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What are gallstones?
Gallstones form when liquid stored in the gallbladder hardens into pieces of stone-like material. The liquid, called bile, is used to help the body digest fats. Bile is made in the liver, then stored in the gallbladder until the body needs to digest fat. At that time, the gallbladder contracts and pushes the bile into a tube—called the common bile duct—that carries it to the small intestine, where it helps with digestion.Gallstone formation is the most common disorder of the biliary tree.
 The gallbladder and the ducts that carry bile and other digestive enzymes from the liver, gallbladder, and pancreas to the small intestine are called the biliary system.
In Western countries gallstones are common and occur mostly in females aged 18-65 years, with an overall prevalence of 11%. Gallstones are common in North America, Europe and Australia, and are less frequent in India, the Far East and Africa. In developed countries the incidence of symptomatic gallstones appears to be increasing and they occur at an earlier age.
There has been much debate over the role of diet in cholesterol gallstone disease; an increase in dietary cholesterol, fat, total calories and refined carbohydrate or lack of dietary fiber have all been implicated. At present the best data support an association between simple refined sugar in the diet and gallstones. Moderate intake of alcohol does not lead to formation of gall stones; this is the negative view in most of the countries. Gallstone formation is multifactorial, and the factors involved are related to the type of gallstone. Cholesterol is held in solution in bile by its association with bile acids and phospholipids in the form of micelles and vesicles. Biliary lipoproteins may also have a role in solubilising cholesterol.
In gallstone disease the liver produces bile which contains an excess of cholesterol either because there is a relative deficiency of bile salts or a relative excess of cholesterol. Such bile, which is supersaturated with cholesterol, is termed 'lithogenic'. Factors initiating crystallisation of cholesterol in lithogenic bile (nucleation factors) are also important; patients with cholesterol gallstones have gallbladder bile which forms cholesterol crystals more rapidly than equally saturated bile from patients who do not form gallstones. Factors favouring nucleation (mucus, calcium, fatty acids, and other proteins) and antinucleating factors (apolipoproteins) have been described. The term 'biliary sludge' describes bile which is in a gel form that contains numerous crystals or microspheroliths of calcium bilirubinate granules and cholesterol crystals as well as glycoproteins. It is an essential precursor to the formation of gallstones in the majority of patients. The majorities of gallstones are asymptomatic and remain so. Only about 10% of those with gallstones develop clinical evidence of gallstone disease.
Complications of Gallstones
Symptomatic gallstones manifest either as biliary pain or as a consequence of cholecystitis. If a gallstone becomes acutely impacted in the cystic duct, the patient will experience pain. The term 'biliary colic' is a misnomer because the pain does not rhythmically increase and decrease in intensity. Instead the pain is typically of sudden onset and is sustained for about 2 hours; its continuation for more than 6 hours suggests that a complication such as cholecystitis or pancreatitis has developed.
Pain is felt in the epigastrium about 5-6 cm above umbilicus (70% of patients) or right upper quadrant (20% of patients) and pain may be felt in the interscapular region or the tip of the right scapula, but other sites include the left upper quadrant, the epigastrium and the lower chest; the pain can be confused with intrathoracic disease, oesophagitis, myocardial infarction or dissecting aneurysm. Combinations of fatty food intolerance, dyspepsia and flatulence not attributable to other causes have been referred to as 'gallstone dyspepsia'. These symptoms are not now recognized as being caused by gallstones and are best regarded as non-ulcer dyspepsia. A plain abdominal X-ray will demonstrate calcified gallstones. Ultrasonography is the method of choice to diagnose gallstones but oral cholecystography and CT can also be used. Oral cholecystography shows whether or not the gallbladder is functioning, and this is useful if oral dissolution therapy is being considered. MRI is the best available diagnosing tool for gall stone complications.
Occlusion of the cystic duct for any prolonged period of time results in acute cholecystitis. Other complications include chronic cholecystitis, and a mucocoele of the gallbladder, in which there is slow distension of the gallbladder from continuous secretion of mucus. If this material becomes infected, an empyema develops. Gallstones in the gallbladder (cholecystolithiasis) migrate to the common bile duct (choledocholithiasis) in approximately 15% of patients and cause biliary colic, but they may be asymptomatic. Rarely, fistulae develop between the gallbladder and the duodenum, colon or stomach. Air will be seen in the biliary tree on plain abdominal radiographs. If a stone larger than 2.5 cm in diameter has migrated into the gut it may impact either at the terminal ileum or occasionally in the duodenum. Rarely, gallstones impacted in the cystic duct cause stricturing in the common hepatic duct (Mirizzi's syndrome), resulting in jaundice.
Cancer of the gallbladder is uncommon, although it is recognised more frequently in an ageing population and in a 'porcelain' gallbladder. In over 95% of patients with gallbladder cancer there are accompanying gallstones. Cancer is usually diagnosed as an incidental histological finding following cholecystectomy for gallstone disease.
Treatment of Gallstones
Asymptomatic gallstones found incidentally are not usually treated because the majority will never give symptoms. Symptomatic gallstones are best treated surgically, and minimal access techniques have largely replaced non-surgical treatment. Many surgeons recommend surgerical treatment because it is said to best.
Gallstones can be dissolved and fragmented in the gallbladder or removed mechanically from the common bile duct. Medical dissolution of gallstones can be achieved by oral administration of the bile acid ursodeoxycholic acid. Radiolucent gallstones, a gallbladder that opacifies on oral cholecystography, stones not larger than 15 mm in diameter, moderate obesityand no or at most mild symptoms are the features which suggest that drug therapy may be feasible. Success can be expected in approximately 75% of patients who are treated this way.
Occasionally, direct contact dissolution therapy is attempted via percutaneous catheters or catheters placed at ERCP. Bile salt therapy is necessary following lithotripsy to dissolve the gallstone fragments within the gallbladder. As in the case of oral bile salt therapy, only 30% of all patients with gallbladder disease are suitable for lithotripsy. All therapeutic methods which retain gall bladder have a chance of gall bladder formation every 5 years.
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