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Tuesday, 20 March 2012

DIAGNOSIS AND MANAGEMENT CHOLELITHIASIS / GALLSTONES

CHAPTER I
INTRODUCTION

Gallstone disease is often found in developed countries and rarely found in developing countries. With the improvement of socio-economic circumstances, changes in western-style food menu as well as improved means of diagnosis, especially ultrasound, the prevalence of gallstone disease in developing countries tend to increase. Gallstone disease is an important health problem in western countries, while in Indonesia a new clinical attention.
Approximately 5.5 million people with gallstones in the UK and 50,000 cholecystectomy performed each year. Cases of gallstones are often found in America, namely in 10 to 20% of the adult population. Every year several hundred thousand patients are undergoing surgery. Two-thirds of gallstones are asymptomatic when the patient does not have any complaints and that evolved into an annual colicky pain is only 1-4%. While the symptoms of patients with symptomatic gallstones develop complications 12% and 50% had colicky pain in the next episode. Risk for people with gallstones have symptoms and complications are relatively small. However, once gallstone colic pain attacks pose a problem specific to the risk of experiencing problems and complications will continue to increase.
Gallstones are commonly found in the gall bladder, but the stones can migrate through the cystic duct into the bile duct into the bile duct stones and called the secondary bile duct stones.
In Western countries 10-15% of patients with gallbladder stones are also accompanied by bile duct stones. In some circumstances, bile duct stones can form in the bile ducts of primary intra-or extra-hepatic without involving the gallbladder. Primary bile duct stones are more common in patients in Asia compared with patients in Western countries.
Journey secondary bile duct stones are not clear, but the complications will be more frequent and severe than asymptomatic gallbladder stones.
In about 80% of cases, is the largest component of cholesterol gallstones. Usually the stone - stone also contains calcium carbonate, phosphate or bilirubinat, but these stones are rarely pure than one component.

CHAPTER II

REVIEW REFERENCES


2.1 Definition of Cholelithiasis
Cholelithiasis also known is synonymous with gallstones, gallstones, biliary calculus. Kolelitiasis term meant to the formation of stones in the gallbladder. Gallbladder stones is a combination of several elements that make up a stone-like material that form in the gallbladder (kolesistolitiasis) or in the bile ducts (koledokolitiasis) or on both.

                             Gambar1. Gambaran batu dalam kandung empedu (Emedicine, 2007)



2.2 Anatomy of the liver and biliary system
The liver is located under the right diaphragm, protected under the right ribs. Normal liver chewy with the smooth surface. The liver is the largest gland in the body weight of 1000-1500 grams. The upper limit of the liver are parallel to the V right intercostal space and a lower limit to the top of the ribs menyerong IX right to left rib VIII. Concave posterior surface of the liver and there is a transverse slit along the 5 cm from the porta hepatis system. Liver consists of two main lobes, right and left. Right lobe is divided into anterior and posterior segment, left lobe is divided into segments by the medial and lateral ligament Falsiformis.
Each lobe is divided into lobuli. Each lobule is a body composed of hexagonal plates of liver cells surrounding the veins of the central cube. Among the plates are called the sinusoid capillaries of Kupffer cells is limited. Kupffer cells function as the heart of defense. Biliary system starts from kanalikulus bile, which is a small channel lined by microvilli complex sekililing liver cells. Kanalikulus bile forming intralobular bile ducts, which drain bile into the bile ducts in the portal tract.
The resulting hepatocyte bile is excreted into the kanalikuli and then housed in a small tract of bile which is located in the heart that would gradually form a larger channel. These channels have epithelium that cabbage can be expanded in stages when the bile duct continues to expand.
Intrahepatic bile ducts are slowly fused to form larger channels that can be channeled into eight segments of the liver bile. In the right liver segments, combined these branches form a channel in the anterior and posterior are then joined to form a duct hepatikus right. In some people, right hepatikus duct is ± 1 cm outside the liver. Duct is then joined by three segments of the left liver segments (left hepatikus duct) into the duct hepatikus communist.
After merging with the cystic duct from the gallbladder, the ducts become the ductus koledokus hepatikus. In some circumstances, the walls of the duct and lumennya koledokus be widened until it reaches the ampulla. Usually koledokus duct length about 7 cm in diameter ranges from 4-12 mm. gall bladder receives its blood supply from the tangle of blood vessels of the largest branch of the right hepatic artery
The gall bladder can accommodate ± 50 ml of bile with a length of 8-10 cm and consists of a fundus, corpus and neck. Mucosa layer to form a small basin near the neck of the so-called Hartman, who could be buried where gallstones



Physiology of the digestive system and biliary
Basic functions of the liver is divided into:
a. Vascular function to store and filter blood. There are two kinds of blood to the liver, the portal blood from the intestine and arterial blood, which they will meet in the sinusoid. The incoming sinusoid blood will be filtered by Kupffer cells.
b. Metabolic functions. Liver plays an important role in the metabolism of carbohydrates, proteins, fats, vitamins.
c. Ekskretorik function. Many materials in the liver excretion in the bile, such as bilirubin, cholesterol, bile acids and other
d. Synthesis function. liver is a source of plasma albumin, globulin plasma lot, and many proteins that play a role in hemostasis.

Bile functions
a. Aids digestion and absorption of fat
b. Metabolite excretion of waste products such as the liver and cholesterol, bilirubin and heavy metals.


Normal Bilirubin Metabolism
Phase Prahepatik
• Establishment of bilirubin. Approximately 250 to 350 mg of bilirubin, or about 4 mg per kg body weight per day established, 70-80% comes from the breakdown of red blood cells mature. While the remaining 20-30% (early labeled bilirubin) comes from other heme proteins that are primarily in the bone marrow and liver. Part of the heme protein is broken down into iron and biliverdin with intermediate products between the enzyme heme0ksigenasi. Another enzyme, biliverdin reductase, converting biliverdin to bilirubin. Early labeled bilirubin formation is increased in several disorders with ineffective erythropoiesis.
• Transport of plasma. Bilirubin is insoluble in water, hence no conjugated bilirubin transport in the plasma is bound to albumin and can not be through the glomerular membrane, hence it does not appear in the urine. Bond weakening in some circumstances such as acidosis, and the use of certain antibiotics

Phase of the intrahepatic
• Liver uptake. Making process is not conjugated bilirubin by the liver requires a cytoplasmic protein or protein receivers, which are given as a symbol of protein Y and Z.
• conjugation. The free bilirubin is concentrated in the liver cells have to form conjugates with bilirubin diglukuronida glukoronik acid or bilirubin bilirubin conjugation or director. This reaction is catalyzed by the microsomal enzyme transferase glukoronil menghasilakn water-soluble bilirubin. In some circumstances this reaction produces only monoglukorida bilirubin, with the second glukoronik acid was added in units of bile through a different enzyme systems, but this reaction is not considered to be physiological. Conjugation of bilirubin other than diglukuronid also formed, but its usefulness is not clear

Phase Pascahepatik
• excretion of bilirubin. Conjugation of bilirubin released into the kanalikulus with other materials. In the intestinal bacterial flora to "dekonyugasi" and reduce the bilirubin into sterkobilinogen and remove most of the stool that gives the brown color. Some is absorbed and released back into the bile, and small amounts reach the urine as Urobilinogen. The kidneys can not remove bilirubin diglukuronida but unkonyugasi. This explains the dark color of urine is typical in disorders of hepatocellular or intrahepatic cholestasis. No conjugated bilirubin is not soluble in water but soluble in fat. Therefore, conjugated bilirubin can not pass the blood-brain barrier or into the placenta. In liver cells, conjugated bilirubin was undergoing a process of conjugation through glukoniltransferase enzymes and bile soluble in the liquid.

Pathophysiology
There are four common mechanism in which hyperbilirubinemia and jaundice may occur:
A. Excessive formation of bilirubin
2. Disturbance was taking conjugated bilirubin by the liver
3. Disorders of bilirubin conjugation
4. The decrease in biliary excretion of conjugated bilirubin from intrahepatic and extrahepatic factors that are functional or mechanical obstruction.
Conjugated hyperbilirubinemia was mainly caused by the first three mechanisms, whereas the fourth mechanism is mainly menghakibatkan conjugated hyperbilirubinemia.
On the obstruction jaundice, conjugated bilirubin excretion decreased. Excretion of bilirubin interference, whether caused by factors of functional or obstructive, mainly resulting in conjugated hyperbilirubinemia. Because conjugated bilirubin is water soluble, the bilirubin can be excreted into the urine, causing urinary bilirubinuria and makes the dark.
Urobilinogen Urobilinogen feces and urine are often reduced and Stool, pale stools. Elevated levels of conjugated bilirubin can be accompanied by evidence of excretion of liver failure, such as elevated levels of serum alkaline phosphatase, AST, cholesterol, and bile salts. Increased bile salts in the blood causing itching in jaundice. Jaundice caused by conjugated hyperbilirubinemia is usually more yellow than the no-conjugated hyperbilirubinemia. Color change from yellow-orange range young or old to yellow-green in the event of total obstruction of bile flow.
The gall bladder is an avocado-shaped pouch that lies just below the right lobe of the liver. Have gallbladder fundus, corpus, infundibulum, and neck. Fundus rounded shape, the tip of his dead-end of the gall bladder. The corpus is a major part of the gall bladder. Is the narrow neck of the gallbladder.
Vesica fellea act as a resevoir of bile with a capacity of about 50 ml. Vesica fellea has an ability to concentrate bile. And to assist this process, the mucosa has folds - the creases permanently interconnected to each other. So that a surface looks like a wasp nest. Thoracic cells that limit also has a lot mikrovilli.
Bile is secreted continuously by the liver into the small bile ducts within the liver. Small bile ducts which unite to form two larger channels that come out of the surface of the liver as the ductus hepatikus communist. Hepatikus duct joined the cystic duct to form the duct koledokus. In many people, united by koledokus ductal pancreatic duct to form the ampulla of Vater before it empties into the small intestine. Terminal part of the second channel and ampla surrounded by circular muscle fibers, known as the sphincter of Oddi.



                                      Figure 3. Anatomical picture of the gallbladder (Emedicine)


Physiology
One function of the liver is to remove the gall, normally between 600-1200 ml / day. Gallbladder can store about 45 ml of bile. Beyond the meal, bile is stored temporarily in the gall bladder, and here the experience of about 50% concentration. The primary function of the gall bladder bile is concentrating with water and sodium absorption. The gall bladder can concentrate solute impermeable, which contained 510 times in hepatic bile and reduce the volume of 80-90%. Lymph vessels and blood vessels absorb water and inorganic salts in the gall bladder so bile in the gall bladder will be more concentrated 10-fold than the liver bile. Periodically, the gall bladder will empty its contents into the duodenum through simultaneous layers of muscle contraction and relaxation of sphincter of Oddi. Normal excitatory contraction and emptying of the gall bladder is the inclusion of acid in the duodenum kimus. The presence of fat in the diet is a powerful stimulus to induce contractions. Hormone CCK also mediates contraction.
Bile flow as a result of contraction and partial emptying of the gallbladder. This mechanism begins with the entry of fatty foods into the duodenum. Fat hormone induces kolesistokinin of duodenal mucosa, then the hormone into the blood, causing the gallbladder to contract. At the same time, smooth muscle located at the distal end of the duct and ampulla coledokus relaxation, allowing the entry of bile into the duodenum thick. Salts - bile salts in bile is important for the emulsification of fat in the intestines and help digestion and absorption of fat.

The process of coordinating these two activities is caused by two things:
• Hormonal:
Fatty substances contained in food once it gets to stimulate duodenal mucosa so that the hormone cholecystokinin is released. This hormone is the most major role in gallbladder contraction.
• Neurogen:
o vagal stimulation associated with the phase of the secretion of gastric juices Cephalik or intestino-intestinal reflex will cause contraction of the gallbladder.
o Stimulation of food that goes directly to the duodenum and sphincter of Oddi. So that in cases where the gall bladder paralysis, bile will stick out a little though.

Slow emptying of bile due to neurological and hormonal disorders play an important role in the development of rock core.

Bile fluid composition


Bile salts
Bile acids from cholesterol. Bile acids from the liver there are two kinds: Amino Acids and Cholat Deoxycholat.
Function of bile salts are:
o Lowering the surface tension of the particles of fat contained in food, so that the particles of fat that can be broken down into small particles to be digested further.
o Helps absorption of fatty acids, monoglycerid, cholesterol and fat-soluble vitamins
Bile salts into the intestinal lumen by intestinal germs work converted into deoxycholat and lithocholat. Most (90%) of bile salts in the intestinal lumen to be absorbed again by the intestinal mucosa, while the remainder will be released with the feces in the form lithocholat. Absorption of bile salts occurs segmented from the distal ileum. So if there is interference in the area for example because of inflammation or resection of the bile salt absorption will be disrupted.

Bilirubin
Hemoglobin released from erythrocytes will burst into heme and globin. Heme united to form a chain with four core pyrole be bilverdin that soon turned into free bilirubin. This substance in the plasma tightly bound by albumin. Most of free bilirubin bound by other substances (conjugation) of 80% by glukuronide. If there is excessive breakdown of red blood cells for example in the form of malaria is very banyak.Dua bilirubin bile duct disease is most often frequency of stone formation (kolelitiasis) and accompanying chronic inflammation (cholecystitis). These two unusual circumstances arise independently, or occur simultaneously.

According to Guyton & Hall, 1997 Bile performs two important functions, namely:
• Bile plays an important role in digestion and absorption of fat, because bile acids do two things among others: bile acids help mengemulsikan particles of fat into smaller particles with the help of the enzyme lipase which is secreted in the pancreatic lymph, bile acids help transport and absorption of ingested fat that the final product toward and through the intestinal mucous membrane.
• Gall worked as a tool to remove some waste products that are important from the blood, including bilirubin, an end product of the destruction of hemoglobin, and excess cholesterol in the form of the liver cells.

Gallbladder emptying is influenced by hormones kolesistokinin, this occurs when fatty foods enter the duodenum about 30 minutes after eating. The basic cause is the emptying of the rhythmic contractions of the gallbladder wall, but the effectiveness of the discharge also require a relaxation of the sphincter of Oddi same time guarding the exit of the common bile duct into the duodenum. Besides kolesistokinin, gallbladder also strongly stimulated by nerve fibers that secrete acetylcholine from the vagus and the enteric nervous system. The gall bladder stores bile pekatnya emptying into the duodenum, especially in response to stimulation kolesistokinin. When fat is present in food, emptying of the gall bladder went badly, but if there is an adequate amount of fat in the diet, normal gall bladder empty completely in about 1 hour.
Bile salts, lecithin, and cholesterol is the largest component (90%) of bile. The rest is bilirubin, fatty acids, and inorganic salts. Bile salts are steroids produced by hepatocytes and is derived from cholesterol. Production arrangements influenced the feedback mechanism which can be increased up to 20 times the normal production if necessary.


Cholelithiasis etiology
Normal bile consists of 70% bile salts (especially colic and Chenodeoxycholic acid), 22% phospholipids (lecithin), 4% cholesterol, 3% protein and 0.3% bilirubin.2 gallstone etiology is still unknown to perfection but the most important is a metabolic disorder caused by changes in the composition of bile, bile stasis and infection of the gallbladder. Meanwhile, a major component of gallstones are cholesterol that usually remains as a liquid. If the bile becomes saturated because of cholesterol, the cholesterol can become insoluble and form a precipitate out of bile.


Risk Factors for Cholelithiasis
Increased incidence of gallstones can be seen in high-risk groups called "4Fs": female (woman), fertile (fertile)-especially during pregnancy, fat (fat), and forty (forty years).
Cholelithiasis can occur with or without risk factors. However, the more risk factors, the greater the possibility for the occurrence of kolelitiasis.
A. Women (two to be more at risk than men)
2. More than 40 years of age.
3. Weight (BMI). People with a Body Mass Index (BMI) tall, have a higher risk for occurred kolelitiasis. This karenakan with higher BMI levels of cholesterol in the gallbladder too high, and also mengurasi bile salts and reduces the contraction / emptying of the gallbladder.
4. Heredity
5. Physical activity
6. Pregnancy (increased risk of pregnancy)
7. Hyperlipidemia
8. Diet high in fat and low fiber
9. Prolonged gastric emptying
10. Long-term intravenous nutrition. Long-term intravenous nutrition resulted in the gall bladder is stimulated to contract, because no food / nutrients through the intestinal tract. Thereby increasing the risk for stone formation is enhanced in the gallbladder.
11. Gallbladder dysmotility
12. Antihiperlipedmia drugs (clofibrate)
13. Other diseases (such as cystic fibrosis, diabetes mellitus, liver cirrhosis, pancreatitis and gallbladder cancer) and diseases of ileus (lack of bile salts)
14. Race / ethnicity (higher incidence in American Indians, followed by whites, a new African people)


Pathogenesis
Gallstones are almost always formed in the gallbladder and bile ducts are rarely on the other, and are classified according to its constituent materials. Gallstone etiology is still unknown to perfection, however, the most important predisposing factor seems to be a metabolic disorder caused by changes in the composition of bile, bile stasis and infection of the gallbladder. Changes in the composition of bile may be the most important in the formation of gallstones, due to deposition of cholesterol in the gallbladder. Stasis of bile in the gall bladder can increase supersaturasi progressive, changes in chemical composition, and deposition of these elements. Bacterial infection in the bile duct may play a role in stone formation in part, through increased and cell desquamation and mucus formation.
Secretion associated with the formation of cholesterol gallstones. In the abnormal conditions, cholesterol may precipitate, causing the formation of gallstones. Various conditions can cause the deposition of cholesterol is: too much water absorption of bile, too much absorption of bile salts and lecithin of the bile, the secretion of too much cholesterol in the bile, the amount of cholesterol in bile is partly determined by the amount of fat eaten because the cells synthesize hepatic cholesterol as one of the products of fat metabolism in the body. For this reason, those who received high-fat diet in a few years, will be prone to the development of gallstones.
Gall bladder stones may migrate into the duct through the cystic duct koledokus. In the journey through the cystic duct, stones may cause obstruction of bile flow is partially or completely, giving rise to biliary colic gejalah. If the stone stops in the cystic duct for its diameter is too large or restrained by a stricture, stones would remain there as a cystic duct stone.


Pathophysiology
Gallstone formation is divided into three stages: (1) the formation of bile supersaturasi, (2) nucleation or formation of rock core, and (3) develop because of increased precipitation. The solubility of cholesterol is an important issue in the formation of all rocks, except for pigment stones. Supersaturasi bile with cholesterol occurs when the ratio of bile acids and phospholipids (mainly lecithin) and cholesterol falls below a certain price. Normally cholesterol is not soluble in aqueous media. Bile is maintained in liquid form by the formation of colloids that have a central core of cholesterol, surrounded by a hydrophilic coat of the bile salts and lecithin. So the excessive secretion of cholesterol or bile acid levels are low, or there is secretion of lecithin, a situation which litogenik.
Stone formation begins only when there is a nidus, or core of cholesterol deposition. At supersaturasi cholesterol levels, cholesterol crystals out of solution forming a nidus, and form a deposition. Saturation at a lower level, probably bacterial, parasitic fragments, loose epithelial cells, or other debris particle required to be used as crystallization seeds.


Cholelithiasis classification
According to the macroscopic description and chemical composition, gallstones in golongkankan above 3 (three) categories:
A. Cholesterol stones
Oval-shaped, multifocal or mulberry and contain more than 70% cholesterol. More than 90% of gallstones are cholesterol (rock containing> 50% cholesterol). Cholesterol dissolved in bile within the hydrophobic micelle, so that the solubility depends on the relative amounts of bile salts and lecithin.
Required for the formation of cholesterol stones three main factors:
a. Supersaturasi cholesterol
b. Hipomotilitas gallbladder
c. Nucleation / rapid formation of nidus.

According to Meyers & Jones, 1990 The physical process of cholesterol stone formation occurs in four stages:
• Supersaturasi bile with cholesterol.
Cholesterol, phospolipid (lecithin) and bile salts is a component that is not soluble in water. The third of these substances in a specific ratio to form a soluble micelle. In the gall bladder is concentrated into three five-to seven-fold. Dissolution of cholesterol depends on the ratio of cholesterol to lecithin and bile salts, normally between 1: 20 to 1: 30. In the circumstances in which cholesterol supersaturasi will be relatively high this ratio can reach 1: 13. At this ratio of cholesterol will be deposited.
Cholesterol levels will be relatively high in the following circumstances:
 Inflammation of the gallbladder wall, water absorption, bile salts and lecithin is much higher.
 People are fatter where higher cholesterol secretion causing supersaturasi.
 A diet high in calories and high cholesterol (western diet)
 Use of anti-cholesterol drugs that high-mobility tissue cholesterol.
 Pool bile acids and bile acid secretion decreased ileum terminale such as the disruption caused by inflammation or resection (enterohepatic circulation disorder).
 Use of tablet KB (estrogen) increased secretion of cholesterol and low levels chenodeoxycholat, whereas the effect chenodeoxycholat dissolve cholesterol stones and lowers cholesterol saturation. Another study states that the tablet KB effect only up to three years.
• Establishment of the nidus.
Core rock that occurs in phase II can be homogeneous or heterogeneous. Heterogeneous rock core can be derived from bile salts, calcium bilirubinat or loose cells in inflammation. Homogeneous rock core from cholesterol crystals themselves facing due to changes in the ratio of bile acids.
• Crystallization / precipitation.
• Growth in stone by the aggregation / precipitation of lamellar cholesterol and other compounds that make up the rock matrix.
To be a stone, a stone that had formed the core should be enough time to develop into a large. In normal circumstances where the strong contraction of the gallbladder and bile normal circulation, which has formed the core of the stone will be pumped out into the small intestine. When the construction is weak gallbladder, cholesterol crystals caused by supersaturasi be attached to the rock core.
It is easy to occur in patients with diabetes mellitus, pregnancy, total parenteral nutrition on giving long after truncal vagotomi surgery, because the situation is less good gallbladder contraction. Excessive mucus secretion from the mucosa of the gallbladder will bind cholesterol crystals and hard pumped out.

2. Pigment stones
Pigment stones is 10% of the total new type of bile containing <20% cholesterol. There are two forms of pure pigment stones are more common and bilirubinat calcium stones. Less pure pigment stones (2 to 5 mm), multiple, very hard and green to black appearance. These rocks contain varying amounts of calcium bilirubinat, polymer bilirubin, bile acids in small amounts of cholesterol (3 to 26%) and many other organic compounds. East area, the dominant bilirubinat calcium stones and is 40 to 60% of all gallstones. This stone is more brittle, brown to black Pathogenesis of pigment stones is different from cholesterol stones. Possibilities include the secretion of pigment in the amount of increased or abnormal formation of the precipitated pigment in bile. Cirrhosis and biliary stasis predisposes to the formation of pigment stones (Sarr & Cameron, 1996). Patients with increased load was conjugated bilirubin (hemolytic anemia), prevalent form of pure pigment stones. In Eastern countries, the high incidence of calcium stones bilirubinat could relate to secondary bacterial invasion of the bile ducts in the stem of the parasite infection Clonorchis sinensis or Ascaris lumbricoides. E. coli B-form is considered mendekonjugasikan glukoronidase bilirubin in the bile, which could support the formation of calcium bilirubinat insoluble. Kind, among others: a. Bilirubinan pigment calcium stones (brown pigment) Also called mud or stone pigment stones, brown or dark brown colored, soft, easy to destroy and contain calcium-bilirubinat as the main component. This brown pigment stones are generally formed in the bile duct in the infected bile. Brown pigment stones are usually found with a diameter of less than 1 cm, yellowish brown, soft and often found in Asia. These stones are formed due to factors stasis and biliary tract infections. Stasis can be caused by sphincter of Oddi dysfunction, strictures, biliary surgery, and parasites. Biliary infection, excess β-glucuronidase activity of bacteria and human (endogenous) play a key role in the pathogenesis of pigment stones in patients in the east. Bilirubin by the enzyme hydrolysis to form conjugated bilirubin can not be precipitated as calcium bilirubinate. Bacterial β-glucuronidase enzyme from the bacteria E. coli and other bacteria in the bile duct. This enzyme can be inhibited by glucarolactone the concentration is increased in patients with low-protein diet and low fat. b. Black pigment stones. Black or brownish black, shapeless, like the rest of the powder and rich black substance that was extracted. Black pigment stones are rock types which are found in patients with chronic hemolysis or cirrhosis of the liver. Black pigment stones are mainly composed of polymerized bilirubin derivatives. Potogenesis stone formation is unclear. Generally, the black pigment stones are formed in the gall bladder with sterile bile. These types of gallstones are generally small, black with a rough surface. Usually these pigment stones containing less than 10% cholesterol. 3. Mixture of stone A mixture of cholesterol stones containing calcium. These stones are found almost around 90% in patients kolelitiasis. These rocks are diverse, dark brown. Most of the stone mixture has the same basic metabolism with cholesterol stones. Cholesterol stones and pigment mixture which contains 20-50% cholesterol.



                                            Figure 4. Classification of stones in the gallbladder

Bilirubin stone formation consists of two phases:
a. Saturation of bilirubin
In the state of non-infectious, bilirubin saturation occurs because of excessive red cell breakdown, such as the malaria and the disease Sicklecell. In the state of saturation of infection due to conversion of conjugated bilirubin into bilirubin unkonjugasi poorly soluble. Conversion occurs because of b glukuronidase enzyme produced by Escherichia coli. In normal circumstances bile containing 1.4 glokaro glukuronidase lactone that inhibits work.
b. Formation of rock core
Stone formation in addition to the core by the calcium salts and also by bacterial cells can be, part of the parasite and worm eggs. Tatsuo Maki reported that 55% of pigment stones with the egg nucleus or a body of the worm Ascaris lumbricoides. While Tung from Vietnam to get 70% of the core stone is of hookworm.
Clinical Manifestations
Patients with gallbladder stones give a new complaint if the stone migrated cystic duct or duct clogging koledokus, so the clinical picture varies from no symptoms (asymptomatic), mild to severe complications due.
Pain in the area found the right hipokondrium, which is sometimes accompanied by biliary colic arising settled / constant. Sometimes pain in the area subkapula dijalarkan up with nausea, vomiting and dyspepsia, flatulen and others. On physical examination tenderness hipokondrium earned the right, may be palpable enlargement of the gallbladder and a positive Murphy sign. Jaundice may also occur. Jaundice observed in 20% of cases, mostly mild (bilirubin <4.0 mg / dl). If the high bilirubin levels, should be considered a stone in the extra hepatic bile duct. Biliary colic is a major complaint in most patients. Visceral pain is coming from spasmetonik transient cystic duct obstruction by stones. Biliary colic is a term implied by the notion that the gall bladder mucosa showed no acute inflammation. Biliary colic usually occurs at night or early morning, lasts a long time between 30-60 minutes, settled, and the pain mainly arises in the epigastric region. Abdominal pain may spread to the right, to the shoulders, back, rarely to the left abdomen and may mimic angina pectoris. Biliary colic must be differentiated with dyspeptic symptoms which are common symptoms in many patients with or without kolelitiasis. Diagnosis and management are good and right can prevent serious complications. Complications from gall bladder stones among other acute cholecystitis, chronic cholecystitis, koledokolitiasis, pancreatitis, cholangitis, secondary biliary cirrhosis, gallstone ileus, hepatic abscess and peritonitis due to perforation of the gallbladder. Complications will be difficult to handle and can be fatal. Most (90-95%) of cases with acute kolesititis kolelitiasis and circumstances arising from cystic duct obstruction that causes inflammation of these organs. Patients with chronic cholecystitis usually have kolelitiasis and has often had attacks of biliary colic or acute cholecystitis. This condition causes a thickening and fibrosis of the gallbladder and in 15% of patients with other diseases such as koledo kolitiasis, panleneatitis and kolongitis. Gall bladder stones may migrate into koledokus duct through the cystic duct (secondary koledokolitiasis) or gall stones may also form in the bile ducts (primary koledokolitiasis). Koledokolitiasis course of the disease is highly variable and difficult to forecast the start of asymptomatic until the onset of significant obstructive jaundice. Bile duct stones (BSE) can be entered into the duodenum of small spontaneously without causing any symptoms or cause temporary obstruction at the ampulla of Vater causing acute pancreatitis and then enter the duodenum (gallstone pancreatitis). BSE is not out spontaneously remains in the bile ducts and can be enlarged. Clinical picture is dominated penyulitnya koledokolitiasis as obstructive jaundice, cholangitis and gallstones pankreatitis.Penderita often have symptoms of acute or chronic kolestitis. Acute form is characterized by sudden severe pain in upper abdomen, especially amid the epigastrium. Then the pain radiating to the back and right shoulder (Murphy sign). The patient may sweat a lot and rolled from side to side during sleep. Nausea and vomiting are common. Pain can last for hours or can be repeated. 3 The symptoms of chronic cholecystitis is similar to the acute phase, but the severity of pain and physical signs are less obvious. Often there is a history of dyspepsia, fat intolerance, heartburn, or prolonged flatulen. Once formed, gallstones can dwell in peace in the gallbladder and cause no problem, or it may cause complications. The most frequent complication is infection of the gallbladder (cholecystitis) and obstruction of the cystic duct or duct koledokus. This obstruction may be temporary, intermittent and permanent. Sometimes stones can break through the gallbladder wall and causes severe inflammation, often leading to peritonitis, or cause rupture of the gallbladder wall. Gall Bladder Stone (Kolesistolitiasis) A. Asymptomatic Contained stones in the gallbladder are often no symptoms (asymptomatic). Can give symptoms of acute pain due to cholecystitis, biliary pain, chronic recurrent abdominal pain or dyspepsia, nausea. The study course of the disease up to 50% of all patients with gallbladder stones, regardless of type, are asymptomatic. Less than 25% of patients who actually have asymptomatic gallstones will experience symptoms that require intervention after wakti period of 5 years. No data are recommending routine cholecystectomy in all patients with asymptomatic gallstones. 2. Symptomatic The main complaint of pain in the epigastrium, right upper quadrant. Another pain of biliary colic that lasted more than 15 minutes, and sometimes new disappeared several hours later. Biliary colic, right upper quadrant pain pascaprandial, usually precipitated by fatty foods, occurs 30-60 minutes after eating, ended after a few hours and then recovered, caused by gallstones, biliary colic is referred to as. Nausea and vomiting often associated with biliary colic attacks. 3. Complication Acute cholecystitis is a complication of gallstone disease is most common and often led to abdominal emergencies, especially among middle-aged and elderly women. Acute inflammation of the gallbladder, cystic duct obstruction related to or in the infundibulum. A typical picture of acute cholecystitis is upper right abdominal pain is sharp and constant, either acute attacks or previous preceded by discomfort in the post-prandial epigastric region. This pain increases with inspiration or with movement and can spread kepunggung or to the end of the scapula. Complaints may be accompanied by nausea, vomiting and decreased appetite, which can last for days. Can be found on examination signs of toxemia, tenderness in the right upper abdomen and the classic signs of "Murphy sign" (the patient stops breathing while the upper right abdomen is pressed). Period which may be palpable found only in 20% of cases. Most patients eventually will have an open or laparoscopic cholecystectomy. Channel Gall stones (Koledokolitiasis) At koledokus duct stones, a history of pain or colic in the epigastrium and right upper abdomen accompanied by signs of sepsis, such as fever and chills in the event of cholangitis. Arise if the attack is generally accompanied by obstructive cholangitis, clinical symptoms will be found that correspond to the severity of cholangitis. Acute cholangitis is usually mild to moderate non-pyogenic bacterial cholangitis is characterized by Charcot's triad is fever and chills, pain in liver area, and jaundice. In the event of kolangiolitis, usually in the form of intrahepatic pyogenic cholangitis, there will be 5 pentade Reynold symptoms, three symptoms of Charcot's triad plus shock, and mental disorder or impairment of consciousness to coma. Koledokolitiasis often cause very serious problems due to mechanical complications and infections that may be life threatening. Koledokus duct stones accompanied by bakterobilia in 75% percent of patients and the presence of bile duct obstruction, acute cholangitis may arise. Severe episodes of acute cholangitis can cause liver abscess. Migration of small gallstones through the ampulla of Vater when there is a general line between the duct and pancreatic duct distal koledokus can cause gallstone pancreatitis. Gallstone lodged in the ampulla will cause obstructive jaundice. Complication Complications that can occur in patients kolelitiasis: 1. Asymptomatic 2. Cystic duct obstruction 3. Biliary colic 4. Acute cholecystitis • Perikolesistitis • Inflammation of the pancreas (pancreatitis) • Perforation 5. Chronic cholecystitis • Hidrop gallbladder • Empyema of the gallbladder • fistula kolesistoenterik • Ileus gallstone (gallstone ileus) 6. Gallstones are secondary (at 2-6% of patients, gastrointestinal and biliary stones shrink back up again) Kolesistokinin secreted by the duodenum because of the food produce gallbladder contraction, so that the stones in the gall bladder was pushed and can cover the cystic duct, the stones can settle or be apart again. If the stone covering the duct sitikus be settled then it will probably occur mukokel, if there is an infection, the mukokel can be an empyema, gallbladder usually surrounded and covered by means of the stomach (colon, omentum), and can also form a fistula kolesistoduodenal. Blockage of the cystic duct may also result in acute cholecystitis who can heal or may lead to necrosis of the wall (can be covered sekiatrnya tools) and can form a kolesistoduodenal fistula or perforation of the gallbladder can occur which results in peritonitis generalisata.3 Gall bladder stones can be advanced into the cystic duct during contraction of the gallbladder. This stone can move forward until the duct koledokus then settle sometimes asymptomatic or can cause colic. A clog in the duct stones koledokus also result in obstructive jaundice, cholangitis, kolangiolitis, and pankretitis. Gallbladder stones can pass into the gastrointestinal tract through a fistula formation kolesitoduodenal. If gallstones are large enough to clog the pad the narrowest part of the gastrointestinal tract (terminal ileum) and cause obstruction ileus. Diagnosis Anamnesis Half to two-thirds of patients are asymptomatic kolelitiasis. Complaints that may arise is dyspepsia are sometimes accompanied by intolerance to fatty foods. At the symptomatic, the chief complaint of pain in the epigastrium, right upper quadrant or perikomdrium. More pain is biliary colic may last more than 15 minutes, and sometimes new disappeared several hours later. Onset of pain but most slowly in 30% of cases arise suddenly. Spread of pain in middle back, scapula, or shoulder to the peak, accompanied by nausea and vomiting. Over a quarter of patients reported that pain was reduced after using antacids. If there kolelitiasis, persistent complaints of pain and increase the time a deep breath. a. Physical examination Gallbladder stones If abnormalities are found, usually associated with complications, such as acute cholecystitis with local or general peritonitis, hidrop gallbladder, gallbladder empyema, or pankretitis. On examination found tenderness with maximum punktum anatomical location of the gall bladder area. Murphy sign positive if tenderness increased when the patient took a deep breath because of an inflamed gallbladder fingertips touched the patient stops breathing. Bile duct stones New bile duct does not cause symptoms in a quiet phase. Sometimes palpable hatidan jaundiced sclera. Need diktahui that if the blood bilirubin levels less than 3 mg / dl, jaundice is not clear. If the blockage of the bile duct to gain weight, there will be clinical jaundice. b. Examination Support Laboratory tests Gallbladder stones are generally asymptomatic showed no abnormalities in laboratory tests. In the event of acute inflammation, leukocytosis may occur. In the event of mirizzi syndrome, will be found a mild increase in serum bilirubin due to suppression by koledukus duct stones. High levels of serum bilirubin may be caused by a stone in the duct koledukus. Serum alkaline phosphatase levels and serum amylase levels may also typically increases whenever there is any acute attacks. Radiological examination Plain photo abdomen Plain abdominal usually do not give a distinctive because it is only about 10-15% of gallbladder stones that are radioopak. Sometimes gallbladder bile containing high levels of calcium can be seen with a plain photo. In the acute inflammation of the gallbladder with an enlarged or hydrops, gallbladder sometimes seen as a soft tissue mass in the upper right quadrant of the picture of the air pressure in the colon, hepatic flexure on.



                                                      Figure 3. Photo rongent on kolelitiasis

Pemeriksaan Ultrosonografi (USG)
Ultrasonography has a degree of specificity and high sensitivity for the detection of gallbladder stones and intrahepatic bile duct dilation and extra hepatic. Ultrasound can also be seen with gallbladder wall thickening due to fibrosis or edema caused by inflammation or other causes. Duct stones found on the distal koledukus sometimes difficult to detect because it was blocked by the air in the intestine. With ultrasound punktum maximum pain on a gangrenous gallbladder stones more clearly than with ordinary palpation.
Ultrasound can provide a fairly complete information concerning:
• Ensure the presence of gallstones
• Demonstrate how the existing gallstones and also its size.
• Looking at the location of gallstones proficiency level. Whether in the gallbladder or in
in the duct.

There are two types of examination using ultrasound, namely:
 transabdominal ultrasonography
This examination is painless, inexpensive and does not harm the patient. Nearly 97% of gallstones can be diagnosed by transabdominal ultrasonography, but less well in identifying gallstones located in the duct and gall stones can only identify with a larger size than 45 mm.

 endoscopic ultrasonography
Endoscopic ultrasonography can provide a better picture than transabdominal ultrasound. Because it is more invasive and can also detect gallstones in the bile ducts located better. The drawback is expensive in terms of cost and pose a risk to patients.

Ultrasonography has a degree of specificity and high sensitivity for the detection of gallbladder stones and intrahepatic bile duct dilation or extrahepatic. You can view a thickened gallbladder wall due to fibrosis or edema due to inflammation or other causes. Duct stones found on the distal koledokus sometimes difficult to detect, because the air in the intestine is blocked. By ultrasonography punktum maximum pain relief for a gangrenous gallbladder stones more clearly than with ordinary palpation.


                                                    Figure 5. photo of USG on kolelitiasis

Kolesistografi
For certain patients, kolesistografi by contrast quite well because it is relatively inexpensive, simple, and accurate enough to see radiolucent stones so that they can count the number and size of the stone. Oral Kolesistografi will fail in a state of paralytic ileus, vomiting, bilirubun serum levels above 2 mg / dl, okstruksi pylorus, and hepatitis due to the circumstances of the contrast can not reach the heart. Kolesitografi oral examination more meaningful to the assessment of gallbladder function.


                                                              Fig 6. results Kolesistografi

CT scan
Showed gallstones and bile duct dilatation.


                                Figure 7. CT scan of upper abdomen showing multiple gallstones

ERCP (Endoscopic Retrograde Cholangio Pancreatography)
Namely a cannula is inserted into the duct and duct koledukus pancreatikus, then the contrast material is injected into the duct. ERCP function facilitates direct visualization of the biliary structures and facilitate access to the duct koledukus distal to retrieve gallstones, but it serves to distinguish ERCP jaundice caused by liver disease (jaundice hepatocellular jaundice due to biliary obstuksi and can also be used to investigate gastrointestinal symptoms in patients who had gall bladder diangkat.ERCP risk of occurrence of these signs of perforation / infection.


Figure 8. ERCP showed gallstones in the extrahepatic duct (short arrow) and intrahepatic duct (long arrow)

Magnetic Resonance-Pancreatography Cholangio (MRCP)
Magnetic resonance-Pancreatography Cholangio or MRCP is a modification of Magnetic Resonance Imaging (MRI), which allows to observe the bile duct and pancreatic duct. MRCP can detect gallstones in the bile duct and also when there is obstruction of the duct.


                                                           Figure 9. The results of MRCP

Management
Conservative
a) lysis of stone with drugs
The majority of patients with asymptomatic gallstones will have no complaints and the number, magnitude and composition of rocks is not related to the onset of complaints during the monitoring. If complaints arise later on so that treatment can generally mild elective.
A common problem that interferes with all substances ever used is a high recurrence rate and the cost incurred. Dissolution of substances beneficial to only show the type of cholesterol gallstones. Randomized prospective study of acid xenodeoksikolat has indicated that the dissolution and complete loss of the stone occurs in about 15%. If the drug is discontinued, the stone recurrence occurred in 50% pasien.10 Less than 10% of gallstones do this and previous medical dissolution sukses.2 must meet the criteria of non-operative therapies such as cholesterol stone diameter <20 mm, the stone is less than 4 stones, good gallbladder function and a patent cystic duct. Acid dissolution therapy with ursodeoksilat to dissolve cholesterol gallstones takes 6-12 months of drug administration and monitoring required to achieve dissolution. Effective therapy in a small stone size of 1 cm with a 50% recurrence rate within 5 years. Contact dissolution Although experience is still limited, the infusion of the potent cholesterol solvent (Methyl-Ter-Butyl-Ether (MTBE)) into the gallbladder through a catheter that has been seen placed percutaneous effective in dissolving gallstones in selected patients. This procedure is invasive and its main disadvantage is the high recurrence rate (50% within 5 years). The method is based on the principle of direct instilasi PTC and solvent of cholesterol into the gallbladder. This procedure is invasive and its main disadvantage is the high recurrence rate. b) lithotripsy (Extarcorvoral Shock Wave Lithotripsy = ESWL) Wave lithotripsy elektrosyok although very popular a few years ago, cost-benefit analysis at this point is limited to patients who have actually been considered for this therapy. Effectiveness of ESWL require adjuvant therapy ursodeoksilat acid. Very popular to use a few years ago, cost-benefit analysis of the current pad to show that this procedure is limited to patients who have been seriously considered for this therapy.

                                               Figure 10. Elektrosyok wave lithotripsy (ESWL)

Operative treatment
a) Open cholecystectomy
This operation is a standard for the treatment of patients with symptomatic gallstones. The most common indications for cholecystectomy were biliary colic recurrence, followed by acute cholecystitis. Severe complications are rare, including CBD trauma, hemorrhage, and infection. Recent data show that mortality in patients undergoing open cholecystectomy in 1989, overall mortality 0.17%, in patients less than 65 years 0.03% while the mortality rate in patients over 65 years the death rate reached 0.5 %.
b) laparoscopic Cholecystectomy
Advantages of this action include more minimal postoperative pain, faster recovery, better cosmetic results, truncate hospitalization and lower cost. Most common indication is recurrent biliary pain. Absolute contraindications are similar to open the action can not tolerate a general anesthetic action and coagulopathy that can not be corrected. Complications of bleeding, pancreatitis, cystic duct stump leak and bile duct trauma. The risk of bile duct trauma is often discussed, but generally range between 0.5-1%. By using the laparoscopic technique better quality of recovery, there is no pain, re-run the normal activities within 10 days, return to work quickly, and all the abdominal muscles intact so it can be used for sporting activities.

                                                  Figure 11. Cholecystectomy laparaskopi

c) Cholecystectomy minilaparatomi.
Modification of action open cholecystectomy with a smaller incision with the effects of lower postoperative pain.
d) Kolesistotomi
Kolesistotomi that can be done with local anesthesia even at the bedside of patients continue to be a useful procedure, especially for patients who are critically ill.
e) Endoscopic retrograde cholangiopancreatography (ERCP)
At ERCP, an endoscope is inserted through the mouth, esophagus, stomach and into the small intestine. Radioopak contrast agent into the biliary tract through a tube in the sphincter of Oddi. In the sphincterotomy, sphincter muscle rather wide open so that gallstones that block the channel will move to the small intestine. ERCP and sphincterotomy was successfully performed in 90% of cases. Less than 4 of every 1,000 patients who died, and 3-7% have complications, so the procedure is safer than abdominal surgery. ERCP is usually effective only performed in patients with bile duct stones are older, the gall bladder was removed.

                              Figure 12. Endoscopic retrograde cholangiopancreatography (ERCP)

Diet Management
In the case of kolelitiasis amount of cholesterol in bile is determined by the amount of fat eaten because the hepatic cells synthesize cholesterol from lipid metabolism, so that the client is recommended / restricted to the liquid diet low in fat. Avoiding high cholesterol is mainly derived from animal fats. Supplement high in protein and carbohydrate powder can be stirred into skim milk and as for additional food such as cooked fruit, rice, sweet potatoes, lean meat, vegetables that do not form a gas, bread, coffee / tea.

Treatment Selection Considerations
1) Location
Locations can be various kinds of gallstones in the gallbladder, cystic duct, koledokus duct, ampulla of Vater, in the heart. Stones in the gallbladder that does not give or gejalagejala complaints (asymptomatic) to let it go. When symptoms occur, usually due to stone migration into the neck of the gallbladder or duct koledokus entered, then this stone to be removed. Migration to the neck of the gall bladder stones will cause cystic duct obstruction. This situation resulted in a chemical irritation of the mucosa of the gallbladder bile was left so that there was an acute or chronic cholecystitis, depending on the severity of mucosal changes. (1) In patients with symptomatic gallbladder stones can be done conventionally or cholecystectomy by laparoscopy.
Gallstone stuck in the cystic duct, cystic duct at the mouth of the duct koledokus, can suppress the duct or duct hepatikus koledokus communist causing obstruction (Mirizzi syndrome). (7) The stone is to be removed by surgery. If not removed will cause obstruction to complications such as cholangitis or sepsis and obstructive jaundice can lead to liver failure or biliary cirrhosis.
Koledokus stone must be removed as it will result in biliary obstruction that can impair liver function to cause liver failure. Apart from that bile flow is not smooth cholangitis can cause complications - sepsis. Expenditure koledokus stone can be done with conventional surgery or by means through which the endoscope with endoscopic sphincterotomy and stone extraction by Dormia basket.
Intrahepatic gallstones or gallstone hepatolitiasis is located in the intrahepatic bile ducts. (4) intrahepatic stones found in 20% of cases with gallstones. (5) The problem is very different intrahepatic stones with biliary stones, others because its management is difficult surgery; some- sometimes required repeated surgery because of frequent relapses and ultimately patients often suffer from liver damage due to obstructive jaundice that long, cholangitis, multiple liver abscesses and sepsis. When the small intrahepatic stones and the number 1 or 2 pieces only and is located in the distal, can be tried out with the Dormia basket through the endoscope. When the operation that required a lot of different operations to another gallstone.
2) Size
Koledokus stones with a diameter of more than 1 cm are broken down first in order to more easily removed by endoscopy. There are several ways to break this stone, namely (i) of the mechanical Litotriptor Suhendra: This is a long way, can now be used mechanical litotriptor BML from Olympus. In principle, this technique after a stone caught in the basket and the basket is tightened the grip of a special tool so that the stone is split. Another way is (ii) hydraulic Litotriptor, (iii) laser Litotriptor, (iv) Litotriptor ultrasonic, (v) Litotriptor "piezoceramic", (vi) "Extracorporeal Shock Wave Lithotripsy" (ESWL), is the most good. After a large gallstone was fragmented into several small parts, with a Dormia basket stone is extracted from the duct koledokus. Smaller stones are elusive to the basket using a balloon catheter removed. Catheter with a balloon that has not blown so that entered into the bile duct to the top of the stones. The balloon then is pulled down and blown up out of the papilla of Vater. Thus small batubatu with bile sludge can be issued.
3) The composition of the rock
Gallbladder stones composed of cholesterol is easily broken down by ESWL. In Indonesia in general, gallbladder stones rather than cholesterol stones that ESWL is less useful. Koledokus duct stones in Indonesia also in general rather than cholesterol stones so that the use of ESWL for stone crushing koledokus apparently not much help.
4) The anatomy of the distal koledokus
Koledokus distal part narrow and elongated stones would make it difficult spending by endoscopy. In this state should be spending stones through surgery.
5) The presence of complications of acute cholangitis or acute pancreatitis
The existence of these complications, complications indicate the need for immediate action. In the acute cholangitis in a while in a state of emergency could be installed pipe nasobilier and adequate antibiotic treatment. After the acute condition is resolved and the patient's general condition had improved to act in a way that is definitive elective surgery or remove the stone through the endoscope to perform sphincterotomy and stone extraction by Dormia basket.
In the acute pancreatitis is usually caused by gallstones block the papilla of Vater small, needs to be done by way of endoscopic sphincterotomy and stone extraction so that the flow of bile and pancreatic juice into the duodenum becomes smooth again.
In everyday practice is not rare circumstances where the patient is sent to a specialist in internal medicine by a surgeon with a problem that after cholecystectomy because of gall bladder stones, the patient remained jaundiced jaundice or even more. Having evaluated the patient was also suffering from stone koledokus that escaped detection. Abdominal ultrasound showed only preoperative gallbladder stones. It is in fact at the clinic, 10-15% of patients with gallbladder stones, also contains a stone in the duct koledokus.
How to avoid it is not difficult to see that the liver function before surgery. When gamma glutamyl transferase (GGT) or alkaline phosphatase greatly increased, especially when bilirubin increased, the suspect in koledokus stone.
On physiology liver gall bladder stones are usually not disturbed. In this case, ultrasound can not always visualize koledokus stone because of the air in the colon and the duct koledokus intrahepatic bile duct and not always in rock koledokus widened. In general it intra and extrahepatic bile duct stones widened in koledokus.
It needs to be done cholangiography such as "Endoscopic Retrograde Cholangio Pancreatography" (ERCP) to confirm the presence or absence of obstruction in the bile duct. Sometimes koledokotomi after surgery, the patient was still there colic and jaundice caused by a stone left in the duct koledokus. It is unknown at the time the patient has not come home from the hospital and sometimes the patient is still in intensive care unit or in the "recovery room" some time after surgery. Certainly less acceptable when the patient is recommended for at laparotomy again to remove the remaining stones.
In this case the act of spending per endoscopic bile duct stones can resolve the issue. In patients with stones accompanied koledokus gallbladder stones when the gallbladder is still well and asymptomatic gall bladder stones the gall bladder stone is left alone while koledokus removed by endoscopy. When overdo bile showed signs of chronic cholecystitis, made of stone koledokus expenditure per endoscopy followed by cholecystectomy via laparoscopy at the next opportunity.

REFERENCES

1. Norman, A. 1999. Penatalaksanaan Batu Empedu
2. Lesmana L. Batu Empedu dalam Buku Ajar Penyakit Dalam Jilid 1. Edisi 3. Jakarta: Balai
Penerbit Fakultas Kedokteran Universitas Indonesia. 2000.380-4.
3. Schwartz S, Shires G, Spencer F. Prinsip-prinsip Ilmu Bedah (Principles of Surgery.
Edisi 6. Jakarta: Penerbit Buku Kedokteran EGC. 2000.459-64.
4. Sjamsuhidayat R, de Jong W. Buku Ajar Ilmu Bedah. Edisi 2. Jakarta: Penerbit Buku
Kedokteran EGC. 2005. 570-9.
5. Price SA, Wilson LM. Kolelitiasis dan Kolesistisis dalam : Patofisiologi. Konsep Klinis
Proses-Proses Penyakit, edisi 4. Jakarta : EGC. 1995. 430-44.
6. Clinic Staff. Gallstones. Available from:
http:/www.6clinic.com/health/digetivesystyem/DG9999.htm.
7. Cholelithiasis. Available from:
http:/www.7.com/healthmanagement/ManagingYourHealth/HealthReference/Disease/InDepth.htm.
8. Latchie M. Cholelitiasis dalam : Oxford Handbook of Clinical Surgery. Oxford University.
1996. 162
9. Kasper DL et al. Cholelitiasis, Cholesistitis, and Cholangitis dalam: Harrisons Manual
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1 comment:

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