Biliary colic

Approximately one-third of patients with gallstones are symptomatic. Biliary colic as the result
of transient obstruction of the cystic duct by sludge or stones is the main complaint in 70%80% of
symptomatic patients. Implicit in the term biliary colic is the fact that the gallbladder mucosa does not
show features of acute inflammation. The pain of biliary colic is thought to be caused by functional
spasms around an obstructed cystic duct; the pain of acute cholecystitis is caused by gallbladder wall
inflammation.
Although it may be variable, biliary pain often has specific characteristics. The pain is episodic
and severe, and it is located in the epigastrium or less frequently in the right upper quadrant, left
upper quadrant, the precordium, and the lower
Abdomen. The pain may be precipitated by eating a large meal, but often no single food is the lone
culprit. Pain may develop without any precipitating events.Typically, the pain has a sudden onset and
rises steeply in intensity over a 15-min interval to a steady plateau lasting as long as 3 h. Resolution of
pain is slower. Pain lasting more than 6 h should raise the suspicion of cholecystitis. The pain may
radiate to the interscapular region or, rarely, to the right shoulder. Vomiting and diaphoresis are not
uncommon. The patient is usually restless and unable to find a comfortable position. Residual
tenderness in the upper abdomen may persist after an attack. The interval between attacks is
unpredictable and may be weeks, months, or years. True biliary
colic should be differentiated from nonspecific dyspepsia. Flatulence, pyrosis, aerophagia, vague
abdominal discomfort,
and fatty food intolerance are common complaints of many patients, whether or not they have
cholelithiasis. The ability to differentiate true biliary pain from nonspecific abdominal symptoms
significantly impacts the success of treating gallstone disease. For example, a cholecystectomy
performed for gallstone-induced biliary colic is usually curative, but symptoms often persist if it is
performed for patients with nonspecific dyspepsia and cholelithiasis. It is worthwhile to clarify
prevalent misunderstandings about biliary pain. First, biliary colic is a misnomer, because the pain is
steady, not intermittent or fluctuating. Second, the pain is primarily epigastric. It is inappropriate to
interpret pain not located in the right upper quadrant as atypical of gallstone symptoms. Third, fat
intolerance is not a feature of biliary colic. Fourth, despite the availability of many imaging techniques
to demonstrate the presence of gallstones, the diagnosis of biliary colic is ultimately based on clinical
judgment.

Acute cholecystitis

The most common cause of acute cholecystitis is obstruction of the cystic duct by gallstones, resulting
in acute inflammation
of the gallbladder. Approximately 90% of cases are associated with cholelithiasis. Obstruction likely
damages the gallbladder mucosa, initiating an inflammatory reaction involving prostaglandins and
other chemical mediators. Although bacteria are commonly found in the gallbladder bile of patients
with acute cholecystitis, this is probably a secondary event. Secondary bacterial infection can progress
to empyema. Most patients with acute cholecystitis have had previous attacks of biliary pain. The pain
of acute cholecystitis typically lasts longer than 3 h and shifts from the epigastrium to the right upper
quadrant with the emergence of localized tenderness and associated vomiting. With time, the intensity
of pain may diminish, but tenderness increases. Fever is common, but is rarely over 38.3C (101F).
The sequence of clinical features represents visceral pain of ductal impaction by stones,proceeding to
gallbladder inflammation with parietal pain. In elderly patients, presenting signs and symptoms may
be especially mild. On physical examination, Murphys sign, an abrupt arrest in inspiration secondary
to pain during direct palpation of the right upper quadrant, may be present . In 30% to 40% of patients,
a palpable mass may be present.
Jaundice is present in 15% of patients with acute cholecystitis, even without choledocholithiasis and
obstruction. The
pathogenesis may involve edema and compression around the inflamed cystic duct. The differential
diagnosis of cholecystitis
includes choledocholithiasis, acute cholangitis, and pyogenic or amebic liver abscesses.

Chronic cholecystitis

Patients with chronic cholecystitis usually have gallstones and have had repeated attacks of biliary
pain or acute cholecystitis. This results in a thickened and fibrotic gallbladder, which shows evaginated
mucosal pouches (RokitanskyAschoff sinuses) on histological examination. It is uncommon for the
gallbladder to be palpable during an attack of pain. The patient may have fewer symptoms referable to
the gallbladder but may present with associated gallstone complications such as recurrent
pancreatitis, choledocholithiasis, and cholangitis.

Choledocholithiasis and cholangitis

Small gallstones passing into the common bile duct from the gallbladder may eventually proceed to
the duodenum. They may also remain in the common bile duct and give rise to complications. The
majority of stones in the common duct have the same composition as those in the gallbladder.
However, some are softer and more brown in color because of deposits of calcium bilirubinate and
other calcium salts, including fatty acid complexes. Common duct stones are frequently associated
with infected bile, which may or may not be clinically apparent. Choledocholithiasis is one of many
causes of obstructive or surgical jaundice, which must be differentiated from hepatocellular or
medical jaundice. Obstruction of the passage of bile results in jaundice and pruritus. The
pathogenesis of pruritus is unclear, although retention of bile salts with irritation of sensory nerve
endings and retention of endogenous opiate agonists have been proposed as mechanisms. Sometimes
pruritus can be the predominant or incapacitating symptom. With biliary obstruction, the feces may be
hypocholic or acholic. Light-colored or clay-colored stools are uncommon in bile duct obstruction
resulting from gallstones because the obstruction is rarely complete, but are
more commonly observed with malignant strictures of the common bile duct. Unlike with malignant
obstruction of the common bile duct, a palpable and nontender gallbladder because of cholelithiasis
(Courvoisier law) is uncommon. The biliary obstruction is usually incomplete, and the gallbladder itself
is likely to be fibrotic, scarred, and nondistensible secondary to chronic cholecystitis. However, the
exceptions to this rule are substantial, with frequent false-positive and false-negative results.
Obstruction of the common bile duct also causes increased intraductal pressure, inhibiting bile flow
and causing the
reflux of bile from the canaliculus into the sinusoids. The normal pressure in the common bile duct is
10 cmH2O to
15 cmH2O. With obstruction, the pressure can rise to above 40 cmH 2O, causing biliary duct dilation.
Therefore,
dilation of the extrahepatic and intrahepatic bile ducts is a valuable sign of common bile duct
obstruction and is best
seen using ultrasonography or a computed tomography (CT) scan. Clinically, the only manifestations
may be mild hepatomegaly
or right upper quadrant tenderness. Prolonged biliary obstruction induces fibrogenesis in the liver,
potentially leading to secondary biliary cirrhosis. Thepropensity for developing cirrhosis varies with the
completeness and duration of obstruction. On average, choledocholithiasis will lead to secondary
biliary cirrhosis after about 5 years. Patients with incomplete obstruction more commonly present with
portal hypertension, and those with complete obstruction present with hepatic failure. Even if the
patient has cirrhosis, every effort should be made to relieve the obstruction, because reversal of portal
hypertension and secondary biliary cirrhosis has been reported. A common complication of
choledocholithiasis is cholangitis. For bacterial infection to occur, biliary obstruction or bile stasis is
always present, although obstruction is not always associated with overt bacterial infection. For
example, cholangitis is extremely common in choledocholithiasis, not uncommon in sclerosing
cholangitis, and relatively uncommon (10%15%) in malignant bile duct strictures. The typical clinical
picture, occurring in 70% of cases, consists of biliary pain, jaundice, and chills and rigors (Charcot
triad). Pain, usually characteristic of biliary colic, occurs in 90% of patients. Bacteremia with chills and
fever occurs in 95%, and clinical jaundice in 80%. Clinical signs are nonspecific, with mild
hepatomegaly, tenderness, and occasionally rebound tenderness. For many patients, cholangitis is a
short and self-limited illness complicating choledocholithiasis or sclerosing cholangitis. However, shock,
multiple liver abscesses, or multiorgan failure may result. Blood cultures are often positive and reflect
the organisms infecting the bile ducts. The most commonly found organisms are E. coli, Klebsiella sp.,
Pseudomonas sp., and enterococci. Coinfection with anaerobes occurs in 15%. Acute pancreatitis may
be precipitated by the passage of stones or sludge in the common bile duct, and sludge or microscopic
stones may account for a significant proportion of cases of idiopathic pancreatitis.

Differential diagnosis
Clinical signs and symptoms

The clinical symptoms and signs of biliary tract disorders are not highly specific. The patients history,
physical findings, and laboratory data should be carefully examined. A clinical impression of biliary
colic should be confirmed by imaging studies. Gallstones are found commonly and may coexist with
other disorders so the finding of gallstones does not exclude
other diseases contributing to or complicating the patients clinical picture. Disorders of other visceral
organs, including the upper gastrointestinal tract, colon, kidneys, and pancreas, should be excluded by
appropriate diagnostic tests. Extraabdominal

disorders that may produce a similar clinical picture include angina pectoris, dissecting aortic
aneurysm, spinal, neuralgia, pleuritis, pericarditis, and uncommon metabolic disorders such as
hereditary angioedema (C1 esterase inhibitor deficiency) and acute intermittent porphyria. In addition
to pain, patients with acute cholecystitis usually present with symptoms and signs of local
inflammation (e.g., right upper quadrant mass, tenderness) and systemic toxicity (e.g., fever,
leukocytosis). The differential diagnosis includes other causes of intraabdominal inflammation or
infection. Acute appendicitis can cause a difficult diagnostic
problem. The periumbilical pain shifting to the right lower quadrant with an inflamed mass may be
confused with biliary colic with an inflamed gallbladder. A gallbladder can below lying or an appendix
can be subhepatic. Fever and leukocytosis are features of both. Ultrasonography or hepatobiliary
scintigraphy may be helpful. It may be difficult to differentiate acute pancreatitis from cholecystitis
because the two conditions produce tenderness in an overlapping area. Gallstones may cause acute
pancreatitis, and cholecystitis and pancreatitis therefore may coexist. Acute cholecystitis alone can be
associated with hyperamylasemia, but pancreatitis often has higher enzyme levels. Biliary scintigraphy
and imaging techniques such as ultrasound and CT scans are helpful diagnostically. Perforated peptic
ulcer usually produces more dramatic pain and peritoneal signs. Plain abdominal radiographs or CT
scans often show free intraabdominal air. If free air cannot be seen and ulcer perforation is still
suspected, an urgent radiographic study with water-soluble contrast should demonstrate the
perforation.

Diagnostic studies
Laboratory tests
In uncomplicated biliary colic, the results of hematological and biochemical tests are normal. In acute
cholecystitis, leukocytosis with a left shift is usually seen, but this does not differentiate it from other
intraabdominal infections. Edema and inflammation of the gallbladder can partially obstruct the
common bile duct, causing mild elevation of the serum aminotransferases and alkaline phosphatase.
Elevation of serum bilirubin can also be associated with the enzyme level changes, especially if the
common hepatic duct or common bile duct is involved in the inflammatory reaction. Bilirubin elevation
is proportional to the degree of obstruction. Alkaline phosphatase, however, is produced by bile
canalicular and ductular cells, and its elevation does not depend on the magnitude or cause of
obstruction. Abdominal pain, fever, and jaundice are often the presenting features of
choledocholithiasis. In such cases, the bilirubin level is usually between 2 mg/dL and 10 mg/dL, and the
alkaline phosphatase is less than five times normal. If the level of bilirubin is above 15 mg/dL, a
neoplastic obstruction should be strongly suspected. If ductal dilatation is documented by
ultrasonography or CT scans, a cholangiogram should be obtained to define the cause and level of
obstruction.