Gallbladder Disease in Children
Allison Rice
Gallbladder disease in children has evolved over the past 25 years.
Historically, disease of the biliary tract was relatively uncommon in pediatrics and typically associated with hemolytic diseases.1
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.
Cholelithiasis and biliary dyskinesia are increasing in frequency as well as a rise in cholecystectomy rates.1,2
Definitions:
Cholecystitis: inflammation and distention of the gallbladder caused by obstruction of the cystic duct6
Acute cholangitis: ascending bacterial infection of the biliary tree caused by an obstruction5
Acute acalculous cholecystitis (AAC): inflammation of the gallbladder, without the presence of gallstones6
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
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
RELEVANT ANATOMY
The gallbladder is situated between the 9th and 10th costal cartilages along the anterior abdominal wall.
Normal gallbladder wall thickness is <3 mm.8
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
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).
Bile excretion is increased by cholecystokinin (CCK), secretin, and vagal input. Excretion is decreased by somatostatin and sympathetic stimulation.5
 Figure 19.1 Blood supply of the gallbladder. (Reprinted with permission from Moore KL, Agur AMR, Dalley AF. Essential Clinical Anatomy. Philadelphia, PA: Wolters Kluwer Health; 2015.) |
EPIDEMIOLOGY AND ETIOLOGY
Incidence
Gallstones are more common in Caucasian children compared with those of African American descent.
Etiology
Congenital malformations of the biliary system.
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
Risk factors for cholesterol stones include obesity and oral contraceptive pills.
Critically ill children and those requiring long-term total parenteral nutrition are predisposed to developing acalculous cholecystitis.7
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.
Younger children often have more vague, atypical symptoms.7
Pain after fatty meals suggests cholelithiasis; however, >75% of patients with cholelithiasis are asymptomatic.1
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
Leukocytosis, fever, and a positive Murphy sign suggest infection.7
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