Gastrointestinal and Abdominal: Gallbladder Flashcards
Gallbladder: Anatomy and Physiology
The gallbladder is located in the right upper quadrant
of the abdomen beneath the liver. The cystic duct exits
at the neck of the gallbladder and joins the common
hepatic duct to form the common bile duct, which
empties into the duodenum at the ampulla of Vater.
This is surrounded by the sphincter of Oddi, which
regulates bile flow into the duodenum (Fig. 7-1).
Bile produced in the liver is stored in the gallblad-
der. Bile is important for the absorption of fat-soluble
vitamins (A, D, E, and K). Cholecystokinin stimulates
gallbladder contraction and release of bile into the
duodenum. The spiral valves of Heister in the cystic
duct prevent bile reflux into the gallbladder. Arterial
supply is from the cystic artery, which most commonly
arises from the right hepatic artery and courses
through the triangle of Calot, which is bounded by the
cystic duct laterally, the common hepatic duct medi-
ally, and the edge of the liver superiorly (Fig. 7-2).
Gallstone Disease
Cholelithiasis is the presence of gallstones within
the gallbladder. Choledocholithiasis refers to stones
in the common bile duct (Fig. 7-3). Biliary colic is pain
produced when the gallbladder contracts against a tran-
siently obstructing stone in the neck of the gallbladder.
There is no inflammatory or infectious process in biliary
colic. Acute cholecystitis produces a constant pain and
refers to inflammation and infection of the gallbladder;
total or partial occlusion of the cystic duct is thought to
be required. The most common organisms cultured
during acute cholecystitis are
Escherichia coli, Klebsiella
,
enterococci,
Bacteroides fragilis
, and
Pseudomonas.
Gallstones within the common bile duct are a major
cause of pancreatitis, known as gallstone pancreatitis.
Gallstone Disease: Pathogenesis
Gallstones are composed of cholesterol, calcium biliru-
binate (pigment), or a mixture of both. Cholesterol
stones make up approximately 75% of gallstones in
Western countries. Stone formation occurs when bile
becomes supersaturated with cholesterol. Cholesterol
crystals then precipitate out of solution and agglom-
erate to form stones.
A high-cholesterol diet causes increased concentra-
tions of cholesterol and may have a role in the patho-
genesis of cholesterol stones. Pigment stones are com-
posed of calcium bilirubinate and are either black or
brown. Black pigment stones are usually found in
the gallbladder and are associated with cirrhosis and
hemolytic processes, such as sickle cell anemia, tha-
lassemia, and spherocytosis. Brown stones
are associ-
ated with chronic biliary tract infection and are often
found in the bile ducts. Patients with
indwelling bil-
iary stents or with intraluminal nonabsorbable sutures
in the ducts from prior surgery are prone to develop-
ing brown stones.
Gallstone Disease: Epidemiology
Approximately 10% of the U.S. population has gall-
stones. The vast majority of people with stones are
asymptomatic. Nevertheless, more than 600,000 chole-
cystectomies are performed in the United States
annually.
Gallstones are found more commonly in women.
Risk factors include obesity, multiparity, chronic total
parenteral nutrition use, high-dose estrogen oral
contraceptives, rapid weight loss, diabetes, and
increasing age. Some ethnic groups such as American
Indians have very high prevalence rates. Spinal cord
injury predisposes to cholesterol stones.
Gallstone Disease: History
As stated, most patients with gallstones are asympto-
matic. Patients with biliary colic usually complain of
right upper quadrant or epigastric pain, often radiating
around the right flank to the back. The pain is usually
postprandial (occurring after eating). Pain episodes
may be precipitated by fatty food intake and last sev-
eral hours before resolving spontaneously. Associated
nausea and vomiting are common.
Cholecystitis implies infection and inflammation
of the gallbladder. The pain of cholecystitis is usually
constant, with progressive worsening. Patients may
have fever, chills, or sweats.
Choledocholithiasis can result in transient or com-
plete blockage of the common bile duct. Patients may
relate episodes of passing dark urine or light-colored
stools caused by the inability of bile pigments to reach
the gastrointestinal tract and from subsequent renal
clearance. Choledocholithiasis can also lead to ascend-
ing cholangitis, demonstrated by right upper quadrant
abdominal pain, fever, and chills.
Pancreatitis owing to choledocholithiasis (gall-
stone pancreatitis) typically manifests with epigastric
pain radiating to the back.
Gallstone Disease: Physical Examination
Physical examination in simple biliary colic reveals
right upper quadrant tenderness but no fever.
Cholecystitis may be associated with fever and signs
of peritoneal irritation, including right upper quad-
rant rebound and guarding. The classic finding in
acute cholecystitis is the arrest of inspiration on deep
right upper quadrant palpation as pressure from the
examiner’s hand contacts the inflamed gallbladder
and peritoneum (Murphy sign). Choledocholithiasis
may be associated with jaundice, in addition to signs
of biliary colic. Cholangitis is classically marked by
fever, right upper quadrant pain, and jaundice
(Charcot triad). Progression of cholangitis to sepsis
defines Reynolds pentad by adding hypotension and
mental status changes to the triad. Patients with gall-
stone pancreatitis have epigastric tenderness. A pal-
pable, nontender, distended gallbladder in the clini-
cal setting of jaundice indicates malignant biliary
obstruction (Courvoisier law).
Gallstone Disease: Diagnostic Evaluation
Laboratory examination in biliary colic is usually unre-
markable. Cholecystitis usually manifests with increased
white blood cell count and minor liver function
test
abnormalities. Choledocholithiasis is classically asso-
ciated with increased serum bilirubin and alkaline
phosphatase. Cholangitis usually causes elevated
serum bilirubin and transaminase levels, as well as
leukocytosis. Gallstone pancreatitis is accompanied
by elevations in serum amylase and lipase.
Ultrasound is the best modality for imaging the
gallbladder and bile ducts, having a sensitivity and
specificity of 98% for the detection of gallstones. On
ultrasound, the gallstones appear as opacities, with
echoless shadows posteriorly (Fig. 7-4). Moving the
patient during ultrasound examination often demon-
strates migration of the stones to the dependent por-
tion of the gallbladder. Ultrasound is also used for
diagnosing acute cholecystitis. Fluid around the gall-
bladder (pericholecystic fluid), a thickened gallblad-
der wall, and an ultrasonographic Murphy sign all
support the diagnosis of acute cholecystitis.
When ultrasound findings are equivocal or acal-
culous cholecystitis is suspected, cholescintigraphy
(e.g., hepatobiliary iminodiacetic acid scan) is almost
100% sensitive and 95% specific for acute cholecystitis.
In this test, a radionucleotide that is injected intra-
venously is taken up in the liver and excreted into the
biliary tree. If the cystic duct is obstructed, as in acute
cholecystitis, the gallbladder does not fill, and the
radionucleotide passes directly into the duodenum.
Choledocholithiasis can be diagnosed by intraop-
erative cholangiography at the time of surgery or pre-
operatively or postoperatively by endoscopic retro-
grade cholangiopancreatography (ERCP). ERCP is
performed by using a specialized side-viewing endo-
scope to visualize the ampulla, where the pancreatic
and biliary ducts enter the duodenum. Using a
catheter passed through the endoscope, contrast
media is injected retrograde and outlines the biliary
tree and pancreatic duct (Fig. 7-5). Magnetic reso-
nance cholangiopancreatography can noninvasively
detect common bile duct stones; however, it lacks the
therapeutic advantage of ERCP for stone extraction.
Gallstone Disease: Complications
Most gallstones are quiescent. When cholecystitis devel-
ops, however, delayed diagnosis may result in gan-
grenous necrosis of the gallbladder wall with perfora-
tion, leading to localized abscess or frank biliary
peritonitis. Emphysematous cholecystitis owing to
Clostridium perfringens
can be seen in diabetic patients.
Gallstone pancreatitis may occur as a result of a
common duct stone causing blockage of the ampulla,
theoretically resulting in bile reflux into the pancre-
atic duct or increased intraductal pressure. (See
Chapter 9, Pancreas.)
Chronic perforation may result in a bilioenteric
fistula. This occurs in older adult patients when a
large gallstone erodes through the gallbladder wall
and causes a fistula to form between the gallbladder
and bowel (usually duodenum, rarely colon). The
large stone can then pass out of the gallbladder,
through the fistula and into the bowel, resulting in
distal bowel obstruction (gallstone ileus). Stone
obstruction of the small bowel typically occurs at the
terminal ileum, whereas the large bowel obstruction
typically occurs at the sigmoid colon. Pneumobilia
and a smooth obstructing mass on imaging studies are
classic findings.
Gallstone Disease: Treatment
For patients with asymptomatic stones found on
workup for other problems, the incidence of symp-
toms or complications is approximately 2% per year.
Cholecystectomy is usually not advised for these
patients. For individuals with biliary colic, laparoscopic
cholecystectomy is a safe and effective procedure. This
is performed electively in most cases. If the preopera-
tive workup suggests that common duct stones may be
present, either ERCP or intraoperative cholangiography
should be performed. (See Appendix for a description
of a typical laparoscopic cholecystectomy.)
Patients with acute cholecystitis should be ade-
quately fluid resuscitated before surgery, as vomiting
and diminished oral intake often results in dehydra-
tion. Intravenous antibiotics should be administered.
Laparoscopic cholecystectomy is the procedure of
choice for removal of the gallbladder (Fig. 7-6). In
the acute setting with gallbladder inflammation and
infection, the procedure tends to be technically more
difficult and has a higher rate of conversion to the
open technique when compared with elective opera-
tions for biliary colic. Rarely, when patients are too ill
to tolerate surgery, a cholecystostomy tube may be
considered. This involves placing a percutaneous
drain into the gallbladder lumen for decompression
and drainage of pus. Cholecystectomy can then be
performed when the patient is stable.
Patients with gallstone pancreatitis require aggressive
fluid resuscitation and close observation. Fortunately,
mild episodes account for 80% of cases; however, severe
fulminant cases can be lethal. Intravenous antibiotics are
only indicated in severe cases with pancreatic necrosis,
infected necrosis, or infectious complications. Early
ERCP is indicated in patients with signs of common bile
duct obstruction (cholangitis, jaundice, dilated common
duct on imaging studies) and in patients with severe dis-
ease. Once pancreatic inflammation subsides, cholecys-
tectomy with intraoperative cholangiography should be
performed during the same hospitalization to reduce
the risk of recurrent pancreatitis and to rule out residual
common duct stones. If stones are present, intraopera-
tive common duct exploration or postoperative ERCP is
performed. The risk of recurrent pancreatitis is approxi-
mately 40% within 6 weeks (see Chapter 9, Pancreas).
Cholangitis, usually caused by choledocholithiasis,
requires rapid diagnosis and treatment. Gram-negative
organisms are the most common cause. Prompt
treatment with intravenous antibiotics, fluid resusci-
tation, and urgent biliary decompression and drainage
are indicated. ERCP with sphincterotomy is the pri-
mary intervention. If the obstructing stone is unable
to be extracted, an indwelling biliary stent can be
passed proximal to the stone to allow decompression
and drainage of infected bile into the duodenum.
Other methods of decompression include percut
aneous transhepatic drainage or open surgical drainage with
common bile duct exploration and T-tube placement.
Overall mortality is approximately 15%.
Gallbladder Cancer: Epidemiology
Carcinoma of the gallbladder is the most common
malignancy of the biliary tract. Cancer of the gallblad-
der is three times more common in females. The inci-
dence is 2.5 in 100,000. Risk factors include gallstones,
porcelain gallbladder, and adenoma. One percent of all
patients who undergo cholecystectomy for gallstones
will be found to have gallbladder carcinoma.
Gallbladder Cancer: Pathology
Adenocarcinoma is the most common histologic
type. Approximately 80% are adenocarcinomas, 10%
are anaplastic, and 5% are squamous cell.
Gallbladder Cancer: History
Unfortunately, most patients usually present with
late-stage disease complaining of vague right upper
quadrant pain. Weight loss, anorexia, and nausea may
also be present.
Gallbladder Cancer: Physical Examination
A right upper quadrant mass may be present.
Obstructive jaundice represents invasion or com-
pression of the common bile duct. Ascites is seen in
advanced cases.
Gallbladder Cancer: Staging
Staging of gallbladder carcinoma is as follows:
Stage I: confined to mucosa/submucosa
Stage II: involvement of muscle layer of gallbladder wall
Stage III: lymph node involvement or extension into
the liver (less than 2 cm liver invasion)
Stage IV: liver invasion greater than 2 cm or distant metastasis.
Gallbladder Cancer: Treatment
The mainstay of treatment for gallbladder cancer is
surgical, because early detection and complete resection
provide the only chance for cure. The extent of resection
is controversial but is based on the stage of disease.
Options include simple cholecystectomy, radical resec-
tion of the gallbladder including partial hepatic resection,
or palliative operation as symptoms arise.
Most cases of early-stage disease are found inciden-
tally after elective laparoscopic cholecystectomy. If the
cancer is stage I and confined to the mucosa/submucosa,
then no additional surgery is indicated. For stage II and
III lesions, where the muscle layer is involved, the
en-bloc resection of the gallbladder with hepatic seg-
ments 4 and 5 as well as radical lymph node dissection
is indicated. Overall, stage IV cancers show no benefit
from attempts at radical resection (except perhaps in
patients with T4N0 disease).