Ep 226 – Gallstones

In this episode, Dr Roger Henderson discusses gallstone disease, one of the most common disorders affecting the biliary system and a frequent cause of abdominal pain, emergency presentations and gastrointestinal complications. He examines how gallstones develop, focusing on the metabolic, hormonal, genetic and environmental factors that contribute to their formation. The discussion then follows the clinical progression from asymptomatic cholelithiasis and biliary colic to acute cholecystitis, choledocholithiasis, ascending cholangitis and gallstone pancreatitis. Dr Henderson reviews the role of ultrasound, laboratory investigations, magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography in diagnosis, before considering current approaches to management, including laparoscopic cholecystectomy and endoscopic intervention. Finally, he highlights important complications and clinical red flags, providing a concise framework for recognising and managing gallstone disease in everyday medical practice.

Key take-home points

• Gallstones are extremely common, and their prevalence increases with age, with women generally affected more often than men.
• Most gallstones are asymptomatic and are discovered incidentally. Asymptomatic gallstones usually do not require treatment unless specific high-risk circumstances are present.
• Gallstones form when substances within bile, particularly cholesterol or bilirubin, become supersaturated and precipitate into crystals that progressively enlarge.
• Cholesterol stones are the predominant type in Western populations, while black pigment stones are associated with haemolysis and brown pigment stones are more closely linked to biliary infection and stasis.
• Gallstone formation is multifactorial, involving metabolic, hormonal, genetic, environmental and biliary factors rather than a single cause.
• Obesity, insulin resistance, diabetes, dyslipidaemia, reduced physical activity and diets high in refined sugars and saturated fats are important risk factors for cholesterol gallstones.
• Rapid weight loss, including through the use of GLP-1 receptor agonist medications, and prolonged fasting can also increase gallstone risk because they reduce gallbladder emptying and promote biliary stasis.
• Biliary colic results from transient cystic duct obstruction, typically producing steady right upper quadrant or epigastric pain after meals, sometimes radiating to the back or right shoulder.
• Unlike acute cholecystitis, uncomplicated biliary colic is usually self-limiting, and patients are generally afebrile with normal laboratory investigations between episodes.
• Acute calculous cholecystitis develops when cystic duct obstruction persists, resulting in gallbladder distension, inflammation and sometimes secondary bacterial infection.
• Ultrasound is the preferred initial imaging investigation for suspected gallstone disease and can demonstrate gallstones, gallbladder wall thickening, pericholecystic fluid and a sonographic Murphy sign.
• Migration of a gallstone into the common bile duct produces choledocholithiasis, which can cause biliary obstruction, jaundice and cholestatic liver enzyme abnormalities.
• Ascending cholangitis is a medical emergency caused by infection in an obstructed biliary system. The classic Charcot triad consists of fever, right upper quadrant pain and jaundice, while hypotension and altered mental status indicate severe disease.
• Gallstones can cause acute pancreatitis when a stone obstructs the pancreaticobiliary outflow near the ampulla, typically producing severe epigastric pain with nausea and vomiting.
• Laparoscopic cholecystectomy is the definitive treatment for recurrent symptomatic gallstones and is generally preferred for acute calculous cholecystitis in suitable patients. Common bile duct stones may require endoscopic retrograde cholangiopancreatography or surgical exploration, while severe cholangitis requires antibiotics together with urgent biliary decompression.

Key references

1. EASL. J Hepatol. 2016;65(1):146-181. doi: 10.1016/j.jhep.2016.03.005.
2. NICE. 2014. https://www.nice.org.uk/guidance/cg188.
3. Fujita N, et al. J Gastroenterol. 2023;58(9):801-833. doi: 10.1007/s00535-023-02014-6.
4. Dasari BV, et al. Cochrane Database Syst Rev. 2013;2013(12):CD003327. doi: 10.1002/14651858.CD003327.pub4.
5. Gurusamy KS, Davidson BR. BMJ. 2014;348:g2669. doi: 10.1136/bmj.g2669.
6. NICE. 2021. https://www.nice.org.uk/guidance/htg584.