gall stone disease+compilcations

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gall stones and its complications


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GALLSTONE disease “ CHOLELITHIASIS” Dr Nishant Sagar

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The Gallbladder and Biliary System with Pancreas

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The Gall Bladder and Bile Ducts Fundus

Anatomical Position of the GB:

Anatomical Position of the GB Gallbladder IVC Lesser Omentum Common Bile Duct GB in situ , anterior view

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What are these pathological specimens? What are their likely chemical composition?

Cholelithiasis (Gallstones):

Cholelithiasis (Gallstones)


INTRODUCTION Definition. CHOLELITHIASIS refers to presence or formation of gallstones in the gallbladder or bile ducts. Gallstones are the most common biliary stones. Overall prevalence of gallstones of 7.9% in men and 16.6% in women In Acute Cholecystitis gallstones are present in about 95% of cases -calculous cholecystitis. The exact incidence of acute Cholecystitis among patients who harbor gallstones is not known but in about 20% of patients who enter a hospital for biliary tract disease have acute cholecystitis . 7


PATHOGENESIS OF GALLSTONES Pathogenesis of cholesterol gallstones involves: 1) cholesterol supersaturation in bile, exceeding their maximum solubilities 2) crystal nucleation-mucin & non mucin GP A1,AII 3) gallbladder dysmotility, The underlying factors implicated are: Metabolic factor Stasis factor Reflux factor Infective factor 8


1.METABOLIC FACTOR The solubility of bile cholesterol depends on the concentration of lithogenic (supersaturated) bile salts and phospholipids(licithin predominantly) in the bile. Cholesterol is insoluble in aquaous solution. It is dissolved in bile acids into micelles along with phospholipids. The normal ratio of bile acid to cholesterol is 25:1. When this ratio fall to 13:1, the cholesterol precipitates and gallstone forms. 9


MICELLES Central core-cholesteral shell-bile salts and lecithin


2.BILE STASIS FACTOR Temporary cessation of bile flow into intestine and stagnation of bile in the gallbladder has increminated a major factor in producing gallstones. Bile flow interruption Impair s enterohepatic circulation  decrease output of bile salts and phospholipids  reduce solubility of cholesterolgallstone formation. 11


3. REFLUX FACTOR Pancreatic enzymes have been dectated in gallbladder of patients suffering from cholelithiasis. Reflux of pacreatic enzymes into gallbladder is also considered to be the cause of cholesterol precipitation Trypsin disturbs colloidal balance and pancreatic phospholipase A which may convert lecithin into toxic lysolecithin.


4.INFECTIVE FACTOR The role of infection in causing stones is unclear. Under “normal” conditions, the biliary tract is sterile Positive cultures found: 11-30% symptomatic stones & chronic cholecystitis 46% of acute cholecystitis 58% with gallstones & CBD stones without cholangitis 94% with gallstones, CBD stones and cholangitis 13


Organisms Gram-negative aerobes most common E. coli Klebsiella Pseudomonas Enterobacter Gram-positive aerobes Enterococcus Streptococcus viridans Anaerobes (~25%) Bacteroides fragilis Clostridium Fungal Candida sp. Parasitic Opisthorchis sp. (Thailand) (Liver fluke) Clonorchis sp. (China) Approximately 50% of positive cultures will have 2 or more different bacteria species present


5.HEMOLYTIC FACTOR -PIGMENTED STONE Hemolysis: - Increases bilirubin production thus forming PIGMENT STONES seen in Hereditary spherocytosis sickle cell anaemia , thalassaemia , malaria mechanical destruction of red cells by prosthetic heart valves. In ducts with benign or malignant strictures Cirrhosis Infestation of biliary tree with clonorchis sinensis and ascaris lumbricoldes . Saints triad: Gallstones, diverticulosis of the colon hiatus hernia. Therefore, it is important to find out which lesion is the cause of the patient’s dyspeptic symptoms. 15


TYPES OF GALL STONES 1. CHOLESTEROL STONES – - . Cholesterol gallstones usually contain >50% cholesterol monohydrate plus an admixture of calcium salts, bile pigments, and proteins 2. PIGMENT STONES Composed almost entirely of calcium bilirubinate. They are mostly small, black and multiple. Some are hard and coral like, others are soft and really concretions of sludge rather than stones.Two types Hemolysis and liver disease are associated with the black stones; the brown, earthy stones more frequently are formed outside the gallbladder and often are associated with bacterial infections of the biliary tract 16

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3. MIXED STONES Cholesterol is the major component. Other components includes calcium bilirubinate, calcium palmitate, calcium carbonate, calcium phosphate and proteins. They are usually multiple and often they are faceted. .

Cholesterol stones:

Cholesterol stones

Pigment stones :

Pigment stones


RISK FACTORS OF GALLSTONES 1 Non modifiable factors Increasing age Female gender Ethnicity Genetics, family history


2 Modifiable factors Pregnancy and parity-GB sludge in 25%,stones in 10% Obesity Low-fiber, high-calorie diet Prolonged fasting Drugs: clofibrate , ceftriaxone Oral contraceptives Low-level physical activities Rapid weight loss (> 1.5 kg/wk) Hypertriglyceridemia /low high-density lipoprotein Metabolic syndrome Gallbladder stasis Specific diseases ( ie , cirrhosis, Crohn’s disease with severe ileal involvement/resection)


Age. People older than age 60 are more likely to develop gallstones than younger people. As people age, the body tends to secrete more cholesterol into bile. 2. Sex. Women are twice as likely as men to develop gallstones. Excess estrogen from pregnancy, hormone replacement therapy, and birth control pills appears to increase cholesterol levels in bile and decrease gallbladder movement, which can lead to gallstones.


3. Ethnicity. American Indians have a genetic predisposition to secrete high levels of cholesterol in bile. In fact, they have the highest rate of gallstones in the United States. The majority of American Indian men have gallstones by age 60. Among the Pima Indians of Arizona, 70 percent of women have gallstones by age 30. Mexican American men and women of all ages also have high rates of gallstones.


4. Family history. Gallstones often run in families, pointing to a possible genetic link. The prevalence of gallstones is increased in families and in identical twins of patients who have gallstones. The genes responsible for biliary lipid transport across the hepatic canaliculi and for lipid metabolism have been identified. ABCG5/G8 CYP7A1 MDR3


5.Metabolic diseases eg. diabetes mellitus, chronic hemolysis,* alcoholic cirrhosis,* biliary infection,* primary biliary cirrhosis, duodenal diverticula,* truncal vagotomy, hyperparathyroidism, low level of high-density lipoprotein cholesterol Diabetes. People with diabetes g enerally have high levels of fatty acids called triglycerides. These fatty acids may increase the risk of gallstones.


6.Weight. a)Overweight . A large clinical study showed that being even moderately overweight increases the risk for developing gallstones. The most likely reason is that the amount of bile salts in bile is reduced, resulting in more cholesterol. Increased cholesterol reduces gallbladder emptying. Obesity is a major risk factor for gallstones, especially in women.


b) Rapid weight loss (> 1.5 kg/wk ). The increased risk associated with rapid weight loss may be due to an increase in the ratio of cholesterol to bile salts in the gallbladder and to bile stasis resulting from a decrease in gallbladder contractions As the body metabolizes fat during prolonged fasting and rapid weight loss—such as “crash diets”—the liver secretes extra cholesterol into bile, which can cause gallstones. In addition, the gallbladder does not empty properly.


7.Diet. Diets high in fat and cholesterol and low in fiber increase the risk of gallstones due to increased cholesterol in the bile and reduced gallbladder emptying 8.Cholesterol-lowering drugs. Drugs that lower cholesterol levels in the blood actually increase the amount of cholesterol secreted into bile. In turn, the risk of gallstones increases.


CLINICAL PICTURE As gallstones move into the bile ducts and create blockage, pressure increases in the gallbladder and one or more symptoms may occur. Symptoms of blocked bile ducts are often called a gallbladder “attack” because they occur suddenly. Gallbladder attacks often follow fatty meals, and they may occur during the night.


Gallstone disease may be thought of as having the following 4 stages: -The lithogenic state, in which conditions favor gallstone formation Asymptomatic gallstones Symptomatic gallstones, characterized by episodes of biliary colic Complicated cholelithiasis


1.SYMPTOMATOLOGICAL FINDINGS Biliary colic is usually caused by the gallbladder contracting in response to hormonal or neural stimulation, usually due to a fatty meal, forcing a stone (or possibly sludge or microlithiasis) against the gallbladder outlet or cystic duct opening, and leading to increased intra-gallbladder pressure and pain. The stones often fall back from the cystic duct as the gallbladder relaxes. As a result, the discomfort progresses in less than an hour to a steady plateau that ranges from moderate to excruciating and remains constant for more than an hour, then slowly subsides over several hours. In some patients the pain is not very severe, which is why patients often have several attacks before seeking medical attention


1.SYMPTOMATOLOGICAL FINDINGS Biliary colic begins quite suddenly and may persist with severe intensity for 15 min to 5 h, subsiding gradually or rapidly. Frequent radiation to the interscapular area, right scapula, or shoulder. It is steady intense dull pressure-like discomfort rather than intermittent as would be suggested by the word colic , which must be regarded as a misnomer, although it is in widespread use. Diaphoresis,nausea and vomiting frequently accompany episodes of biliary pain. Biliary colic may be precipitated by eating a fatty meal, by consumption of a large meal following a period of prolonged fasting, or by eating a normal meal; it is frequently nocturnal, occurring within a few hours of retiring. One group suggested that the pain had a circadian pattern, peaking at 9:30 PM . In most cases, the pain has a characteristic pattern and timing for individual patients


WARNING FEATURES An episode of biliary pain persisting beyond 5 hours should raise the suspicion of acute cholecystitis. An elevated level of serum bilirubin and/or alkaline phosphatase suggests a common bile duct stone Fever or chills (rigors) with biliary pain usually imply a complication, i.e., cholecystitis, pancreatitis, or cholangitis


2. PHYSICAL FINDINGS Patients with simple biliary colic are not usually ill appearing and do not have fever or tachycardia. There are no peritoneal signs since the pain is purely visceral without gallbladder inflammation. However, voluntary guarding may be encountered depending upon the severity of the pain 35

Treatment :

Treatment SURGERY- laparoscopic cholecystectomy has become the "gold standard" for treating symptomatic cholelithiasis. 1) the presence of symptoms that are frequent enough or severe enough to interfere with the patient's general routine (2) the presence of a prior complication of gallstone disease, i.e., history of acute cholecystitis, pancreatitis, gallstone fistula, etc (3) the presence of an underlying condition predisposing the patient to increased risk of gallstone complications e.g., calcified or porcelain gallbladder (4)Patients with very large gallstones (>3 cm in diameter) and patients having gallstones in a congenitally anomalous gallbladder might also be considered for prophylactic cholecystectomy

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MEDICAL- Ursodeoxycholic acid (UDCA) 10–15 mg/kg per day for 6 months to 2 years, therapy should be limited to radiolucent stones smaller than 5 mm in diameter. Pigment stones are not responsive to UDCA therapy there is also the factor of taking an expensive drug for up to 2 years Stones larger than 15 mm in size rarely dissolve

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Acute cholecystitis Choledocholithiasis Pancreatitis Acute cholangitis Gallstone ileus Gallbladder cancer

Acute cholecystitis:

Acute cholecystitis Acute inflammation of the gallbladder wall usually follows obstruction of the cystic duct by a stone

Clinical features:

Clinical features Acute cholecystitis often begins as an attack of biliary pain that progressively worsens. Approximately 60–70% of patients report having experienced prior attacks that resolved spontaneously. As the episode progresses, however, the pain of acute cholecystitis becomes more generalized in the right upper abdomen, Peritoneal signs of inflammation such as increased pain with jarring or on deep respiration may be apparent. Vomiting is relatively common and may produce symptoms and signs of vascular and extracellular volume depletion. Jaundice is unusual early in the course of acute cholecystitis but may occur when edematous inflammatory changes involve the bile ducts and surrounding lymph nodes.

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low-grade fever is characteristically present, but shaking chills or rigors are not uncommon. The RUQ of the abdomen is almost invariably tender to palpation. An enlarged, tense gallbladder is palpable in 25–50% of patients. Deep inspiration or cough during subcostal palpation of the RUQ usually produces increased pain and inspiratory arrest (Murphy's sign). Abdominal distention and hypoactive bowel sounds from paralytic ileus, but generalized peritoneal signs and abdominal rigidity are usually lacking, in the absence of perforation

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The triad of sudden onset of RUQ tenderness, fever, and leukocytosis is highly suggestive. Typically, leukocytosis in the range of 10,000–15,000 cells per microliter with a left shift on differential count is found. The serum bilirubin is mildly elevated [<85.5 mol/L (5 mg/dL)] in fewer than half of patients one-fourth have modest elevations in serum aminotransferases (usually less than a fivefold elevation). Ultrasound will demonstrate calculi in 90–95% of cases and is useful for detection of signs of gallbladder inflammation including thickening of the wall, pericholecystic fluid, and dilation of the bile duct. The radionuclide (e.g., HIDA) biliary scan may be confirmatory if bile duct imaging is seen without visualization of the gallbladder .


COMPLICATIONS OF CHOLECYSTITIS Mucocele,hydrops and empyema Gangrene and Perforation Fistula Formation and Gallstone Ileus Limey Bile and Porcelain Gallbladder

Treatment of acute cholecystitis:

Treatment of acute cholecystitis Medical Therapy Although surgical intervention remains the mainstay of therapy for acute cholecystitis and its complications, a period of in-hospital stabilization may be required before cholecystectomy. Oral intake is eliminated, nasogastric suction may be indicated, and extracellular volume depletion and electrolyte abnormalities are repaired. Meperidine or nonsteroidal anti-inflammatory drugs (NSAIDs) are usually employed for analgesia because they may produce less spasm of the sphincter of Oddi than drugs such as morphine .

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Intravenous antibiotic therapy is usually indicated in patients with severe acute cholecystitis, even though bacterial superinfection of bile may not have occurred in the early stages of the inflammatory process. Antibiotic therapy is guided by the most common organisms likely to be present, which are E. coli , Klebsiella spp., and Streptococcus spp. Effective antibiotics include ureidopenicillins such as piperacillin or mezlocillin, ampicillin sulbactam, ciprofloxacin, moxifloxacin, and third-generation cephalosporins. Anaerobic coverage by a drug such as metronidazole should be added if gangrenous or emphysematous cholecystitis is suspected. Imipenem/meropenem represent potent parenteral antibiotics that cover the whole spectrum of bacteria causing ascending cholangitis. They should, however, be reserved for the most severe, life-threatening infections when other regimens have failed

Surgical treatment:

Surgical treatment The optimal timing of surgical intervention in patients with acute cholecystitis depends on stabilization of the patient. Urgent (emergency) cholecystectomy or cholecystostomy is probably appropriate in most patients in whom a complication of acute cholecystitis such as empyema, emphysematous cholecystitis, or perforation is suspected or confirmed. Uncomplicated acute cholecystitis should undergo early elective laparoscopic cholecystectomy, ideally within 72 hours after diagnosis.. Delayed surgical intervention is probably best reserved for (1) patients in whom the overall medical condition imposes an unacceptable risk for early surgery and (2) patients in whom the diagnosis of acute cholecystitis is in doubt Seriously ill or debilitated patients with cholecystitis may be managed with cholecystostomy and tube drainage of the gallbladder. Elective cholecystectomy may then be done at a later date .


Choledocholithiasis Passage of gallstones into the CBD occurs in 10–15% of patients with cholelithiasis. The overwhelming majority of bile duct stones are cholesterol stones formed in the gallbladder, which then migrate into the extrahepatic biliary tree through the cystic duct. Primary calculi arising de novo in the ducts are usually pigment stones developing in patients with (1) hepatobiliary parasitism or chronic, recurrent cholangitis; (2) congenital anomalies of the bile ducts (especially Caroli's disease); (3) dilated, sclerosed, or strictured ducts; or (4) an MDR3 (ABCB4) gene defect leading to impaired biliary phospholipids secretion (low phospholipid–associated cholelithiasis).

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CBD stones should be suspected in gallstone patients who have any of the following risk factors: 1) a history of jaundice or pancreatitis, (2) abnormal tests of liver function (3) ultrasonographic or MRCP evidence of a dilated CBD or stones in the duct


Diagnosis The diagnosis of choledocholithiasis is usually made by cholangiography preoperatively by endoscopic retrograde cholangiogram (ERCP) or MRCP or intraoperatively at the time of cholecystectomy


TREATMENT When CBD stones are suspected prior to laparoscopic cholecystectomy, preoperative ERCP with endoscopic papillotomy and stone extraction is the preferred approach if intraoperative cholangiography reveals retained stones, postoperative ERCP can be carried out. The need for preoperative ERCP is expected to decrease further as laparoscopic techniques for bile duct exploration improve


complications Cholangitis Obstructive Jaundice Pancreatitis Secondary Biliary Cirrhosis

Cholangitis :

Cholangitis Cholangitis may be acute or chronic, and symptoms result from inflammation, which usually is caused by at least partial obstruction to the flow of bile. The characteristic presentation of acute cholangitis involves biliary pain, jaundice, and spiking fevers with chills (Charcot's triad) Bacteria are present on bile culture in 75% of patients with acute cholangitis early in the symptomatic course.. Blood cultures are frequently positive leukocytosis is typical. Nonsuppurative acute cholangitis is most common and may respond relatively rapidly to supportive measures and to treatment with antibiotics. In suppurative acute cholangitis , however, the presence of pus under pressure in a completely obstructed ductal system leads to symptoms of severe toxicity—mental confusion, bacteremia, and septic shock.

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Response to antibiotics alone in this setting is relatively poor, multiple hepatic abscesses are often present, and the mortality rate approaches 100% unless prompt endoscopic or surgical relief of the obstruction and drainage of infected bile are carried out. Endoscopic management of bacterial cholangitis is as effective as surgical intervention. ERCP with endoscopic sphincterotomy is safe and the preferred initial procedure for both establishing a definitive diagnosis and providing effective therapy.


Pancreatitis Suspect when you have (1)back pain or pain to the left of the abdominal midline (2) prolonged vomiting with paralytic ileus o (3) a pleural effusion, especially on the left side (4) elevations in serum amylase and lipase

Secondary Biliary Cirrhosis:

Secondary Biliary Cirrhosis Secondary biliary cirrhosis may complicate prolonged or intermittent duct obstruction. Once established, secondary biliary cirrhosis may be progressive even after correction of the obstructing process, and increasingly severe hepatic cirrhosis may lead to portal hypertension or to hepatic failure and death. Prolonged biliary obstruction may also be associated with clinically relevant deficiencies of the fat-soluble vitamins A, D, E, and K.


IMAGING STUDIES a) Ultrasonography : Non-invasive and cost-effective 95-98% sensitive, 98% specific for documenting presence of gallstones-acoustic "shadowing" of opacities that are within the gallbladder lumen and that change with the patient's position Biliary sludge is material of low echogenic activity that typically forms a layer in the most dependent position of the gallbladder Can also assess emptying function of GB 80-95% sensitive, 78-80% specific for cholecystitis Operator dependant 59






c) CT Scanning: CT Scans are not the first line test for the diagnosis of cholelisthiasis. Less sensitive than ultrasound for detecting stones (50-70%) or cholecystitis. More expensive However it does provide important information regarding the nature, extent location of biliary dilatation and the masses in and around the biliary tract a nd pancreas.

CT Scan:

CT Scan


d) . MRCP Cost prohibitive Most often used to detect common bile duct obstruction




e) Abdominal plain film rarely useful as 10-15% of stones radiopaque enough to be seen. diagnose emphysematous cholecystitis, porcelain gallbladder, limey bile, and gallstone ileus.

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Radionuclide scan – hepatobiliary iminodiacetic acid (HIDA) are rapidly extracted from the blood and are excreted into the biliary tree in high concentration even in the presence of mild to moderate serum bilirubin elevations. Failure to image the gallbladder in the presence of biliary ductal visualization may indicate cystic duct obstruction, acute or chronic cholecystitis, or surgical absence of the organ. Such scans have some application in the diagnosis of acute cholecystitis.

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Good for detecting cystic duct obstruction or CBD obstruction Also very useful in determining bile leaks after cholecystectomy Acute cholecystitis: 94% sensitive, 65-85% specific Chronic cholecystitis: 65% sensitive, 6-10% specific Overall false positive (no filling of cystic duct or gallbladder) 15-20% This is lowered with administration of morphine to 2%

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