Gallstone diseases and related disorders

Published on 11/04/2015 by admin

Filed under Surgery

Last modified 11/04/2015

Print this page

This article have been viewed 6380 times

Gallstone diseases and related disorders

Introduction

Gallstones and related disorders account for all but a small proportion of biliary tract disease in most countries. Gallstone disease is also known as cholelithiasis and choledocholithiasis is when stones are present in the bile ducts.

Most gallstone-related disease presents with pain, typically located in the epigastrium or right hypochondrium (right upper quadrant or RUQ). The character of the pain varies but in most cases, it is acute and intermittent. Less commonly, gallstone disease presents as pain and jaundice caused by a stone passing into and obstructing the common bile duct.

Structure and function of the biliary system

Bile collects in canaliculi between hepatocytes and drains via collecting ducts within the portal triads into a system of ducts within the liver. These progressively increase in diameter until they become the right and left hepatic ducts which fuse to form the common hepatic duct. This is joined further distally by the cystic duct to become the common bile duct (Fig. 20.1). The common bile duct is 4–5 cm long and passes down behind the duodenum then through the head of the pancreas to drain via the ampulla of Vater into the medial wall of the second part of the duodenum. In most cases, the main pancreatic duct joins the common bile duct at the ampulla although it may enter the duodenum independently. The sphincter of Oddi within the ampulla prevents reflux of duodenal contents into the common bile duct and pancreatic duct.

Fig. 20.1 Surgical anatomy of the gall bladder, biliary tract and pancreas
The coeliac trunk (the foregut artery) arises from the aorta and divides into the hepatic, splenic and left gastric arteries. The hepatic artery divides into right and left branches, mirrored by the extrahepatic right and left hepatic ducts. These join caudally to form the common hepatic duct; this in turn is joined by the cystic duct to form the common bile duct (CBD). The porta hepatis consists of the hepatic arteries, the extrahepatic bile ducts and the portal vein

The gall bladder is a muscular sac lined by mucosa characterised by a single, highly folded layer of tall columnar epithelial cells. The lining epithelium is supported by loose connective tissue containing numerous blood vessels and lymphatics. Mucus-secreting glands are found at the neck of the gall bladder but are absent from the body and fundus. The proximal part of the duct is disposed into a spiral arrangement called the spiral valve, the function of which is not well understood. The gall bladder lies in a variable depression in the under-surface of the right hepatic lobe and is covered by the peritoneal envelope of the liver. The common bile duct is a fibrous tissue tube lined by a simple, tall columnar epithelium. Normally it is up to 0.6 cm in diameter and this can be measured on ultrasound scanning.

Bile is made continuously by the liver and passes along the biliary tract to the gall bladder where it is stored. Bile is concentrated there by as much as 10 times by a process of active mucosal reabsorption of water. Lipid-rich food passing from stomach to duodenum promotes secretion of the hormone cholecystokinin-pancreozymin (CCK) by endocrine cells of the duodenal mucosa. This hormone stimulates contraction of the gall bladder, squeezing bile into the duodenum. Bile salts (acids) act as emulsifying agents and facilitate hydrolysis of dietary lipids by pancreatic lipases. If biliary tract obstruction prevents bile from reaching the duodenum, lipids are neither digested nor absorbed, resulting in passage of loose, pale, foul-smelling fatty stools (steatorrhoea). Furthermore, the fat-soluble vitamins (A, D, E and K) are not absorbed. The lack of vitamin K soon leads to inadequate prothrombin synthesis and hence defective clotting. If surgery is necessary in a patient with obstructive jaundice, this may pose problems of haemostasis.

Pathophysiology of the biliary system

Gallstone composition

In developed countries, most gallstones are of mixed composition and contain a predominance of cholesterol; this is mixed with some bile pigment (calcium bilirubinate) and other calcium salts. A small proportion is virtually ‘pure’ cholesterol stones (‘cholesterol solitaire’). In Asia, most gallstones are composed of bile pigment alone. The composition and pathogenesis of the various types of gallstone are summarised in Table 20.1 (and see Fig. 20.2), and some examples are illustrated in Figure 20.3.

Table 20.1

Composition and pathogenesis of gallstones

Fig. 20.2 X-ray of radiopaque gallstone
Plain abdominal X-ray showing large radiopaque gallstone in the right upper quadrant. Note that the stone is obviously laminated, having built up in layers over many years. Note also that only 10% of mixed stones are radiopaque

Fig. 20.3 Types of gallstone
(a) Thick-walled chronically inflamed gall bladder found to be obstructed at its neck by a single stone. Note the stone is an aggregate of many smaller stones
(b) Multiple small gallstones in the gall bladder, all of much the same ‘generation’.
(c) Gall bladder containing one huge stone and multiple smaller stones. These stones all fitted together with adjoining facets.
(d) Different types of gallstones—pale irregular stones of different ages on the left and a pigment ‘jack’ stone on the right

The physical structure of mixed gallstones gives an insight into their sequence of formation. There is usually a small core of organic material, often containing bacteria. The main body of the stone is made up of concentric layers, demonstrating that stones form in a series of discrete precipitation events. Furthermore, in the same gall bladder, there are often several ‘families’ of gallstones, each of a different size. This suggests each generation began at a different time, presumably due to some transient change in local conditions. All families then build up at the same rate by lamination, leading to the range of different sizes. Radioisotope dating studies have shown that the average gallstone is 11 years old when removed!

The main factors in stone formation are: (a) changes in concentration of the different constituents of bile, (b) biliary stasis and (c) infection. It is likely that several subtle abnormalities combine synergistically to bring about precipitation of bile constituents.

Bile salts and lecithin are responsible for maintaining cholesterol in a stable micelle formation. The normal micellar structure of bile supports a greater concentration of cholesterol than could otherwise be held in solution and is therefore inherently unstable. An excess of cholesterol in proportion to bile salts and lecithin is probably one of the main factors in cholesterol stone formation. This is supported by the fact that patients in whom the terminal ileum has been resected or who have chronic distal ileal disease have a three-fold risk of developing cholesterol-rich stones. The mechanism is likely to be as follows: the terminal ileum is the main site for reabsorption of bile salts and when it is diseased or has been removed, reabsorption declines, leading to bile salt loss via the bowel and, eventually, a decline in the bile salt pool. The remaining bile salts are then insufficient to maintain the micellar structure of cholesterol in suspension.

Precipitation from bile is enhanced by biliary stasis. This occurs if the gall bladder becomes obstructed or contractility becomes defective. It is not known whether obstruction of the gall bladder outlet is a primary event in formation of stones but it probably plays a part in their continued accretion. Obstruction can be caused by dysfunction of the spiral valve in the cystic duct, by reflux of duodenal contents (which may be infected) or by small stones already formed. The muscular gall bladder wall is damaged by longstanding inflammation or infection which interferes with its ability to empty. Pregnancy is also a predisposing factor.

Investigation of gall bladder pathology

When gallstone disease is suspected, investigation has the following objectives:

• Exclude haematological and liver abnormalities and other metabolic disorders

• Establish if gallstones are present in the gall bladder and/or common duct and whether the gall bladder wall is thickened

• Assess the integrity and patency of the bile duct system and the pancreatic duct (if there is any suggestion of obstruction)

Blood tests for haematological and liver abnormalities: Haemolytic disorders such as hereditary spherocytosis, thalassaemia and sickle-cell trait should be considered as they may predispose to pigment stones. Liver function tests (LFTs) are indicated to look for indications of common duct stone obstruction if there is any suggestion of jaundice and to exclude other liver abnormalities.

Imaging in investigating gall bladder pathology: Ultrasonography (see Fig. 20.4) can reliably identify stones in the gall bladder and any increase in thickness of the wall (caused by inflammation or fibrosis). Ultrasound also provides a simple and accurate means of demonstrating dilatation of the common duct system, often indicating distal duct obstruction. Unfortunately, it is unreliable for directly identifying bile duct stones, particularly at the lower end, because the image tends to be obscured by overlying duodenal gas. Ultrasound has the great advantage of being suitable for use in the seriously ill or jaundiced patient as it is non-invasive and can be performed at the bedside.