Gallstones are formed by the abnormal aggregation of bile components, and can develop in any part of the biliary tree. Cholelithiasis is the presence of stones in the gallbladder or bile ducts, and is very common; up to 20% of those over 60 years of age have gallstones.
Bile, produced in the liver, drains into the common hepatic duct via the left and right hepatic ducts. The common hepatic duct then joins with the cystic duct, leading from the gallbladder, to form the common bile duct. This is then joined by the pancreatic duct to form the ampulla of Vater (not shown on the diagram), which drains into the duodenum through the sphincter of Oddi (also not shown).
When the sphincter is open the bile drains directly into the duodenum. When the sphincter is closed, between meals, the bile backs up along the biliary tree and is stored in the gallbladder.
(*Please see below for the picture reference.)
Gallstones can be formed from cholesterol, bile pigments, calcium carbonate (very rare) or, in 80% of cases, a mixture of these.
Cholesterol gallstones: are formed when there a higher proportion of cholesterol relative to bile salts causing the cholesterol to precipitate out and form crystals. Pigmented stones: are most common in the Far East due to the high prevalence of malaria and other parasitic diseases. Parasitic diseases cause haemolysis and consequently an increased production of bilirubin. Calcium carbonate stones: form due to increased calcium excretion in the bile.
Many different factors have been identified in the pathogenesis of gallstones. A typical patient is said to exhibit the ‘five F’s’:
However, the majority of patients will not fit this sterotype! Other factors involved are smoking, diabetes, pregnancy, oral contraceptives, or other gastrointestinal disease and previous surgery.
Most patients with gallstones will remain asymptomatic. However, 10% will experience one of the complications of gallstone disease, depending on the location.
Biliary colic occurs when a stone lodges in the neck of the gallbladder. This is not a true colic; the pain is constant when it occurs, but the condition occurs intermittently. The pain has the following characteristics:
Treatment involves symptomatic relief until the attack has subsided, followed by an elective cholecystectomy (removal of the gallbladder).
ΔΔ: pancreatitis, duodenal ulcer, other abdominal colics e.g. renal colic. May overlap with other gallstone diseases.
Acute cholecystitis is inflammation of the gallbladder secondary to a bacterial infection of the gallbladder wall. This almost always occurs due to gallstone disease. Pain associated with this exhibits the same characteristics as biliary colic, but does not subside. Additional signs are:
Pain relief and antibiotics (e.g. cefuroxime) are given initially, and cholecystectomy is ideally performed within 72 hours. This is usually performed laparoscopically unless there is a possibility perforation has occurred. If early surgery is not an option the patient may be treated conservatively until the attack resolves, followed by an elective cholecystectomy.
ΔΔ: pancreatitis, perforation of duodenal ulcer, hepatitis, acute appendicitis.
Chronic inflammation in the absence of infection can lead to a less specific clinical picture of vague abdominal pain, distension, nausea and fat intolerance.
ΔΔ: peptic ulcers, irritable bowel syndrome, pancreatitis, gastrointestinal tumour.
If the stone completely obstructs the gallbladder neck the lumen may fill with pus. In most cases this requires emergency cholecystectomy, but in those unable to withstand this procedure an emergency cholecystostomy can be performed (see below). This involves removal of the stones and drainage of the pus. Cholecystectomy can be performed when the patient’s condition has stabilised.
If a stone passes out of the gallbladder and lodges in the common bile duct, then obstructive jaundice may occur. This may be accompanied by cholangitis or biliary colic.
Obstruction of the common bile duct results in an overflow of conjugated bilirubin into the blood, resulting in conjugated hyperbilirubinaemia. The excess bilirubin is excreted in the urine giving the classical dark colour. Due to the blockage less bilirubin is excreted in the faeces, hence the abnormal pale colour. Pruritis may result from deposition of bilirubin in the dermis. LFT’s typically show normal liver transaminase levels but with elevated serum alkaline phosphatase.
Courvoisier’s law: ‘If in the presence of jaundice the gallbladder is palpable, then the jaundice is unlikely to be due to a stone’ (Ludwig Courvoisier, 1843-1918, Professor of Surgery, Basle, Switzerland). This is based on the principle that if the obstructive jaundice is caused by a gallstone, the gallbladder will be thickened and fibrosed, and therefore cannot distend under increased retrograde pressure. However, there are some rare exceptions to the rule, for example a gallstone forming in situ in the common bile duct, so the gallbladder has no pathology and therefore can distend.
Gallstones in the common bile duct are not usually seen on ultrasound, but can be suspected if dilatation of the biliary tree is present. Endoscopic retrograde cholangiopancreatography (ERCP) confirms the diagnosis and allows removal of the stones. Sphincterotomy of the sphincter of Oddi is also performed in this procedure. Cholecystectomy may be necessary at a later date.
ΔΔ: other causes of obstructive jaundice:
Gallstones can also lodge in opening of the pancreatic duct, resulting in pancreatitis. The following symptoms are associated with this condition:
ERCP and stone removal may be necessary.
ΔΔ: other causes of acute abdomen, myocardial infarction.
Infection of the bile duct causes RUQ pain, jaundice and signs of infection, which can be mistaken for cholecystitis. Infection occurs due to bile stasis secondary to obstruction of the bile duct with a stone. The increased pressure caused by the stone allows the bacteria to escape into the systemic circulation to cause sepsis.
Empirical antibiotics are given until blood culture results are obtained. Biliary drainage can be performed by ERCP.
In chronic cholecystitis the inflammation can weaken the gallbladder wall and stones can ulcerate through to the adjacent intestine, creating a fistula. If the stones are large enough they can cause mechanical obstruction of the intestine; most commonly the stones lodge in the ileocaecal valve.
Typical signs and symptoms of small bowel obstruction occur: pain, distension, constipation preceded by vomiting. Abdominal x-ray will show air in the biliary tree (pneumatobilia) and/or gallstone in the intestine.
Gallstone ileus requires emergency removal of the stone by laparotomy. Cholecystectomy may be performed electively following this procedure.
ΔΔ: other causes of small bowel obstruction – impacted faeces, strictures of the intestinal wall (e.g. in Crohn’s disease), extrinsic lesions (e.g. postoperative adhesions), paralytic ileus.
Ultrasound: most stones can be visualised on US, and dilatation of the biliary tree above the site of obstruction can be seen. It is quick and non-invasive, but does not allow accurate assessment of gallbladder function.
Plain abdominal x-ray: most stones are not radio-opaque, but this is a useful screening test.
ERCP: In this procedure an endoscope is passed down the oesophagus, through the stomach and into the duodenum until the sphincter of Oddi is visualised. Radiocontrast is then injected into the ampulla of Vater, and x-rays are taken to assess blockages or stones (fluoroscopy). If neccessary, instruments such as wires, baskets or balloons can be inserted into the common bile duct or the pancreatic duct to remove stones or place stents.
This is the most accurate method of assessing gallstone disease, and allows concurrent therapeutic intervention if stones are seen. However, there is a risk of developing pancreatitis or cholangitis.
MRCP: (magnetic resonance cholangiopancreatography) is non-invasive and produces better images than ERCP. However no interventions can be performed at the same time, and ERCP may be still be required. As such, local policy and clinical judgement often determine which imaging modality the patient receives.
Removal of the gallbladder is usually performed laparoscopically, with a camera port at the umbilicus and a minimum of two more ports containing instruments placed inferior to the ribs, e.g. epigastric and anterior axillary line. The gallbladder is dissected away from the surrounding tissues, and the cystic duct and cystic artery are clipped and cut. The gallbladder is then removed through one of the ports in a small bag.
The traditional open procedure was more invasive and resulted in a longer post-operative recovery period. As such, it is rarely performed, unless laparoscopic surgery is contraindicated, or complications arise during the operation. The open procedure involved an incision in the right upper quadrant, and you may come across patients with a scar in this location (shown below).
In this procedure a stoma is created to allow drainage of bile and pus. The gallbladder is punctured e.g. by trocar needle, and a catheter is inserted. Radiocontrast is injected through the catheter and the location is confirmed by x-ray. Any stones are removed, samples of bile and pus are sent for analysis e.g. MC&S, and the catheter is sutured in place and allowed to freely drain.
This procedure is sometimes used when the patient is too ill to undergo a cholecystectomy, or when local factors complicate matters e.g. empyema. However, it isn't a very common procedure.
*Picture of biliary system adapted from procto-med.com, accessed via creativecommons.org. All other images created by the author.
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