlying cause. Any other cause for the cholangitis identified should also be managed as appropriate.

Prognosis

The mortality of cholangitis is around 5-10% in those who are given antibiotic therapy. Early ERCP and early antibiotic therapy have both been found to improve patient outcomes.

Factors which increase the mortality rate include delayed diagnosis, liver failure, cirrhosis, CKD, hypotension, female gender, and >50yrs

Porcelain gallbladder

• It is a calcification of the gallbladder caused by excessive gallstones, although the exact cause is not clear.

• This condition occurs predominantly in overweight female patients of middle age.

• It is usually found incidentally on plain abdominal x-rays or other imaging because most patients are asymptomatic.

• It is a morphological variant of chronic cholecystitis.

• Inflammatory scarring of the wall, combined with dystrophic calcification transforms the gallbladder into a porcelain-like vessel. Removal of the gallbladder (cholecystectomy) is the recommended treatment.

• The risk of cancer in a porcelain gallbladder is 15%.

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