Cholelithiasis

Cholestasis

1. Cholelithiasis
In
Children

2. Pathogenesis
For gallstones of any type to develop, some or all of
the following need to occur
Alterations in the proportion of bile constituents
Nucleation
Changes in gallbladder motility
Infection (Infection appears to be important only for
brown pigment gallstone formation).

3. Classification
Cholesterol stones
Pigment stones
Black pigment stones
Brown pigment stones
In children, >70% of gallstones are the pigment
type, 15-20% are cholesterol stones, and the
remainder are composed of a mixture of
cholesterol, organic matrix, and calcium bilirubinate

4. Cholesterol Stones
More than 50% of cholesterol by weight
with variable amounts of proteins and calcium salts
This mainly occurs due to super saturation of bile salts
with cholesterol
Commonly seen in
Obesity
Ileal resection
Jejunoilael bypass
Ileal Crohn’s disease

6. Pigment Stones

7. Black Pigment Stones
50% are radiopaque, due to high content of calcium carbonate
and phosphate
Cholesterol concentration 10%-30%
Shiny, hard & spiculated
Commonly seen in
Chronic hemolytic anaemias like sickle cell anaemia, hereditary
spherocytosis etc
Cirrhosis & Chronic cholestasis
Total parenteral nutrition
Ceftriaxone therapy
Infants born to morphine abusers

9. Brown Pigment Stones
Soft, soap-like or greasy in consistency
Seen in biliary infestations like biliary ascariasis
More commonly found in the extrahepatic ducts
and even in the intrahepatic ducts

11. 0-12MONTHS 1-5YEARS 6-18YEARS
Prematurity Hepatobiliary disease Cystic fibrosis
TPN Abdominal surgery Hemolytic disease
Abdominal surgery Artificial heart valve Obesity
Sepsis Drugs – Cefrtiaxone Abdominal surgery
Bronchopulmonary
dysplasia
Malabsorption Oral contraceptives
Hemolytic disease Cystic fibrosis Hepatobiliary disease
Malabsorption
Hemolytic disease
TPN
Necrotising enterocolitis TPN Malabsorption/IBD
Hepatobiliary disease Pregnancy

12. Clinical Presentation
Typical biliary symptoms (40%-50%): right upper
quadrant or epigastric pain with or without nausea,
vomiting and fat intolerance.
Non-specific abdominal pain (20%-30%).
Acute abdomen (5%-10%): due to acute
cholecystitis, pancreatitis or cholangitis.
Asymptomatic (20%).

13. General Features
Pruritis
Xanthomas
Sinus bradycardia
Hepatosplenomegaly
Pale stools
Steatorrhoea

14. Diagnosis
Laboratory test results commonly are normal. The white blood cell
count may be normal. In a small fraction of patients, there is
transient mild elevation of serum bilirubin, aminotransferase, and
alkaline phosphatase levels.
Diagnosis is made using USG abdomen
A stone, as small as 1.5 mm, can be detected by ultrasonography.
The sensitivity and specificity of ultrasonography exceeds 95% for
gallbladder cholelithiasis, but only 50%-75% for choledocholithiasis
Axial CT may also be helpful in demonstrating stones

16. Management
Gallstones
Gall
bladder
Asymptomatic
Normal GB
wall
Observation
Symptomatic CBD
Asymp
tomatic
Surgery (LAP or Open
cholecystectomy)
Hemolytic
disease
Septate GB
Thickened &
Contracted GB
Stones > 2 cm
Porcelain GB
Surgery/
Endoscopic
intervention

17. Medical Management
Nonsurgical therapy consists of
Administration of bile salts or
Extracorporeal shock wave lithotripsy.
Ursodeoxycholic acid and chenodeoxycholic acid are
two bile salts that have been used. Both of these bile
salts decrease cholesterol secretion into bile so that bile
becomes desaturated of cholesterol.
Extracorporeal shock wave lithotripsy has been used in
association with administration of bile acids to
disintegrate stones.

18. Prevention
Gallstones can be prevented by
Initiating children on TPN with early limited enteral
feeds.
Pancreatic supplements in cystic fibrosis.
Weight control in obese children.
Using choleretics in chronic cholestasis.