GALLSTONES AND ITS

COMPLICATIONS

PATHOGENESIS

RISK FACTORS

Age: Increasing age*

Body habitus: Obesity, rapid weight loss
Childbearing: Pregnancy
Drugs: Fibric acid derivatives (or fibrates), contraceptive steroids, postmenopausal
estrogens, progesterone, octreotide (Sandostatin), ceftriaxone (Rocephin)
Ethnicity: Pima Indians, Scandinavians
Family: Maternal family history of gallstones
Gender: Females
Hyperalimentation: Total parenteral nutrition, fasting
Ileal and other metabolic diseases: Ileal disease (Crohn's disease), resection or
bypass,* high triglycerides, diabetes mellitus, chronic hemolysis,* alcoholic
cirrhosis,* biliary infection,* primary biliary cirrhosis, duodenal diverticula,*
truncal vagotomy, hyperparathyroidism, low level of high-density lipoprotein
cholesterol
*--Risk factors for pigment gallstone formation.
--Risk factor for cholesterol and pigment gallstone formation.

Case
46yo F w RUQ pain x4hr, after a fatty meal,

radiating to the R scapula, also w nausea. Pt is

pain-free now.
No prior episodes
Minimal RUQ tenderness, no Murphys
WBC 8, LFT normal
RUQ U/S reveals cholelithiasis without GB
wall thickening or pericholecystic fluid

CASE

denotes
gallstones

denotes the
acoustic shadow
due to absence of
reflected sound
waves behind the
gallstone

Symptomatic cholelithiasis
aka biliary colic
The pain occurs due to a stone obstructing the

cystic duct, causing wall tension; pain resolves

when stone passes
Pain usually lasts 1-5 hrs, rarely > 24hrs
Ultrasound reveals evidence at the crime scene
of the likely etiology: gallstones
Exam, WBC, and LFT normal in this case
Treatment: Laparoscopic cholecystectomy

CASE
66 years-old male with past medical history of

diabetes mellitus, c/o RUQ pain > 24hrs

radiating to the R scapula, started after fatty
meal, a/w nausea, vomiting, fever
Exam: Palpable, tender gallbladder, guarding,
+Murphys = inspiratory arrest
WBC 18, Mild LFT

Case

Curved arrow

Straight arrow

Two small stones at

GB neck

Thickened GB wall

pericholecystic fluid
= dark lining outside
the wall

U/S: gallstones, wall thickening (>4mm), GB

distension, pericholecystic fluid, sonographic
Murphys sign (very specific)
Diagnosis: ?

EMPHYSEMATOUS CHOLECYSTITIS

CASE

A 72 year old woman with heart faliure, hypertension

and diabetes came to the office with a chief complaint
of chills, abdominal pain, nausea and vomiting
followed by inability to pass flatus 8 hours prior to
consult.
On physical examination the patient was febrile and
appeared dehydrated. Abdominal exam: distension
and increased bowel sounds. No jaundice.
Labs: Hyperglycemia, mild renal failure,
hypernatremia and leukocytosis.

CASE

CHOLECYSTOENTERIC FISTULA

A 43-year-old woman visited our

outpatient clinic in March
2004 with a six-month history of colic
pain, nausea and vomiting. She had a past
history of hyperthyroidism.
Physical examination revealed a tender
right upper abdomen
and jaundice. The laboratory blood tests
showed increased
levels of bilirubin 9 mg/dl
alkaline phosphatase 145 U/l (<140 U/l),
g-glutamyltransferase
161 U/l (<40 U/l), alanine transaminase
1240 U/l (<40 U/l), aspartate
transaminase 688 U/l (<35 U/l)
and lactate dehydrogenase 888 U/l (<480
U/l), while the
serum amylase was normal.
Ultrasonography showed
slightly dilated intrahepatic ducts, an
extended gallbladder
with multiple stones

CASE

MIRIZZI'S SYNDROME

One study has shown that acute cholecystitis resolves without

complications in approximately 83% of patients but results in
gangrenous cholecystitis in 7%,
gallbladder empyema in 6%,
perforation in 3%, and
emphysematous cholecystitis in less than 1%
When the level of leukocytosis exceeds 15,000 cells/mm,
particularly in the setting of worsening pain, high fever
(temperature >102 F), and chills, suppurative cholecystitis
(empyema) or perforation should be suspected, and urgent
surgical intervention may be required.

CASE
46yo F p/w RUQ pain, jaundice, acholic

stools, dark tea-colored urine, no fevers

Known history of cholelithiasis
Exam: unremarkable
WBC 8, T.Bili 8, AST/ALT 90/75, HepB/C
neg
Ultrasound: Gallstones, CBD not dilated
Diagnosis: ?

CASE

MRCP

EUS

CHOLEDOCHOLITHIASIS

Fifteen percent of patients with gallbladder stones also have CBD stones.
Conversely, of patients with ductal stones, 95% also have gallbladder stones

Stones in the CBD usually come to rest at the lower end of the ampulla of Vater.
Obstruction of the bile duct raises bile pressure proximally and causes the ducts to
dilate. Pressure in the CBD is normally 10 to 15 cm H2O and rises to 25 to 40 cm
H2O with complete obstruction. When pressure exceeds 15 cm H2O, bile flow
decreases, and at 30 cm H2O, bile flow

The bile duct dilates to the point that it can be detected on either ultrasonography
or abdominal CT in approximately 75% of cases. In the patient who has had
recurrent bouts of cholangitis, the bile duct may become fibrotic and thus unable to
dilate. Moreover, dilatation of the duct is sometimes absent in patients with
choledocholithiasis because the obstruction is low-grade and intermittent

CHOLEDOCHOLITHIASIS

Acute obstruction usually causes biliary pain and jaundice

Obstruction that develops gradually over several months may
manifest initially as pruritus or jaundice alone.
If bacteria proliferate, life-threatening cholangitis may
result
The physical findings are usually normal if obstruction of the CBD is
intermittent.
Mild to moderate jaundice may be noted when obstruction has
been present for several days to a few weeks.
Deep jaundice without pain, particularly with a palpable
gallbladder (Courvoisier's sign), suggests neoplastic obstruction of the
CBD, even when the patient has stones in the gallbladder.
With long-standing obstruction, secondary biliary cirrhosis may
result, leading to physical findings of chronic liver disease.

CHOLEDOCHOLITHIASIS
Elevated serum bilirubin and alkaline

phosphatase levels are seen with CBD

obstruction
Serum bilirubin level >10 mg/dL suggests
malignant obstruction or coexisting hemolysis
A
transient spike in serum aminotransferase or
amylase (or lipase) levels suggests the passage
of a stone

TREATMENT

CASE
46yo F p/w fever, RUQ pain, jaundice
If also altered mental status and signs of

shock
VS tachycardic, hypotensive
ABCs, Resuscitate

2 large bore IV, Foley, Continuous monitor

1-2L fluid bolus, repeat until resuscitated

Diagnosis: ?

CHOLANGITIS

Stone in the common bile duct causing bile stasis Bacterial

superinfection of stagnant bile Early bacteremia

Charcot's triad (pain, jaundice, and fever) is present in 70% of

patients Pain may be mild and transient and is often accompanied by
chills Mental confusion, lethargy, and delirium suggest sepsis

Fever in 95% RUQ tenderness in 90% Jaundice in 80% Peritoneal

signs in 15% Hypotension and mental confusion coexist in 15% and
suggest gram-negative sepsis

Leukocytosis in 80%, but remainder may have normal white blood cell
count with band forms Serum bilirubin level >2 mg/dL in 80%
Serum alkaline phosphatase level is usually elevated Blood cultures
are usually positive, especially during chills or fever spike; two
organisms are grown in cultures from one half of patients

CASE
46yo F w RUQ pain x4hr, after a fatty meal,

radiating to the R scapula, also w nausea. Pt is

pain-free now. Has had multiple prior attacks
of similar RUQ pain
No prior episodes
Minimal RUQ tenderness, no Murphys
WBC 8, LFT normal
RUQ U/S reveals cholelithiasis with GB wall
thickening, no pericholecystic fluid

CHRONIC CHOLECYSTITIS

Chronic inflammation of the gallbladder is the indication for nearly 3% of

cholecystectomies in adults.
Pathophysiology is poorly understood.
repeated episodes of low-grade gallbladder obstruction, resulting in recurrent
mucosal trauma .
There is little correlation between the number of choleliths or their overall
volume and the degree of gallbladder wall inflammation.
In fact, 12% to 13% of patients who have chronic cholecystitis have no
demonstrable stones.
No role of Bacterial infection of the bile
As each episode of acute inflammation resolves, neutrophilic infiltration is
replaced with lymphocytes, plasma cells, macrophages, and eosinophils. Focal
ulcerations and necrotic tissue are replaced by granulation tissue and collagen
deposits. The gallbladder wall may become thickened or remain thin. The
mucosa can remain intact, develop accentuated folds, or be flattened.

CHRONIC CHOLECYSTITIS

The symptoms of chronic cholecystitis

vary :
classic severe biliary colic
vague
or nonspecific complaints.
intermittent
episodes of nausea,
reflux
symptoms,
food
intolerance, or bloating.
lowgrade fever,
mild
upper abdominal discomfort, or
chronic
fatigue.
Not infrequently patients who have chronic cholecystitis have
been treated for gastritis, ulcer disease, or irritable bowel
syndrome without appreciable improvement in their
complaints.
HIDA with CCK helps

Dx: ?

PORCELAIN GALLBLADDER

Take Home Points

As always, ABC & Resuscitate before Dx

Understanding the definitions is key
Is this acute cholecystitis? (fever, WBC, tender on exam
with positive Murphys)
Or simply cholelithiasis vs ongoing chronic
cholecystitis? (no fever/WBC)
Is patient sick or toxic-appearing, to suspect empyema,
gangrene or even perforation?
Elicit h/o jaundice, acholic stools, tea-colored urine
Rule out cholangitis, because this will kill the patient
unless dx & tx early