Explanation about gallbladder disease in children

2. • Provide a brief review of Bile and
Gallbladder Physiology and gallstone
formation
• Screen procedures to identify Fatty Liver
and gallbladder disorders
• Identify Children at risk for developing
Fatty Liver and Gallbladder disorders

5. The liver's cells (hepatocytes) excrete bile
into canaliculi, which are intercellular
spaces between the liver cells. These
drain into the right and left hepatic ducts,
after which bile travels via the common
hepatic and cystic ducts to the
gallbladder.
The gallbladder, which has a capacity
of 50 milliliters (about 5 tablespoons),
concentrates the bile 10 fold by
removing water and stores it until a
person eats. At this time, bile is
discharged from the gallbladder via
the cystic duct into the common bile
duct and then into the duodenum (the
first part of the small intestine), where
it begins to dissolve the fat in ingested
food.

6. Synthesis of bile acids is a major route
of cholesterol metabolism in most
species other than humans.
The Liver produces about 800 mg of
cholesterol per day and about half of
that is used for bile acid synthesis.
20-30 grams of bile acids are secreted.
90% of excreted bile acids are
reabsorbed by in the ileum.
Bile is also used to break down fat
globules into tiny droplets.

7. 56 cases collected ( plus 6 HEN)
57% Male /43% Female (4 HEN Boys and 2
Girls) Average age 13.76
46.6% fatty liver positive
5.8 % of total ultrasound positive for GB
disease, and represents1.48% of total
patients in the study
34% of all GB disease BMI% 99 or
over 98% of the cases BMI% ≥85

8. GallBladder disease in
children
•Cholecystitis
•Cholelithiasis
•Sludge
•Polyps
•Septation
•Dilated or Contracted
• Non Specific
Thickened Wall
•Phrygian Cap
Related To:
Fatty Liver
Focal Fat Sparing
Hyper echoic Nodes
Hepatomegaly
Spleen Enlargement
Ascites
Pleural Fluid
Pancreatitis
Cirrhosis?

9.  History of cardiac or abdominal surgery Prolonged parenteral
nutrition Hemolytic disease
 Hepatobiliary obstructive disease
 Obesity
 Rapid decreases in weight Systemic Infection
Acute renal failure Prolonged fasting
Low calorie diet Certain medications Organ
transplant

10. •Persistently Abnormal liver
enzymes
•Acute or persistent epigastric or
non- specific abdominal pain,
postprandial
•Rapid decline in BMI
•Family history of Gall bladder
disease
•persistently elevated GGT or
Total Bilirrubin

11. 201
2

12.  Cholecystitis calculous and
Acalculous.
 In the pediatric population most
gallbladders that are removed for
acute cholecystitis show evidence of
chronic inflammation.
 Mechanism of Chronic Inflammation :
 Cholesterol crystals and/or calcium
bilirubinate→ stone →inflammation→
chronic obstruction→ decreased
contractile → biliary stasis→
Inflammation of the gallbladder wall

13. • Acalculus Cholecystitis:
Similar manner but from different etiologic
mos
t often associated with systemic illness or
infection→ Increased mucous production,
dehydration, and increased pigment →
increase cholesterol saturation and biliary
stasis→
hypofunction→ biliary sludge → obstruction
→
inflammation, edema → compromised blood
flow and bacterial infection

14. Abstract
Cholesterol, the major component of Summary gallstones, is held in solution in
the bile by formation of micelles in which phospholipids and bile-salts are
involved. The ratio of cholesterol to bile-salts plus phospholipids determines
cholesterol solubility. Although the bile produced by the liver in patients with
gallstones is abnormal, some features of gallbladder function might favor stone
formation. Of the hepatic factors contributing to gallstone formation a high
cholesterol content of bile, a low bile-salt pool, and interruption of the
enterohepatic circulation seem to be important. One hypothesis for gallstone
formation relates to events at the plasma membrane of the bile canaliculus, but
whether the critical factor here is an increase in the amount of cholesterol
passing through the membrane or an abnormal cholesterol to phospholipid ratio
remains controversial. It seems likely that an understanding of the mechanism
for gallstone formation will come from an investigation of the problem at the
cellular, subcellular, or molecular level. This review ends with a note on the
prospects for treatment, which should be directed at affecting the cholesterol to
phospholipid plus bile-salt ratio or at the cholesterol precipitate directly by using
detergent agents.
IanA.D Bouchier * Based on the Goulstonian Lecture delivered before the Royal
College of Physicians, in London, on April 7, 1971.

15. The two types of gallstones are cholesterol
stones and pigment stones. Cholesterol stones
are usually yellow-green and are made primarily
of hardened cholesterol. They account for about
80 percent of gallstones. Pigment stones are
small, dark stones made of bilirubin. Gallstones
can be as small as a grain of sand or as large
as a golf ball. The gallbladder can develop just
one large stone, hundreds of tiny stones, or a
combination of the two

16. women—especially pregnant, use of hormone
replacement therapy, or birth control pills (decrease
gallbladder movement) people over age 60 (As people age,
the body tends to secrete more cholesterol into bile)
American Indians (Pima Indians of Arizona, 70% of women
have
gallstones by age 30)
Mexican Americans
overweight or
obese (
Bile salts Cholesterol GB
emptying
people who fast or lose a lot of weight quickly
people with a family history of gallstones (possible
genetic link) people with diabetes (high levels of fatty acids
called triglycerides) people who take cholesterol-lowering
drugs
The Classic 4 F’s still apply: Female, Fertile, Forty, Fat

17. • Typical symptoms of RUQ pain, nausea,
vomiting.
• Tenderness to palpation or mass at RUQ
• Leukocytosis and jaundice
• The pain and tenderness are less localized in
younger children
• Epigastric pain mimic RUQ pain
• Epigastric pain or discomfort postprandial
• Atypical presentation: Sleep apnea
and sleep disturbance

18. 29/11/2017
Pediatric gallstones (Cholelithiasis)
47
*
Prof.Dr. Saad S Al Ani
Thelocation of the stone
Gallbladder wall thickening
Thepresenceof gallbladder sludge
Pericholecystic fluid

19. Pediatric gallstones (Cholelithiasis)
Prof.Dr. Saad S Al Ani
Ultrasounography of RUQ findings:
• Thick GBwall
• Stonesin GB
• Absence of echoes posterior to the calculi
"Shadowing"

22. Definition
Acute acalculous cholecystitis (AAC)is an inflammation of
the gallbladder, which is not associated with the presence of
gallstones
Prevalence
Account for > 50% of pediatric cholecystitis cases.
Symptoms :
• Abdominal pain (mild to severe), more pronounced at
right upper quadrant
• Fever.

23. Etiology :
Most AAC presented with an underlying clinical condition :
• Cardiac surgery
• Asystemic medical illness
• Leukemia
• End stage liver disease,
• Hemolytic uremic syndrome,
• Cystic fibrosis
Risk Factor
• Prolonged fasting,
• Total parenteral nutrition,
• Intravenous opiate narcotics,
• Volume depletion (shock),
• Multiple transfusion
• Sepsis. Tsakayannis et al.8

24. Infectious Causes of AAC
Bacterial
• Salmonella typhi,
• Streptococcus pyogenes,
• Acinetobacter baumannii,
• Streptococcus pneumoniae,
• Staphylococcus epidermidis,
• Burkholderia cepacia, and
• Stenotrophomonas maltophilia
Viral
• Hepatitis A
• Epstein-Barr Tsakayannis et al.

25. Abdominal Ultrasonography :
• Increased gallbladder wallthickness
(>4–5 mm)
• Pericholecystic fluid
• Presence of mucosal membrane sludge
The presence of at least two of these US criteria,
inaddition to the absence of gallstones, defines the
diagnosis of AAC in pediatric.

26. (A) Transverse image : Diffuse gallbladder wall thickening and
pericholecystic fluid.
(B) Longitudinal image : Diffuse wall thickening, anechoic lumen, and
no evidence of cholelithiasis.
The patient had a positive sonographic Murphy's sign.(Courtesy: Kristin
Fickenscher, Kansas City,MO.

27. •Biliary Sludge is a mixture of particulate
matter and mucous from the bile
•The composition of particulate matter varies
1. Cholesterol Crystals and calcium
2. Drugs particles since the bile is one of
the major routes of excretion of drugs
3 Sludge has been associated with
conditions:
1. Pregnancy
2. Rapid weight loss
3. Medications ( ceftriaxone, Octreotide)
4. Bone marrow and solid organ

28. Cholesterosis might contribute to
the formation of the GB polyps
Cholesterosis accumulated in the mucosal
service of the GB

29. Complete Sludge with stone
formation

31. Resembling growth in the gall bladder wall
True polyps are abnormal accumulation of mucous
membrane tissues that would normally be shed by the
body
Main types of polyps
Cholesterol
Polyp/Cholesterosis
Cholesterosis with fibrous
dysplasia Adenomyomatosis
Hyperplastic
cholecystosis
Adenocarcinoma
It affects 5% of adult, the causes uncertain, but there is a
correlation between increase age, and presence of Gall
stone.
The polyps are detected by abdominal ultrasound

32. Figure 1. Focal hepatic steatosis.
Prasad S R et al. Radiographics 2005;25:321-331
©2005 by Radiological Society of North America

33. Hamer O W et al. Radiographics 2006;26:1637-1653
©2006 by Radiological Society of North America

34. Figure 7. Focal fat accumulation in the liver at US. Transverse image shows, adjacent to the
left portal vein, a geographically shaped area of high echogenicity that represents
accumulation of fat (f) in the falciform ligament, with posterior acousticattenuation.
Hamer O W et al. Radiographics 2006;26:1637-1653
©2006 by Radiological Society of North America

35. •Septate gallbladder is a very rare anomaly
that has an asymptomatic course and is
detected as an incidental finding without
clinical relevance. Rarely,
however, septate gallbladder causes
recurrent attacks abdominal pain or
becomes complicated by cholelithiasis.
•The pinpoint communication between
the cavities causes stagnation,
inflammation or stone formation.
•Symptoms are usually caused by
pressure in the small chambers of the
gallbladder along with delayed emptying
which may sometimes favor early
Cholecystectomy
• Ultrasonography is the modality of choice.

36. • Hepatocytes take up the
radiopharmaceutical in minutes
after injection
• Hepatic ducts seen in fifteen
minutes
• Gallbladder seen within 45 to 60
miutes
• GBEF >40

38. This test examines the gallbladder and the ducts which connect to
the liver.

41. •Although gallbladder disease is relatively
uncommon in the pediatric population, the
rate has increased in the past 10 years.
•Pediatric gallbladder disease was commonly
associated with hemolytic diseases or
hemoglobinopathies; however, now other
factors are recognized.

42. •Incidence of Gallbladder disease is on the
rise on overweight children.
•Gallbladder disease should be in the differential
diagnosis of any pediatric patient who presents
with localized pain in the epigastric, RUQ or ill-
defined, Jaundice or dyspepsia and
asymptomatic patients with BMI of ≥85
•Consider Liver ultrasound as primary tool
over more expensive and invasive
procedures
•HB Scan helps identify adequate GB