Gallbladder Disease in Children
Allison Rice
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Gallbladder disease in children has evolved over the past 25 years.
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Historically, disease of the biliary tract was relatively uncommon in pediatrics and typically associated with hemolytic diseases.1
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The increase in incidence is due to multifactorial causes that parallel the rise in pediatric obesity, improved diagnostic modalities, and improved survival of critically ill patients.
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Definitions:
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Cholecystitis: inflammation and distention of the gallbladder caused by obstruction of the cystic duct6
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Acute cholangitis: ascending bacterial infection of the biliary tree caused by an obstruction5
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Acute acalculous cholecystitis (AAC): inflammation of the gallbladder, without the presence of gallstones6
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Biliary colic: postprandial abdominal pain, typically in the right upper quadrant (RUQ) or epigastric region, caused by failure of gallbladder to fully contract typically from the presence of a stone, without signs of inflammation5
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Biliary dyskinesia: vague RUQ pain and a low ejection fraction on hepatobiliary iminodiacetic acid scan (<35%), in the absence of gallstones or gallbladder wall thickness4
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RELEVANT ANATOMY
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The gallbladder is situated between the 9th and 10th costal cartilages along the anterior abdominal wall.
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Normal gallbladder wall thickness is <3 mm.8
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Normal common bile duct diameter in neonates to 1-year olds is <1.6 mm. In childhood to early adolescence, it is <3 mm.8
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Arterial supply to common bile duct is from the right hepatic and gastroduodenal artery branches at the 9- and 3-o’clock position, respectively (Figure 19.1).
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Bile excretion is increased by cholecystokinin (CCK), secretin, and vagal input. Excretion is decreased by somatostatin and sympathetic stimulation.5
EPIDEMIOLOGY AND ETIOLOGY
Incidence
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Gallstones are more common in Caucasian children compared with those of African American descent.
Etiology
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Congenital malformations of the biliary system.
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Pigmented gallstones are frequently seen in those with hemolytic disorders, which form when bilirubin is conjugated with calcium as a result of hemolysis. Specific conditions include sickle cell anemia, thalassemias, red blood cell enzymopathies, Wilson disease, and Gilbert syndrome.4
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Risk factors for cholesterol stones include obesity and oral contraceptive pills.
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Critically ill children and those requiring long-term total parenteral nutrition are predisposed to developing acalculous cholecystitis.7
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Klebsiella, Escherichia coli, Enterobacter, Pseudomonas, and Citrobacter are the most common pathogens found in acute cholangitis.5
CLINICAL PRESENTATION
Classic presentation: A child presents with RUQ pain, nausea, and vomiting.
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Younger children often have more vague, atypical symptoms.7
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Pain after fatty meals suggests cholelithiasis; however, >75% of patients with cholelithiasis are asymptomatic.1
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Signs of acute cholecystitis include RUQ abdominal tenderness, frequently with nausea and vomiting. Inspiratory arrest on palpation over the gallbladder, known as Murphy sign, is a classic physical examination finding.1
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Leukocytosis, fever, and a positive Murphy sign suggest infection.7
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