CHOLELITHIASIS,

CHOLEDOCHOLITHIASIS,
PANCREATITIS
CHOLELITHIASIS
 DEFINITION

Cholesterol stones account for more than 90% of all gallstones in Western
industrialized countries. Cholesterol gallstones usually contain >50%
cholesterol monohydrate plus an admixture of calcium salts, bile pigments,
proteins, and fatty acids.
 EPIDEMIOLOGY

Gallstone formation increases after age 50. In the United States, the third
National Health and Nutrition Examination Survey (NHANES III) has
revealed an overall prevalence of gallstones of 7.9% in men and 16.6% in
women.
 PATHOGENESIS

Cholesterol is essentially water insoluble and requires aqueous dispersion

into micelles, which require the presence of a second lipid to solubilize the
cholesterol.
Cholesterol and phospholipids are secreted into bile, which are converted
into mixed micelles consisting of bile acids, phospholipids, and cholesterol.
Bile also consist lecithin and bilirubin.
 The most important is increased biliary secretion of cholesterol. This may
occur in association with obesity, the metabolic syndrome, high-caloric and
cholesterol-rich diets and increased hepatic uptake of cholesterol from
blood.
 While supersaturation of bile with cholesterol is an important prerequisite for
gallstone formation.
An important mechanism is nucleation of cholesterol monohydrate crystals, which
is greatly accelerated in human lithogenic bile.
Vesicle fusion leads to liquid crystals, which, in turn, nucleate into solid cholesterol
monohydrate crystals.
Cholesterol monohydrate crystal nucleation and crystal growth probably occur
within the mucin gel layer.
 A third important mechanism in cholesterol gallstone formation is
gallbladder hypomotility.
The incidence of gallstones is increased in conditions associated with
infrequent or impaired gallbladder emptying such as fasting, parenteral
nutrition, or pregnancy and in patients using drugs that inhibit gallbladder
motility.
 SYMPTOMS

The most specific and characteristic symptom of gallstone disease is biliary

colic that is a constant and often long-lasting pain.
Biliary colic begins quite suddenly and may persist with severe intensity for
30 min to 5 h, subsiding gradually or rapidly.
Nausea and vomiting frequently accompany episodes of biliary pain.
 DIAGNOSIS

Ultrasonography of the gallbladder is very accurate in the identification of

cholelithiasis and has replaced oral cholecystography.
Stones as small as 1.5 mm in diameter may be confidently identified
provided that firm criteria are used (e.g., acoustic shadowing of opacities
that are within the gallbladder lumen).
 TREATMENT

Recommendation for cholecystectomy in a patient with gallstones should

probably be based on assessment of three factors:
(1) The presence of symptoms that are frequent enough or severe enough to
interfere with the patients general routine;
(2) The presence of a prior complication of gallstone disease, acute
cholecystitis, pancreatitis.
(3) Patients with very large gallstones (>3 cm in diameter) might be
considered to cholecystectomy.
 DRUGS
This therapy should be limited to radiolucent stones smaller than 5 mm in
diameter. The dose of UDCA (Ursodeoxycholic acid) should be 1015 mg/kg
per day.
CHOLEDOCHOLTHIASIS
 DEFINITION AND EPIDEMIOLOGY
Choledocholithiasis is the presence of at least one gallstone in common bile
duct.
Passage of gallstones into the CBD occurs in 1015% of patients with
cholelithiasis. The incidence of common duct stones increases with
increasing age of the patient, so that up to 25% of elderly patients may have
choledocholithiasis.
 PATHOPHYSIOLOGY

Passage of gallstones into the CBD occurs in 1015% of patients with

cholelithiasis. The incidence of common duct stones increases with
increasing age of the patient.
The overwhelming majority of bile duct stones are cholesterol stones
formed in the gallbladder, which then migrate into the extrahepatic biliary
tree through the cystic duct.
 CLINICAL MANIFESTATION

Common duct stones may remain asymptomatic for years, may pass
spontaneously into the duodenum, or (most often) may present with biliary
colic.
 DIAGNOSIS
CBD stones should be suspected in gallstone patients who have any of the
following risk factors:
1. A history of jaundice or pancreatitis.
2. Abnormal tests of liver function.
3. Ultrasonographic or MRCP evidence of a dilated CBD or stones in the duct.
 TREATMENT
The widespread use of laparoscopic cholecystectomy and ERCP has
decreased the incidence of complicated biliary tract disease and the need
for choledocholithotomy and T-tube drainage of the bile ducts.
PANCREATITIS
 DEFINITION

Pancreatitis is a serious condition where the pancreas become inflamated

over a short period of time.
 ETIOLOGY

Gallstones continue to be the leading cause of acute pancreatitis in most

series (3060%). The risk of acute pancreatitis in patients with at least one
gallstone <5 mm in diameter is fourfold greater than that in patients with
larger stones.
Alcohol is the second most common cause, responsible for 1530% of cases
in the United States.
 EPIDEMIOLOGY

The annual incidence ranges from 1345/100,000 persons. Acute

pancreatitis results in >250,000 hospitalizations per year. Hospitalization
rates increase with age, are 88% higher among blacks, and are higher
among males than females.
 PATHOGENESIS

The initial phase is characterized by autodigestion, pancreatitis results when

proteolytic enzymes (e.g., trypsinogen, chymotrypsinogen) are activated in
the pancreas acinar cell rather than in the intestinal lumen.
 The second phase of pancreatitis involves the activation, sequestration of
leukocytes and macrophages in the pancreas, resulting in an enhanced
intrapancreatic inflammatory reaction.
 The third phase of pancreatitis is due to the effects of activated proteolytic
enzymes and cytokines, released by the inflamed pancreas. Activated
proteolytic enzymes, especially trypsin, not only digest pancreatic and
peripancreatic tissues. The active enzymes and cytokines then digest
cellular membranes and cause proteolysis, edema, interstitial hemorrhage,
vascular damage, coagulation necrosis, fat necrosis, and parenchymal cell
necrosis.
HOW TO DIAGNOSIS
 SYMPTOMS

Abdominal pain is the major symptom of acute pancreatitis. Pain may vary
from a mild discomfort to severe and constant. Characteristically, the pain,
which is steady and boring in character, is located in the epigastrium and
periumbilical region, and may radiate to the back, chest and lower
abdomen. Nausea and vomiting frequent complaints.
 PHYSICAL EXAMINATION

Physical examination, Abdominal rigidity is present to a variable degree, but

compared with the intense pain, these signs may be less impressive. Bowel
sounds are usually diminished or absent. An enlarged pancreas may be
palpable.
 LABORATORY DATA

Serum amylase and lipase values threefold. Serum lipase is the preferred
test. After 37 days, even with continuing evidence of pancreatitis, total
serum amylase values tend to return toward normal.
 CT-SCAN

Two types of pancreatitis are recognized on imaging as interstitial or

necrotizing based on pancreatic perfusion. CT imaging is best evaluated 35
days into hospitalization when patients are not responding to supportive
care to look for local complications such as necrosis.
 The diagnosis is established by two of the following three criteria:
(1) Typical abdominal pain in the epigastrium that may radiate to the back
(2) Threefold or greater elevation in serum lipase and/or amylase
(3) Confirmatory findings of acute pancreatitis on cross-sectional abdominal
imaging.
 ACUTE PANCREATITIS MANAGEMENT

The management of acute pancreatitis begins in the emergency ward. After

a diagnosis has been confirmed, aggressive fluid resuscitation is initiated,
intravenous analgesics are administered, severity is assessed, and a search
for etiologies that may impact acute care is begun.
 FLUID MANAGEMENT
Intravenous fluids of lactated Ringers or normal saline are initially bolused
at 1520 cc/kg (10501400 mL), followed by 3 mg/kg per hour (200250
mL/h), to maintain urine output >0.5 cc/kg per hour.
A targeted resuscitation strategy with measurement of hematocrit and BUN
every 812 h is recommended to ensure adequacy of fluid resuscitation
 CHRONIC PANCREATITIS
Chronic pancreatitis is a disease process characterized by irreversible
damage.
 ETIOLOGY

Although alcohol has been believed to be the primary cause of chronic

pancreatitis, other factors contribute to the disease because not all heavy
consumers of alcohol develop pancreatic disease.
There is also a strong association between smoking and chronic
pancreatitis.
 PATHOPHYSIOLOGY

Inflammatory process in the pancreas are becoming more clearly

understood. Irrespective of the mechanism of injury, it is becoming
apparent that stellate cell activation that results in cytokine expression and
production of extracellular matrix proteins
 Cause acute and chronic inflammation and collagen deposition in the
pancreas. Thus, the condition is defined by the presence of histologic
abnormalities, including chronic inflammation, fibrosis, and progressive
destruction of both exocrine and eventually endocrine tissue (atrophy).
 CLINICAL MANIFESTATON

Patients with chronic pancreatitis seek medical attention predominantly

because of two symptoms: abdominal pain or maldigestion and weight loss.
The abdominal pain may be quite variable in location, severity, and
frequency.
Eating may exacerbate the pain, leading to a fear of eating with consequent
weight loss. Maldigestion is manifested as chronic diarrhea, steatorrhea,
weight loss, and fatigue
 TREATMENT CHRONIC PANCREATITIS

A Whipple procedure, total pancreatectomy, and autologous islet cell

transplantation have been used in selected patients with chronic
pancreatitis