Gallstones in history:
Gallstones can be traced back to 21st Egyptian dynasty. They were discovered in the mummy of a Priestess of Arnan (1000 BC). The first clinical description of gallstones was by Gordon Taylor 4th century BC – symptoms in Alexander the Great. Historically, surgeons have been closely involved in management of gallstone disease. Emil Kocher, a Swiss surgeon, performed drainage of gallbladder for empyema 1878, and was awarded the Nobel prize. Carl Langenbuch, a German surgeon, was first to perform a open cholecystectomy late 1800s. The first laparoscopic cholecystectomy was performed in 1985 by Muhe in Germany.
Epidemiology of Gallstones:
Gallstones are very common, but often asymptomatic. The incidence of gallstones is as follow:
- 8% of population >40 yrs
- 20% of population >60 yrs
- 24% females
- 12% males
Approximately 1-2% of the above group develop any problems or complications from their gallstones.
Types of gallstones:
There are various types of gallstones, and are classified dependent on their constituency and may be calcified:
- Cholesterol or mixed stones (90%)
- Cholesterol stones – more than 50% cholesterol
- Mixed stones – 20 – 50% cholesterol
- Pigment(bilirubin) stones (10%) – less than 20% cholesterol
Cholesterol stones are associated with:
- high fat diet
- oestrogens (female,pregnancy,OC)
- loss of bile salts (ileal resection,Crohn’s)
- rapid weight loss
Pigment stones are associated with:
- haemolytic disorders
- biliary infection (parasitic)
Pathogenesis of gallstones:
Bile consists of bile salts(deoxycholate etc), bilirubin, cholesterol, metal ions, phospholipids and mucin. Gallstones form due to a failure to maintain a solubilized state of bilirubin and cholesterol and this imbalance in bile constituents leads to precipitation of crystals. Cholesterol stones form due to an imbalance in the concentration of cholesterol, bile salts and lecithin (phospholipid). Pigment stones form due to an over production of bilirubin.
Clinical presentation of gallstones:
Gallstones may present in a variety of ways. The clinical manifestation is dependent on mobility, passage and position of gallstones.
Biliary colic is biliary pain which may be precipitated by eating any food, (not only fatty food). When a stone lodges in the cystic duct, there is a functional spasm of cystic duct due to obstruction by stone. This results in sudden onset of pain usually in the epigastrium, and may radiate to (R)UQ or back, but can be (L)UQ.
The pain increases in intensity and may last for hours. “Colic” is a misnomer as the pain is usually steady. The pain is associated with nausea and/or vomiting.
There is usually no fever or rise in inflammatory markers.
Biliary colic is usually self limiting, but acute management of biliary colic involves diagnosis which is established with ultrasound scan which is 95% sensitive.
Treatment is usually with analgesia particularly NSAIDs.
Acute cholecystitis occurs when a gallstone causes obstruction of cystic duct
This results in inflammation of gallbladder wall which causes pain. The pain is usually in epigastric region and then to (R)UQ pain –visceral to parietal development. The pain can last for many hours. The pain is associated with nausea +/- vomit and symptoms of systemic toxicity such as
- rise in CRP
Diagnosis is made by ultrasound (and or CT scan).
Management of acute cholecystitis involves gut rest and analgesics, with the administration of IV fluids and IV antibiotics. Acute cholecystitis usually settles in 5 – 7 days.
30– 40% of patients with acute cholecystitis will have a palpable mass, often due to omentum adherent to gallbladder. A further 15% will have jaundice even without stones in common bile duct(CBD), due to inflammation , this is referred to as – Mirizzi’s syndrome.
Mirizzi’s syndrome is rare (0.1%) and is caused by a stone impacted in Hartmann’s pouch., which results in inflammation and oedema and consequent compression of common hepatic duct(CHD) or common bile duct(CBD). This can lead to erosion of stone into duct sometimes.
Diagnosis of Mirizzi’s syndrome is by ultrasound which reveals dilated intrahepatic ducts and an inflamed gallbladder. A CT scan may be necessary, and
- MRCP/ERCP useful to define anatomy.
- Management of Mirrizi’s syndrome is usually with IV fluids and antibiotics, and
- an ERCP and stent to control jaundice. There is often resolution with time.
- Mucocele and Empyema of gallbladder
If there ia a prolonged episode of acute cholecystitis and the individual presents late, the stone may obstruct gallbladder resulting in a mucoid collection in gallbladder or mucocele.
If this becomes an infected collection in gallbladder, it is referred to as an empyema of the gallbladder. The person will present with a palpable (R)UQ mass and sepsis.
Empyema of gallbladder is diagnosed by US or CT scan. Acute management is dependent on viability of gallbladder ie. no signs of ischemia. If the gallbladder is viable, pateint is treated with IV fluid and IV antibiotics and a percutaneous drainage of empyema performed under image guidance. If there is any suggestion of ischemia, an acute cholecystectomy is warranted.
With a long delay in presentation, a large gallstone can erode through wall of the gallbaldder into adjacent structures, usually duodenum, causing a cholecystoduodenal fistula(rarely colon). Rarely, this can lead to the gallstone blocking the small bowel obstruction called a gallstone ileus. Gallstone ileus with bowel obstruction is diagnosed by CT scan, and after fluid resuscitation, laparotomy and stone retrieval.
This is effectively due to repeated attacks of acute cholecystitis. There is a resultant thickened and fibrotic gallbladder and deposition of calcium within wall. This results in a theoretical increased risk of gallbladder cancer.
Acute cholangitis is caused by passage of gallstones into CBD causing obstruction of bile flow. The obstruction of bile flow causes Charcot’s triad:
- (R)UQ pain
- There will be a resultant
- Deranged liver function, both cholestatic and rise in transaminases
There may be haemodynamic instability and if severe can lead to sepsis and multiorgan failure.
Diagnosis is made by US/CT/MRCP which reveals dilated biliary ducts
Acute management involves IV fluids and IV antibiotics. If stone does not pass, then an ERCP and extrication of stone is mandatory.
Acute pancreatitis is the inflammation of the pancreas gland and is caused by the passage of a gallstone with resulting obstruction of pancreatic duct. This results in
- Severe epigastric pain
- Haemodynamic instability
- Diagnosis is made by raised serum amylase( >1000 usually diagnostic)
- There will also be a
- Raised whi/CRP
- Abnormal liver function tests
Imaging is not usually used for diagnosis, unless it is unclear, whereby CT scan is diagnostic.
Acute management is supportive
- IV fluids/gut rest
Most cases are mild and resolve as stone passes, otherwise ERCP and stone removal. Approximately 15% will be severe with risk of complications(necrotising pancreatitis, pseudocyst) and mortality
Management of asymptomatic gallstones:
If asymptomatic and discovered incidentally, gallstones should be observed. There is no evidence that prophylactic cholecystectomy is beneficial
If the gallbladder is calcified(porcelain), cholecystectomy is indicated as there is a risk of gallbladder malignancy
Management of symptomatic gallstones:
Once an episode of biliary colic has occurred, there is a chance of recurrent episodes. Cohort studies suggest an 30-50% chance of recurrent attacks per year and only about 30% of individuals will be painfree with longterm observation.
The management plan dependent on patient and dependent and overall risk.
Laparoscopic cholecystectomy is recommended for people who don’t want risk of further attacks
Definitive management for acute cholecystitis is laparoscopic cholecystectomy. There is an option of acute versus delayed laparoscopic cholecystectomy, but there is no difference in morbidity, mortality, conversion rates and hospital stay.
After the acute episode has settled, the recommendation is laparoscopic cholecystectomy within the 4-6 weeks after index admission.
If there has been an episode of severe necrotising pancreatitis, then delay to surgery may be appropriate and is dependent on the severity and complications.
This is a low risk procedure which is usually performed laparoscopically. There is a small conversion rate to an open procedure of 3-5%. The complication rate is low at approximately 2%, with a risk of bile duct injury of about 0.5%. As with all types of surgery there is a risk of mortality but this is low at approximately 0.3%