Dr Arun Aggarwal Gastroenterologist explained about Gall Bladder diseases in detail.

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Gall Bladder diseases

• Dr Arun Aggarwal Gastroenterologist

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• Ascertaining the true prevalence of GB disease is
  difficult as most patient with GB disease are
  asymptomatic.
• Various studies have shown prevalence rate
  ranging from 0.13 2.

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Gall stones
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INTRODUCTION

• Gallstone disease is one of the most common and
  costly of all digestive diseases.
• The third National Health and Nutrition
  Examination Survey estimated that 6.3 million men
  and 14.2 million women aged 20 to 74 in the
  United States had gallbladder disease.

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Major risk factors for the development of
gallstones

• Age
• Female sex
• Genetic
• Pima Indians and certain other Native Americans
• Chileans
• Pregnancy
• Obesity
• Rapid weight loss
• Very low calorie diet
• Surgical therapy of morbid obesity
• Cirrhosis
• Hemolytic anemias
• Hypertriglyceridemia

• Medications
• Estrogen and oral contraceptives
• Clofibrate
• Ceftriaxone
• Octreotide
• Terminal ileal resection
• Gallbladder stasis
• Diabetes mellitus
• Total parenteral nutrition
• Postvagotomy
• Octreotide or somatostatinoma
• Spinal cord injury
• Reduced physical activity
• Cystic fibrosis

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• Age exceedingly rare in children except in the
  presence of hemolytic states in addition, lt5 of
  all cholecystectomies are performed in children.
• Sex F gt M
• Pregnancy frequency and no of pregnancies. Sex
  hormones induce a variety of physiologic changes
  in the biliary system, which ultimately cause
  bile to become supersaturated with cholesterol,
  thereby promoting gallstone formation. These
  changes normalize 1-2 months following delivery.

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obesity
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• Diabetes mellitus mechanism is not well
  understood. Hepatic insulin resistance appears to
  be important . Other contributing factors may be
  hypertriglyceridemia and autonomic neuropathy
  leading to biliary stasis due to gallbladder
  hypomotility.
• Serum lipids positively associated with
  apolipoprotein E4 phenotype and elevated serum
  triglycerides. Negative association exists
  between gallstones and high density lipoprotein.
• There is no conclusive evidence linking elevated
  serum cholesterol and gallstones.

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• Cirrhosis due to reduced hepatic synthesis and
  transport of bile salts and nonconjugated
  bilirubin, high estrogen levels, and impaired
  gallbladder contraction in response to a meal.
• Gall bladder stasis In the normal state, the
  gallbladder avidly absorbs water from bile. Thus,
  if bile remains within the gallbladder for a
  prolonged period, it can become overly
  concentrated with cholesterol, thereby promoting
  stone formation. Can occur with spinal cord
  injuries, prolonged fasting and the use of TPN,
  and excess somatostatin.

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• Short bowel syndrome Two factors are thought to
  contribute biliary stasis due to lack of enteral
  stimulation and, in patients with ileal
  resection, interruption of the enterohepatic
  circulation of bile acids results in a reduction
  in hepatic bile acid secretion and an altered
  composition of hepatic bile which becomes
  supersaturated with respect to cholesterol.

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• Crohns disease Gallstones in patients with
  ileal Crohn's disease (or those who have
  undergone ileal resection) are frequently pigment
  based, reflecting an increased concentration of
  bilirubin conjugates, unconjugated bilirubin, and
  total calcium in the gallbladder bile due to
  altered enterohepatic cycling of bilirubin.

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Protective factors

• Statins
• Ascorbic acid
• Coffee (in moderation)
• Vegetable protein
• Poly and mono unsaturated fats

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CLINICAL FEATURES

• When considering gallstone disease it is helpful
  to categorize patients into the following
  clinical groups
• Gallstones on imaging studies but without
  symptoms
• Typical biliary symptoms and gallstones on
  imaging studies
• Atypical symptoms and gallstones on imaging
  studies
• Typical biliary symptoms but without gallstones
  on imaging studies

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Biliary type symptoms

• Biliary colic recurrent pain attacks
• Complication of gall stones acute cholecystitis,
  acute biliary pancreatitis, acute cholangitis, or
  choledocholithiasis with extrahepatic cholestasis.

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Biliary colic

• Usually caused by the gallbladder contracting in
  response to hormonal or neural stimulation
  usually due to a fatty meal, forcing a stone (or
  possibly sludge or microlithiasis) against the
  gallbladder outlet or cystic duct opening, and
  leading to increased intragallbladder pressure
  and pain.
• The stones often fall back from the cystic duct
  as the gallbladder relaxes. As a result, the
  discomfort progresses in less than an hour to a
  steady plateau that ranges from moderate to
  excruciating and remains constant for more than
  an hour, then slowly subsides over several hours.
  
• Despite the term "colic", the pain is usually
  constant and not colicky. The classic attack is
  described as an intense dull pressure-like
  discomfort in the right upper or mid abdomen or
  in the chest that may radiate to the back and the
  right shoulder blade . The pain classically
  follows ingestion of a fatty meal (about one to
  two hours after) and usually does not occur
  during fasting.

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• The pain is often associated with diaphoresis,
  nausea and vomiting. It is not exacerbated by
  movement and not relieved by squatting, bowel
  movements, or flatus.
• After the attack, the physical examination is
  usually normal with the possible exception of
  residual upper abdominal tenderness.
• Prolonged or recurrent cystic duct blockage can
  progress to total obstruction causing acute
  cholecystitis.

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Diagnosis

• Biliary colic is the most accurate predictor of
  gallstone disease.
• Imaging studies can detect gallstones, there is
  no clinical or laboratory test that can make the
  diagnosis of biliary colic.
• The diagnosis is based upon a meticulous history.
• Physical exam usually not ill appearing, no
  fever/ tachycardia, no peritoneal signs,
  voluntary guarding.

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Labs

• LFT
• GGT
• Amylase, lipase
• CBC
• UA
• Imaging studies

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GGT

• GGT is sensitive for detecting hepatobiliary
  disease, but its usefulness is limited by its
  lack of specificity.
• Elevated levels can occur in pancreatic disease,
  myocardial infarction, renal failure, chronic
  obstructive pulmonary disease, diabetes, and
  alcoholism.
• GGT be used to evaluate elevations of other serum
  enzyme tests (eg, to confirm the liver origin of
  an elevated alkaline phosphatase or to support a
  suspicion of alcohol abuse in a patient with an
  elevated AST and an ASTALT ratio of greater than
  21).
• An elevated GGT with otherwise normal liver tests
  should not lead to an exhaustive work-up for
  liver disease.

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USG

• Most useful test.
• It is non-invasive, readily available, relatively
  inexpensive, and does not subject the patient to
  ionizing radiation.
• Accuracy of USG is operator dependent.
• USG must be conducted with the patient having
  fasted, because stones are best seen in a
  distended gallbladder when they are surrounded
  with bile.

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Ultrasound images of a gallbladder adenomatous
polyp (left ) compared to a gallstone (right).
Note the shadow cast by the stone (red arrow)
compared to the absence of a shadow behind the
polyp.
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AXR

• Plain abdominal x-rays are generally not useful
  in looking for gallstones in symptomatic
  patients. Only about 10 of gallstones have
  enough calcium in their composition to make them
  sufficiently radio-opaque to be visible on a
  plain radiograph. 

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Oral cholecystography

• OCG is based upon an orally administered contrast
  agent that is absorbed through the intestine,
  taken up by the liver, and secreted into bile.
  Gallstones appear as filling defects within the
  contrast .

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• CT abdomen
• Endoscopic ultrasonographhy

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Management of biliary colic

• Pain control.
• Can usually be achieved with IV meperidine, which
  is preferred to morphine since it has less of an
  effect on sphincter of Oddi motility.
• NPO to prevent the release of cholecystokinin.
• IV fluids if vomiting
• Anticholinergic agents, which are useful in the
  management of renal colic due to their smooth
  muscle relaxation effects, do not appear to help
  biliary colic.

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Prophylactic treatment to prevent further attacks
and/or the development of complications

• To remove the offending stones to prevent
  recurrent attacks of biliary colic and the
  occurrence of more severe complications.
• Surgical removal of the gallbladder vs medical
  dissolution of the stones while sparing the
  gallbladder.

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• Cholecystectomy is the most commonly recommended
  modality. The gallbladder along with its
  contained stones is removed under general
  anesthesia.
• Open vs laproscopic.
• Laparoscopic procedure has been associated with
  an increased risk of common bile duct injury.
• Laparoscopic procedure may require conversion to
  an open procedure due to a variety of technical
  or patient issues.

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• Interestingly, several other symptoms appeared to
  be improved after cholecystectomy including
  abdominal bloating, dyspepsia, heartburn, fat
  intolerance, nausea and vomiting.
• However, these observations should not be
  interpreted as suggesting that gallstones are a
  possible cause of all these complaints.
• Relief of symptoms may have been due to the
  natural history of some of these disorders, a
  placebo response, or other nonspecific effect of
  the procedure.

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Gallstones but without symptoms

• These patients are unlikely to develop symptoms
  and when they do occur they are generally mild.
• Thus, patients should be educated about symptoms
  potentially related to gallstones (principally
  biliary colic) without recommending specific
  therapy to address the gallstones.

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Typical biliary symptoms and gallstones

• Such patients should generally undergo treatment
  (generally cholecystectomy) since they are likely
  to develop recurrent symptoms, which can be
  severe.

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Atypical symptoms and gallstones

• Such patients should undergo a search for
  non-gallstone-related causes of symptoms.
• If investigation is unrevealing, treatment of
  gallstones can be considered with the
  understanding that the rate of persistent
  symptoms is high.

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Typical biliary symptoms but without gallstones 

• Clinical suspicion for gallstone disease should
  be maintained in such patients.
• A repeat extracorporeal ultrasound should be
  obtained.
• If results are unrevealing, Endoscopic US and
  collection of duodenal bile for microscopy should
  be considered.
• If results continue to be unrevealing, a search
  for other causes of the pain is reasonable.

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Nonsurgical treatment of gallstone disease

• Symptomatic gallstones are uncommonly treated
  with medical therapy alone.
• Ursodiol may have a role to enhance gallstone
  dissolution and perhaps reduce symptoms in
  patients with mild symptoms or those who are not
  candidates for laparoscopic surgery (grade 2 B).
• ESWL and contact lithotripsy will likely be
  limited to specialized centers with experience in
  these techniques and in the majority of cases as
  an adjunct to endoscopic or other invasive
  treatments.
• In patients with stones too large for dissolution
  therapy, lithotripsy (plus bile salts) provided
  that patients have fewer than three noncalcified
  stones (Grade 2B).

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• Acute cholecystitis

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• Syndrome of right upper quadrant pain, fever, and
  leukocytosis associated with gallbladder
  inflammation.
• Usually related to gallstone disease.
• Pain may radiate to the right shoulder or back.
  Characteristically, acute cholecystitis pain is
  steady and severe. Associated complaints may
  include nausea, vomiting, and anorexia.
• Should be suspected when a patient presenting
  with the clinical manifestations outlined above
  is found to have gallstones on an imaging study.
• Left untreated, symptoms of cholecystitis may
  abate within 7 to 10 days. However, complications
  can occur at high rates.
• Most common complication is the development of GB
  gangrene (up to 20 of cases) with subsequent
  perforation (2 of cases).

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Radionuclide imaging/ Scintigraphy

• IV administered Technetium-99m hepatic
  iminodiacetic acid (Tc-99m HIDA) is secreted from
  liver in to hepatic bile ducts, but unable to
  enter GB if cystic duct is obstructed.
• If GB is not seen in 60 min do delayed imaging
  at 4 hrs or administration of morphine.
• Morphine increases pressure at sphincter of oddi
  and forces bile in to GB if cystic duct is
  patent.
• Complications of acalculous cholecystitis
  (gangrene and perforation) can be identified by
  spill of radionuclide into peritoneal cavity.

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• Ultrasound of the right upper quadrant in a
  patient with acute cholecystitis reveals marked
  thickening of the gallbladder wall (arrow) with
  fluid surrounding the distended gallbladder
  (arrowhead).

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Treatment of acute cholecystitis

• Admit
• Analgesia (opioids)
• Antibiotics (unasyn/ zosyn/ rocephin flagyl)
  (grade 2C)

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Treatment of acute cholecystitis
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• Acute cholangitis

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• Clinical syndrome characterized by fever,
  jaundice, and abdominal pain that develops as a
  result of stasis and infection in the biliary
  tract.
• The classic triad of Charcot fever, right upper
  quadrant pain, and jaundice occurs in only 50
  to 75 of patients .
• Confusion and hypotension can occur in patients
  with suppurative cholangitis, producing Reynold's
  pentad, which is associated with significant
  morbidity and mortality.

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Differential diagnosis

• Biliary leaks
• Liver abscess
• Infected choledochal cysts
• Cholecystitis
• Mirizzi syndrome (chronic cholecystitis and large
  gall stones resulting in compression of common
  hepatic duct)
• Right lower lobe pneumonia/empyema

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Treatment

• Antibiotics (unasyn/ zosyn/ meropenem/ rocephin
  flagyl)
• Establishment of biliary drainage (ERCP/ open
  surgical decompression)
• IV fluids
• Correction of coagulopathy
• Monitoring

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• 80 of patients with acute cholangitis will
  respond to conservative management and antibiotic
  therapy.
• Biliary drainage can be performed on an elective
  basis.
• In 15- 20 of cases, cholangitis fails to settle
  over the first 24 hours with conservative therapy
  alone, requiring urgent biliary decompression.
• Indications for urgent biliary decompression
  include
• Persistent abdominal pain
• Hypotension despite adequate resuscitation
• Fever greater than 39ºC (102ºF)
• Mental confusion, which is a predictor of poor
  outcome

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Diagnosis and treatment of acute cholangitis with
ERCP. Left Multiple small stones in the lower
common bile duct (arrow). Ultrasonography had
shown borderline dilatation of the common bile
duct but no stones. Right After sphincterotomy
and stone extraction, the common bile duct is
free of stones.
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Following cannulation of the distal common bile
duct during an ERCP examination (black arrow
indicates cannula), contrast material was
injected, outlining a large stone producing
complete obstruction of the distal duct (white
arrow).
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Acalculous cholecystitis / Biliary dyskinesia

• FgtM
• Associated with systemic infection / surgery /
  trauma.
• Risk factors prolonged fasting, PN, sepsis.
• Abdominal pain RUQ, worse after eating.
• Examination and routine workup is generally
  normal.
• USG shows GB wall thickness gt 3.5 mm.
• Hepatobiliary scintigraphy scan is usually
  diagnostic (ejection fraction lt35).
• Cholecystectomy is usually helpful.

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Sphincter of oddi dysfunction

• There is effectively an obstruction at the level
  of sphincter that may be caused by fibrosis /
  inflammation / elevated sphincter tone.
• Symptoms usually similar to GB dyskinesia.
• ERCP with Manometry is usually diagnostic.
• Sphincterotomy is the treatment of choice.
• Cholecystectomy does not provide relief.

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Benign masses of gall bladder

• Usually polyps primary or secondary
• Primary polyps include
• -Cholesterol polyps
• -Inflammatory polyps
• -hyperplastic adenomyoma
• -Adenoma
• -Heterotopic gastric and pancreatic tissue
• Can present with sign and symptoms of biliary
  colic
• USG usually diagnostic

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• Malignant tumors of GB usually follows
  acute/chronic cholecystitis, rare in children.
• Congenital abnormalities of GB rare, often found
  incidently during imaging/surgery.
• Absent GB can be associated with extra hepatic
  biliary atresia, GB may appear absent in cystic
  fibrosis(recurrent attacks of cholecystitis can
  lead to fibrosis/atrophy of GB).
• Double GB rare, usually asymptomatic.

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Disease process USG Radio nuclide imaging CT MRI / MRCP ERCP Misc.
GB stone
Acute cholecystitis
Acute acalculous cholecystitis
Chronic acalculous cholecystitis
Sphincter of oddi spasm
Biliary leak post cholecystectomy
Bile duct obstruction cholangiogram
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