Gallbladder disease in the pediatric population causes pain and results in significant morbidity. The diagnosis is frequently delayed in this population because of its relative infrequency compared with disease in adults; this results in additional illness, pain, and missed school days for the child and missed work for the parent. More serious complications may develop, such as acute cholecystitis, choledocholithiasis, cholangitis, and pancreatitis.
Even though gallbladder disease is relatively uncommon in the pediatric population, pediatric patients account for a disproportionate number of cholecystectomies; this rate has been rising in recent years. Pediatric gallbladder disease is most commonly associated with hemolytic diseases or hemoglobinopathies; however, other risk factors are recognized.
Extended administration of total parenteral nutrition (TPN) or prior extensive bowel resection increases the risk of gallbladder disease, a cause that will likely continue to increase as survival rates improve in extremely low birth weight infants. Sadly, as childhood obesity reaches near epidemic proportions in the United States, gallbladder disease related to dietary factors is becoming more prominent. [1, 2]
Gallbladder and biliary tract disease should be in the differential diagnosis of any pediatric patient who presents with right-upper-quadrant pain, jaundice, or unremitting dyspepsia with normal endoscopic gastric findings. Asymptomatic gallstones and symptomatic pigment gallstones in children are common indications for surgery. Noncalcified gallstones due to long-term cholestasis or TPN may respond to medical therapy such as ursodeoxycholic acid.  As in adults, laparoscopic cholecystectomy is the most feasible option for most patients. 
Aside from gallstones, cholestasis, and biliary dyskinesia, the pediatric population can experience congenital abnormalities of the gallbladder, including gallbladder perforation, hydrops of the gallbladder, gallbladder atresia, and choledochal cysts.
The introduction of laparoscopy revolutionized the practice of surgery. Trocars have been described since 25 BCE, when these devices were used to drain "bad humors" from the abdomen. The first endoscopic examination was performed in 1901 by a German gynecologist. This technique was further developed in the early part of the 20th century but remained prohibitively dangerous as a consequence of uncontrolled increases in abdominal pressure and an inability to maintain internal temperature.
By 1970, laparoscopy was commonly used by gynecologists. In 1987, the French physician Mouret performed the first human laparoscopic cholecystectomy. While performing laparoscopy for a gynecologic procedure on a woman known to have biliary colic, he tilted his camera upwards and found that he was able to remove her gallbladder without making additional incisions. This forever changed the treatment of gallbladder disease. In 1992, a National Institutes of Health (NIH) consensus conference concluded that laparoscopy was the treatment of choice for cholecystectomy. 
With the development of the laparoscopic cholecystectomy, the annual number of cholecystectomies has increased from 500,000 to 700,000.  Few true contraindications to a laparoscopic technique are recognized; the leading contraindication is unclear anatomy. Open cholecystectomy remains a safe and viable alternative when laparoscopy is not feasible and is commonly performed in infants and children with more uncommon diseases of the biliary tree.
Surgical intervention has evolved to single-incision laparoscopic cholecystectomy (SILC) and needle port–assisted SILC. These approaches, in adults, have been shown to have equal efficacy, with longer operating times and improved cosmesis. 
Bile secretion begins in the bile canaliculus in the liver. From here, bile enters the terminal channels (the canals of Hering), which gradually enlarge as they approach the portal canal. Bile flows from the centrilobular cells in zone 3 toward the portal triads in zone 1. These ducts anastomose to form hilar intrahepatic ducts, which, in turn, become the main hepatic ducts.
The porta hepatis and the right and left hepatic ducts join to form the common hepatic duct (CHD). Generally, the right and left hepatic ducts join outside the liver; however, in 5% of the population, this occurs inside the liver or at the location where the cystic duct joins the right hepatic duct. In 70% of the population, the cystic duct directly enters the CHD. Other possibilities include a cystic duct that runs parallel to the CHDor a cystic duct that runs anterior or posterior to the bile duct before medially joining the bile duct.
The common bile duct (CBD) lies inside layers of the lesser omentum and is anterior to the portal vein and to the right of the hepatic artery. It passes retroperitoneally behind the first portion of the duodenum, behind the head of the pancreas, and enters into the second part of the duodenum. The CBD then passes through the duodenal wall to join the main pancreatic duct, thus forming the ampulla of Vater and resulting in the duodenal papilla on the duodenal side. The sphincter of Oddi surrounds the bile and pancreatic ducts while they are inside the duodenal wall.
Arterial supply of the bile ducts is mostly from the right hepatic artery. The blood supply of the CBD arises from branches of the hepatic and gastroduodenal arteries. Injury to these vessels may lead to stricture of the bile ducts.
Lymphatics from the lower portion of the CBD drain into glands near the head of the pancreas. Lymphatic drainage from the rest of the biliary tree empties into the hilum of the liver.
The gallbladder stores bile created by the liver. This system allows controlled release of bile into the duodenum as needed for lipid solubilization. The gallbladder sits below the right hemiliver. It is divided into a fundus that lies between the transverse colon and the rectus abdominis and ninth costal cartilage, a body that lies close to the duodenum, an infundibulum, and a neck. The Hartmann pouch is an outpouching of the infundibulum that lies close to the neck of the gallbladder. When gallstones are impacted in this area, they obstruct the cystic duct and produce cholecystitis or obstruction of the adjacent CHD, which may lead to Mirizzi syndrome.
The neck of the gallbladder is connected to the cystic duct, which then empties into the CBD. The spiral valve of Heister, formed by the mucous membrane of the neck, regulates the flow of bile.
Arterial supply to the gallbladder comes from the cystic artery, which is usually a branch of the right hepatic artery. Venous drainage is provided by the cystic vein, which usually empties into the portal vein or directly into the hepatic sinusoids. Lymph drainage empties into a lymph gland near the neck of the gallbladder. The celiac axis supplies sympathetic innervation of the gallbladder; visceral pain is conducted through this and is frequently referred to the right subcostal, epigastric, and scapular regions. Parasympathetic innervation arises from both branches of the vagus nerve.
Tubuloalveolar glands aid in the production of mucus in the neck of the gallbladder. Rokitansky-Aschoff sinuses are invaginations of the surface epithelium that may extend through the muscularis and may be a source of inflammation secondary to bacterial stasis and proliferation within the sinuses. The ducts of Luschka sit along the hepatic surface of the gallbladder and directly open into the intrahepatic bile ducts. These may be a source of bile leak after cholecystectomy.
Anatomic variations are common and are likely related to injury to the CBD. Care must be taken to properly identify the anatomy of each individual patient; when the anatomy is unclear, intraoperative cholangiography should be performed to avoid potential serious duct injury.
Acquired disorders of the gallbladder include the following:
Hydrops of the gallbladder
Acute and chronic cholecystitis
Hydrops or acute distention of the gallbladder with edema but without inflammation of the gallbladder wall may be a symptom of severe sepsis or shocklike states. Acute hydrops has been associated with Kawasaki disease and Henoch-Schönlein purpura.
Acalculous cholecystitis is uncommon in children but may arise after successful resuscitation from sepsis or shock when a previously unrecognized hydrops of the gallbladder becomes infected. This is confirmed by ultrasonographic findings that reveal a nonfunctioning, distended gallbladder without gallstones.
Cholestasis is defined as a failure of bile to move through the biliary system and may lead to liver disease. Symptoms and treatment depend on the primary disease process but generally include jaundice, pruritus, xanthomata, hepatomegaly, dark urine, hypopigmented stools, and, possibly, splenomegaly. In neonates, this disorder is also known as neonatal direct hyperbilirubinemia or neonatal hepatitis. Causes of cholestasis in pediatric patients include congenital anomalies, prolonged dependence on parenteral nutrition, cholangitis, hepatitis, pregnancy, and prolonged illness. 
In the pediatric population, cholelithiasis most commonly presents at puberty but can occur at any point in development. Underlying medical causes of gallstones are present in more than 50% of patients with calculous cholecystitis. In infants, the presence of gallstones is generally related to an extended period of fasting, required parenteral nutrition, or abdominal surgery. These gallstones are generally mixed cholesterol-calcium bilirubinate stones. Cholesterol stones (see the image below) have surpassed hemolytic stones as the principal type of gallstones in pediatric patients. The etiology and risk factors remain similar to those seen in adults; a high-fat diet is the primary predisposing factor.
Hemolytic processes that result in gallstones in pediatric patients include sickle cell anemia, hereditary spherocytosis, and thalassemia. Stones found in these diseases are black-pigment stones predominantly composed of calcium bilirubinate. Medications such as ceftriaxone, furosemide, octreotide, ceftriaxone, and cyclosporin have been linked to gallstone formation.
Cholecystitis refers to inflammation of the gallbladder. Acute cholecystitis occurs secondary to an obstructing stone in the cystic duct that results in bile stasis and bacterial overgrowth. Chronic cholecystitis occurs as a result of several attacks of acute cholecystitis and results in an ulcerated and scarred gallbladder epithelium.
Although gallstones are the most common cause of cholecystitis in adults and children, acalculous cholecystitis may occur following local inflammation or infection. Typhoid fever, scarlet fever, measles, and AIDS have been associated with acalculous cholecystitis, as have Mycoplasma, Streptococcus group A and B, Shigella, and Escherichia coli infections. Shock, sepsis, hyperalimentation, fasting, intravenous narcotics, and transfusions are risk factors in the development of acute acalculous cholecystitis following surgery.
Cholangitis is caused by an ascending infection of the biliary tract and usually occurs after a gallstone blocks the CBD. The most commonly involved organisms include E coli and Klebsiella, Pseudomonas, and Enterococcus species.
Choledocholithiasis occurs in 11% of children with cholelithiasis and almost 20% of pediatric patients with gallstone pancreatitis. This condition is caused by the passage of stones through the cystic duct with entrapment at the papilla of Vater.
Pediatric gallbladder disease stems from numerous causes. The following are some of the best-described causes  :
Partial or complete obstruction of the biliary ductal system
Metabolic-related and stress-related causes (eg, short bowel syndrome with reduced bile salt absorption)
However, numerous less defined causes have been recognized, including the association between previous abdominal or renal surgery and gallstones or the development of acalculous cholecystitis.
Congenital abnormalities of the gallbladder are rare. On the other hand, cholelithiasis has an incidence rate of 0.15-0.22% in the pediatric population. Although the incidence of pediatric cholelithiasis has tripled over the past decade, the number of children with cholelithiasis who have hemolytic disease has decreased over the past decade, reflecting either an increase in the incidence of cholesterol cholelithiasis and biliary dyskinesia or an increase in the recognition and willingness to treat these diseases in children.  The increased willingness to treat these diseases may be due to increasingly widespread use of laparoscopy in children.
Possible reasons for a rise in gallbladder disease incidence include improved availability of ultrasonography for assessment of abdominal pain, high teenage pregnancy rates, and increased prevalence of childhood obesity. Although gallbladder disease in pediatric populations historically was a sign of an underlying hemolytic disease, cholesterol stones in children with obesity are currently the most common cause of gallbladder disease. Female adolescents are 11-22 times more likely to have gallbladder disease than male adolescents are.
One study reported that in 224 pediatric patients who underwent cholecystectomy, the mean weight was 58 kg.  Surgery was performed secondary to symptomatic cholelithiasis in 166 patients, secondary to gallbladder dyskinesia in 35, secondary to pancreatitis in seven, in combination with splenectomy in six, secondary to cholecystitis in fives, secondary to choledocholithiasis in one, and secondary to acalculous cholecystitis or polyp in the remaining two. Gallstone formation is seen in 20% of patients with sickle cell disease prior to adolescence. 
When pediatric gallbladder disease is treated appropriately and in a timely fashion, the prognosis is excellent. Most patients recover from a cholecystectomy and return to regular activities within a week. If left untreated, cholecystitis can lead to significant illness. Some patients have diarrhea, gastritis, esophagitis, and colicky abdominal pain after cholecystectomy, particularly after the ingestion of foods high in sugar. This is termed postcholecystectomy syndrome and may occur in as many as 30% of patients.
The epidemic of childhood obesity and poor diet in the United States will likely result in higher rates of gallbladder disease. Any child who presents with symptoms of gallbladder disease should be evaluated and counseled regarding appropriate dietary management. 
Before consenting to surgical treatment of gallbladder disease, both the patient and the family should be educated regarding the risks of both laparoscopic and open cholecystectomy. Described risks should included the following:
Retained stone in the CBD
CBD injury 
Hepatic artery injury
Conversion from a laparoscopic procedure to an open one
Damage to adjacent structures
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