SEQULAE OF GALL STONE MIGRATION

COMMON BILE DUCT STONE (CHOLEDOCHOLITHIASIS) AND JAUNDICE - MECHANISM.

      Gallstone that becomes lodged in the neck of the gallbladder can cause infection and inflammation of the gallbladder (cholecystitis). Usually, it takes six hours to develop the infection of gall bladder with obstructed stone at cystic duct. At this stage of gall bladder infection there will be persistent pain abdomen with or without vomiting and sometime associated with fever also. There is a classical presentation that each meal can cause pain especially after fatty foods. If the stone is impacted in the cystic duct, it leads to gall bladder inflammation. After this pain, sometime the impacted stone may come back to gall bladder and pain will go off. But at the same time the stone may slip down into the common bile duct and cause blockage of bile duct at any part of the common bile duct or even common hepatic duct.

(1) COMMON BILE DUCT STONES (CHOLEDOCHOLITHIASIS) WITH BILE DUCT BLOCK. 

      Gallstones can block the bile transport tube (bile ducts) through which bile flows from the liver to the small intestine. Gall stones from gall bladder can migrate down to the bile duct and block the bile ducts. Bile duct blockage may lead to bile duct infection and present as pain abdomen, fever and jaundice (Charcot’s Triad).

Presence of this persistent infection sometime damages the circulatory system and may end up with fall in blood pressure or increase in pulse rate and also. There will be change in patient orientation and patient will be restless. The presence of pain abdomen, fever and jaundice with hypotension (Fall in blood pressure) and change in orientation are bad prognostic signs. (Reynold’s Pentad).

The presence of bile duct stone is suspected with clinical features and Liver Function Test (LFT) and confirmed by special investigation like MRCP.

(2) COMMON HEPATIC DUCT STONES.

          The slipped stones from gall bladder usually present in the common bile duct and has the tendency to come down to ampulla of Vater because of the bile flow is towards the ampulla of Vater. But sometime multiple bile duct stones can present in the common hepatic duct also. The possible reasons for common hepatic duct stones are migration of multiple stones from the gall bladder or lithogenic bile with production of multiple stones at the common hepatic duct itself. Another important reason for common hepatic duct stone is Choledochal cyst in which there will be abnormal dilatation of bile duct with decreased motility of bile duct. This condition present since birth and commonly present during second or third decade of life.

          The diagnosis of common hepatic duct stone is by ultrasonography of abdomen and confirmed with MRCP. The treatment is directed towards the cause of common hepatic duct stone. In case of gall stone disease with common hepatic duct stone the treatment is ERCP with removal of ductal stones followed by laparoscopic cholecystectomy. But in case of associated condition like Choledochal cyst needs surgical excision of the cyst with cholecystectomy with hepaticojejunostomy.

(3) INTRAHEPATIC DUCTAL STONES

Intrahepatic stone is a part of the calculus of bile duct, referring to the stones located proximal to the confluence of the left and/or right hepatic ducts. Intrahepatic stones include brown pigment stones (calcium bilirubin stones), cholesterol stones, and their mixture. Intrahepatic stones are usually accompanied with extrahepatic stones and have properties of multiple complications, high postoperative recurrence rates, and serious systemic damage. The diagnostic approach, at present, mainly depends on imaging. And the healing therapies now prefer endoscopic treatment approaches to traditional surgical treatment approaches. Endoscopic treatments involve endoscopic retrograde cholangiopancreatography (ERCP). The surgical treatment mainly includes bile duct incision and lithotomy, hepatic resection, reconstruction of bile duct stricture, and liver transplantation. Various treatment strategies have been proposed as mentioned above since there is no extremely effective procedure for the management of intrahepatic stone. So, it is more important to find out the etiology and pathogenesis of intrahepatic stones to prevent the disease from happening and developing rather than curing. Although the pathogenesis of intrahepatic stones has not been disclosed clear so far, it is still reported to be related with the environment, nutritional status, bile duct infection, cholestasis, parasites, the variation of bile duct, bile metabolic defect, and so forth. These factors may cooperate to induce intrahepatic stones. Among these factors, cholestasis, infection, and anatomic abnormity of bile duct and bile metabolic defect occupy the most important positions.

INTRAHEPATIC STONES-POSSIBLE REASONS

Cholestasis

Bile is produced by liver cells and finally excreted into duodenum to help in digestion and absorption fatty foods. the coordination of gallbladder contraction and Sphincter of Oddi (SO) relaxation is also playing important role in the process of bile excretion. Bile salts are the major solutes, which form the main permeability power of the bile flow. Any factor which affects bile production and excretion can cause cholestasis. Cholestasis is essential for the formation of intrahepatic stone, both pigment stones and cholesterol stones. It can be caused by viruses, bacteria, parasites, drugs or toxins, stones, tumours, self-immunity, genetic metabolic defects, and obstruction. Cholestasis provides time and place for the bile components deposited and then form shaped stones, while cholestasis also means toxic bile acid accumulated to cause biliary walls injury and inflammation. And these then provide a condition for ascending infection. This is a vicious cycle. Once biliary sludge formed, bile duct obstruction is aggravated.

Infection

Intrahepatic bile duct infection includes bacteria and parasites. Infection is perhaps the prime cause for pigment stones. Almost in all the patients with intrahepatic stone, bacteria can be detected on bile culture. The pathogenesis of bacterial infection has been explained relatively clearly. The bacteria in bile duct produce β-glucuronidase which can hydrolyze conjugated bilirubin to unconjugated bilirubin. Then, unconjugated bilirubin and ionized calcium will combine together and form calcium bilirubinate deposited.

Parasites, such as Ascaris, liver fluke and Schistosoma, account for intrahepatic stone as well. They can not only damage the epithelium of bile duct to cause inflammation but also form the nucleus of stones with their body Besides, these worms have high glucuronidase activity, which deconjugates bilirubin and forms pigment stones. Similarly, an association between liver fluke infection and intrahepatic stone is well recognized. As one kind of liver fluke, Clonorchis sinensis (C. sinensis) infection is believed to be associated with intrahepatic stones, especially pigment stones.

Anatomic Abnormality of Bile Duct

Intrahepatic stones are easy to occur in intrahepatic bile duct with anatomic variation and poor bile evacuation. For example, the left hepatic duct is slender and meets common hepatic duct at nearly a right angel, and there is often a corner when the right posterior segmental duct meets the right hepatic duct. The two cases mentioned above lead to bile excretion disorder and cholestasis. So, the stones of right posterior lobe type and left lobe type are the most common ones. Apart from normal physiological and anatomical influence, the congenital or acquired anatomic abnormity, deformity, or disease, such as anastomotic stricture, congenital choledochal cyst, and Caroli's disease, can also increase the morbidity of intrahepatic stones. an independent risk factor of residual stones, cholangitis, and stone recurrence after treatment

The common pathological changes in intrahepatic stone are stones, strictures, dilation, chronic proliferative cholangitis, cholangiocarcinoma, hepatic parenchymal fibrosis, and hepatic atrophy. Stricture is the major pathological change and the common reason for stone recurrence and surgical treatment failure.

Bile Metabolic Defect

The most important reason for cholesterol stones is the imbalance of bile components associated with bile metabolic defect. The mechanisms may be related to the increase of cholesterol, the reduction of bile acid, and phospholipid secretion defects.

Besides, the changes of bile components and the over secretion of mucins caused by the activation of arachidonic acid leads to cholestasis and promote crystallization of cholesterol, resulting in cholesterol stones or stones rich in cholesterol.

Treatment of intrahepatic stones are difficult. The commonly recommended treatment protocol is to remove the stones by endoscopic method like ERCP. But the recurrence rate is high with bile duct stricture. In that case bile duct exploration with removal stones along with hepaticojejunostomy is recommended. If the stones are confined to one side of liver, then the hepatic resection of affected side of the liver will be ideal option. Rarely patients with extensive intrahepatic bile duct stones involving both lobe of liver with persistent ongoing infection may necessitate to have liver transplantation.

(4) ACUTE BILIARY PANCREATITIS – GALL STONE INDUCED PANCREATITIS.

    The pancreatic duct is a tube that runs from the pancreas to the duodenum (proximal small intestine). Most of the time pancreatic duct joins with common bile duct to open into duodenum at a common point. Pancreatic juices, which aid in digestion, flow through the pancreatic duct in to the duodenum. So, any block in the lower part of bile duct can cause blockage of pancreatic duct also.

    Any blockage of pancreatic duct usually by the gallstone can cause inflammation of the pancreas (pancreatitis). Pancreatitis causes intense, constant upper abdominal pain and usually requires hospitalization. Pain is associated with vomiting, abdominal distension and sometime patient with pancreatitis will not be able to take oral food. This may end up with severe inflammation of pancreas with severe pancreatic tissue damage known as acute severe pancreatitis.

     Extension of this is known as pancreatic necrosis in which a part of pancreatic tissue loses its viability (Necrosis). There may be associated infection of this necrosed pancreas known as acute necrotizing pancreatitis with infection. Depending on the intensity of the pancreatic damage and associated infection may end up with one or more organ failures.

     Organ failure means dysfunction of a particular organ. For example, change in the blood urea or serum creatinine in case of kidney damage (AKI). Sometime may ends up with breathing difficulty in case of respiratory failure which may require assisted ventilation (ARDS). Sometime this systemic infection damages the circulatory system and may end up with fall in blood pressure with increase in the pulse rate (SHOCK). Rarely, there will be change in patient orientation and patient will be restless. The presence of hypotension (fall in blood pressure) and change in orientation are bad prognostic signs.

(5) GALL STONE ILEUS

         It is an extreme rare condition in which usually large gall stone migrate into the intestine usually through the fistulous communication between the gall bladder and nearby organ like duodenum. This migrated stone sometime causes the block in the food passage. This may end up with features suggestive of intestinal obstruction. Here patients usually present with pain in abdomen along with abdominal distension and vomiting. Investigation like erect X ray of abdomen confirms the intestinal obstruction. Ultrasonography of the abdomen confirms the gall stones and MRCP confirms the fistulous communication between gall bladder and other organ. Usually, this condition requires surgical intervention. The aim of the surgeries is to remove the gall bladder, close the fistulous communication and remove or dis impact the blocked stone from the obstructed intestine.

(6) MIRIZZI’S SYNDROME

       This is a separate entity in which there will be communication between gall bladder and bile duct. Impaction of gall stone at one particular place gives constant pressure over a particular area and leads to the development of artificial communication between gall bladder and common bile duct. This leads to migration of gall stone into the common bile duct. This is divided in to four types depending on the extend of the bile duct involvement.

       In Type I Mirizzi’s syndrome, the bile duct involvement is only extraneous impression of gall stone over the bile duct and actually no communication between bile duct and gall bladder.

       In Type II Mirizzi’s syndrome there will be communication between bile duct and gall bladder is less than 33% of bile duct circumference.

       In Type III Mirizzi’s syndrome there will be communication between bile duct and gall bladder and the involvement is between 33% to 66% of bile duct circumference.

       In Type IV Mirizzi’s syndrome the bile duct involvement will be more than 66% of bile duct circumference.  The reason behind this problem is due to long term presence of ongoing inflammation of gall bladder due to stones. This gives external impression over bile duct as in Type I Mirrizi’s syndrome and abnormal communication between gall bladder and bile duct in other types of Mirizzi’s syndrome.

       In type I Mirizzi’s syndrome careful laparoscopic cholecystectomy is the treatment of choice.

       Type II Mirizzi’s syndrome is managed with laparoscopic cholecystectomy with bile duct stone removal with laparoscopic repair of the defect over a T-tube. In case any technical difficulty the same procedure can be done by open technique.

       But in Type III and Type IV Mirizzi’s syndromes are managed with laparoscopic technique or open surgical technique and will require gall bladder removal, bile duct stone removal and joining the bile duct with jejunum known as hepaticojejunostomy.