Gallstones are calculi formed in the gallbladder by the accretion of bile components. They may remain in the gallbladder or pass into other parts of the biliary tree (cystic duct, common bile duct or ampulla of Vater).
Stones have a core of organic material and bacteria. The bulk of the stone comprises of concentric layers, suggesting formation by repeated precipitation. There are three main types: cholesterol, pigment and mixed stones.
Mixed stones are the most common (80 per cent), containing 20 to 80 per cent cholesterol. They also contain other constituents, such as calcium carbonate, and so may be radiologically visible.
Pigment stones (14 per cent) are associated with excessive bilirubin production and so are commonly found with chronic haemolysis (for example, in sickle cell anaemia and hereditary spherocytosis).
1. Epidemiology and pathophysiology
Gallstones are predominantly a western condition. By the age of 60 years, 10 per cent of men and 20 per cent of women will have gallstones; however, only 10 per cent will develop symptoms five years from diagnosis.
Cholesterol gallstones develop when the bile contains excess cholesterol and inadequate bile salts. Two other factors are important: efficiency of gall bladder contraction, and presence of specific proteins in the bile and liver.
A sluggish, poorly contracting gall bladder predisposes to over-concentration of bile and cholesterol precipitation; while presence of specific proteins in the bile and liver can promote or inhibit cholesterol precipitation into gallstones.
In females, raised estrogen in pregnancy or from hormonal contraception may increase cholesterol levels in bile and decrease gall bladder motility, resulting in gallstones.
Important predisposing factors for gallstones are pregnancy, diabetes and obesity.
This has led to the medical student mantra that the typical gallstone patient is a 'fair, fat, fertile female of forty'.
Many patients, however, do not fit this handy description. Causation may be influenced by a combination of other factors, namely inherited body chemistry and diet. The relationship between diet and gallstone formation is poorly understood.
Low-fibre, high cholesterol diets and diets high in starchy food may contribute to stone formation.
Other nutritional factors that may increase gallstone risk include rapid weight loss (for example, post-bariatric surgery), eating fewer meals per day and constipation.
Pigment stones are commonly seen in the developing world; risk factors include haemolysis, cirrhosis and biliary tract infections.
3. Gallstone disease and symptomatology
Presence of stones in the gallbladder is known as cholelithiasis. Should the stones migrate into the biliary tree, the condition is referred to as choledocholithiasis. Asymptomatic, 'silent' stones do not usually require treatment. Symptoms often begin after many years, once stones reach a certain size (>8mm).
Cholelithiasis may lead to acute cholecystitis, characterised by retention of bile in the gallbladder, associated inflammation and commonly, secondary infection by intestinal micro-organisms.
Patients experience right upper quadrant pain which may radiate to the right shoulder. There may be associated nausea, vomiting and fever.
The gallbladder is usually impalpable and jaundice occurs in a minority. Murphy's sign (pain on inspiration during palpation at the costal margin of the right upper quadrant) may be present.
In choledocholithiasis, stones may obstruct the biliary tree, which can lead to acute ascending cholangitis or acute pancreatitis secondary to obstruction of the exocrine pancreas. Obstruction can cause secondary systemic bacterial sepsis and is a medical emergency.
Clinical features of cholangitis classically manifest as Charcot's triad (right upper quadrant pain, fluctuant jaundice and swinging pyrexia with rigors). Patients are unwell with a leukocytosis and raised bilirubin and alkaline phosphatase.
Biliary colic is a further symptom complex in gallstone disease, occurring when there is sudden, complete obstruction of the cystic duct by a stone. The patient experiences severe and steady right upper quadrant pain. Pain may also be felt in the epigastrium, left upper quadrant and occasionally praecordially.
It may last minutes to hours and often occurs post-prandially. Associated nausea is not uncommon and vomiting may signify the end of an attack.
Clinically, the patient is not usually febrile but may be tachycardic if pain is severe.
Symptoms should settle within 24 hours; prolonged symptoms may suggest acute cholecystitis.
Ultrasound is the most common diagnostic tool used and can identify the number and size of stones (so long as they are >1-2mm). It can also visualise the pancreas and quantify dilatation of the bile ducts proximal to the obstruction site.
Endoscopic retrograde cholangiopancreatography (ERCP) is preferred for identifying stones in the common bile duct. During ERCP, therapeutic procedures, such as stone removal or sphincterotomy of the ampulla of Vater, are possible.
Management depends on whether the condition is acute or chronic. With chronic cholecystitis, a patient with mild symptoms may be managed conservatively with lifestyle advice and adherence to a low-fat diet. Severe episodic pain responds to opiate analgesia with consideration of an early cholecystectomy.
Acute cholecystitis will respond in 90 per cent of cases to conservative measures, such as analgesia, adequate hydration and appropriate antibiotics. An elective cholecystectomy can then be performed during the same inpatient admission.
When surgery is indicated, laparoscopic cholecystectomy is the preferred procedure, usually requiring an overnight hospital stay. Bile duct injury is the commonest complication (0.5 to 2 per cent of cases).
- Dr Croton is a GP in Birmingham
- Sanders G, Kingsnorth AN. Clinical review: gallstones. BMJ 2007; 335: 295.
- MIMS Online. Patient resources: gallstones. www.mims.co.uk/news/882343/Gallstones/
- 5-Minute Clinical Consult: cholelithiasis. www.unboundmedicine.com/5minute/ub/view/ 5-Minute-Clinical-Consult/116129/all/Cholelithiasis