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"Gallstone disease is one of the most common and costly of all digestive diseases. The pain is often associated with diaphoresis, nausea and vomiting. It is not exacerbated by movement and not relieved by squatting, bowel movements, or flatus. Get the full details on PPT<br>"<br>
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Gall Bladder diseases DrArun AggarwalGastroenterologist
Ascertaining the true prevalence of GB disease is difficult as most patient with GB disease are asymptomatic. Various studies have shown prevalence rate ranging from 0.13 – 2%.
INTRODUCTION Gallstone disease is one of the most common and costly of all digestive diseases. The third National Health and Nutrition Examination Survey estimated that 6.3 million men and 14.2 million women aged 20 to 74 in the United States had gallbladder disease.
Major risk factors for the development of gallstones • Age • Female sex • Genetic • Pima Indians and certain other Native Americans • Chileans • Pregnancy • Obesity • Rapid weight loss • Very low calorie diet • Surgical therapy of morbid obesity • Cirrhosis • Hemolytic anemias • Hypertriglyceridemia • Medications • Estrogen and oral contraceptives • Clofibrate • Ceftriaxone • Octreotide • Terminal ileal resection • Gallbladder stasis • Diabetes mellitus • Total parenteral nutrition • Postvagotomy • Octreotide or somatostatinoma • Spinal cord injury • Reduced physical activity • Cystic fibrosis
Age: exceedingly rare in children except in the presence of hemolytic states; in addition, <5% of all cholecystectomies are performed in children. Sex: F > M Pregnancy: frequency and no of pregnancies. Sex hormones induce a variety of physiologic changes in the biliary system, which ultimately cause bile to become supersaturated with cholesterol, thereby promoting gallstone formation. These changes normalize 1-2 months following delivery.
Diabetes mellitus: mechanism is not well understood. Hepatic insulin resistance appears to be important . Other contributing factors may be hypertriglyceridemia and autonomic neuropathy leading to biliary stasis due to gallbladder hypomotility. Serum lipids: positively associated with apolipoprotein E4 phenotype and elevated serum triglycerides. Negative association exists between gallstones and high density lipoprotein. There is no conclusive evidence linking elevated serum cholesterol and gallstones.
Cirrhosis: due to reduced hepatic synthesis and transport of bile salts and nonconjugated bilirubin, high estrogen levels, and impaired gallbladder contraction in response to a meal. Gall bladder stasis: In the normal state, the gallbladder avidly absorbs water from bile. Thus, if bile remains within the gallbladder for a prolonged period, it can become overly concentrated with cholesterol, thereby promoting stone formation. Can occur with spinal cord injuries, prolonged fasting and the use of TPN, and excess somatostatin.
Short bowel syndrome: Two factors are thought to contribute: biliary stasis due to lack of enteral stimulation; and, in patients with ileal resection, interruption of the enterohepatic circulation of bile acids results in a reduction in hepatic bile acid secretion and an altered composition of hepatic bile which becomes supersaturated with respect to cholesterol.
Crohn’s disease: Gallstones in patients with ileal Crohn's disease (or those who have undergone ileal resection) are frequently pigment based, reflecting an increased concentration of bilirubin conjugates, unconjugated bilirubin, and total calcium in the gallbladder bile due to altered enterohepatic cycling of bilirubin.
Protective factors Statins Ascorbic acid Coffee (in moderation) Vegetable protein Poly and mono unsaturated fats
CLINICAL FEATURES When considering gallstone disease it is helpful to categorize patients into the following clinical groups: • Gallstones on imaging studies but without symptoms • Typical biliary symptoms and gallstones on imaging studies • Atypical symptoms and gallstones on imaging studies • Typical biliary symptoms but without gallstones on imaging studies
Biliary type symptoms Biliary colic: recurrent pain attacks Complication of gall stones: acute cholecystitis, acute biliary pancreatitis, acute cholangitis, or choledocholithiasis with extrahepatic cholestasis.
Biliary colic 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 intragallbladder 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. Despite the term "colic", the pain is usually constant and not colicky. The classic attack is described as an intense dull pressure-like discomfort in the right upper or mid abdomen or in the chest that may radiate to the back and the right shoulder blade . The pain classically follows ingestion of a fatty meal (about one to two hours after) and usually does not occur during fasting.
The pain is often associated with diaphoresis, nausea and vomiting. It is not exacerbated by movement and not relieved by squatting, bowel movements, or flatus. After the attack, the physical examination is usually normal with the possible exception of residual upper abdominal tenderness. Prolonged or recurrent cystic duct blockage can progress to total obstruction causing acute cholecystitis.
Diagnosis Biliary colic is the most accurate predictor of gallstone disease. Imaging studies can detect gallstones, there is no clinical or laboratory test that can make the diagnosis of biliary colic. The diagnosis is based upon a meticulous history. Physical exam: usually not ill appearing, no fever/ tachycardia, no peritoneal signs, ± voluntary guarding.
Labs LFT GGT Amylase, lipase CBC UA Imaging studies
GGT GGT is sensitive for detecting hepatobiliary disease, but its usefulness is limited by its lack of specificity. Elevated levels can occur in pancreatic disease, myocardial infarction, renal failure, chronic obstructive pulmonary disease, diabetes, and alcoholism. GGT be used to evaluate elevations of other serum enzyme tests (eg, to confirm the liver origin of an elevated alkaline phosphatase or to support a suspicion of alcohol abuse in a patient with an elevated AST and an AST:ALT ratio of greater than 2:1). An elevated GGT with otherwise normal liver tests should not lead to an exhaustive work-up for liver disease.
USG Most useful test. It is non-invasive, readily available, relatively inexpensive, and does not subject the patient to ionizing radiation. Accuracy of USG is operator dependent. USG must be conducted with the patient having fasted, because stones are best seen in a distended gallbladder when they are surrounded with bile.
Ultrasound images of a gallbladder adenomatous polyp (left ) compared to a gallstone (right). Note the shadow cast by the stone (red arrow) compared to the absence of a shadow behind the polyp.
AXR Plain abdominal x-rays are generally not useful in looking for gallstones in symptomatic patients. Only about 10 % of gallstones have enough calcium in their composition to make them sufficiently radio-opaque to be visible on a plain radiograph.
Oral cholecystography OCG is based upon an orally administered contrast agent that is absorbed through the intestine, taken up by the liver, and secreted into bile. Gallstones appear as filling defects within the contrast .
CT abdomen Endoscopic ultrasonographhy
Management of biliary colic Pain control. Can usually be achieved with IV meperidine, which is preferred to morphine since it has less of an effect on sphincter of Oddi motility. NPO to prevent the release of cholecystokinin. IV fluids if vomiting + Anticholinergic agents, which are useful in the management of renal colic due to their smooth muscle relaxation effects, do not appear to help biliary colic.
Prophylactic treatment to prevent further attacks and/or the development of complications To remove the offending stones to prevent recurrent attacks of biliary colic and the occurrence of more severe complications. Surgical removal of the gallbladder vs medical dissolution of the stones while sparing the gallbladder.
Cholecystectomy is the most commonly recommended modality. The gallbladder along with its contained stones is removed under general anesthesia. Open vs laproscopic. Laparoscopic procedure has been associated with an increased risk of common bile duct injury. Laparoscopic procedure may require conversion to an open procedure due to a variety of technical or patient issues.
Interestingly, several other symptoms appeared to be improved after cholecystectomy including abdominal bloating, dyspepsia, heartburn, fat intolerance, nausea and vomiting. However, these observations should not be interpreted as suggesting that gallstones are a possible cause of all these complaints. Relief of symptoms may have been due to the natural history of some of these disorders, a placebo response, or other nonspecific effect of the procedure.
Gallstones but without symptoms These patients are unlikely to develop symptoms and when they do occur they are generally mild. Thus, patients should be educated about symptoms potentially related to gallstones (principally biliary colic) without recommending specific therapy to address the gallstones.
Typical biliary symptoms and gallstones Such patients should generally undergo treatment (generally cholecystectomy) since they are likely to develop recurrent symptoms, which can be severe.
Atypical symptoms and gallstones Such patients should undergo a search for non-gallstone-related causes of symptoms. If investigation is unrevealing, treatment of gallstones can be considered with the understanding that the rate of persistent symptoms is high.
Typical biliary symptoms but without gallstones Clinical suspicion for gallstone disease should be maintained in such patients. A repeat extracorporeal ultrasound should be obtained. If results are unrevealing, Endoscopic US and collection of duodenal bile for microscopy should be considered. If results continue to be unrevealing, a search for other causes of the pain is reasonable.
Nonsurgical treatment of gallstone disease Symptomatic gallstones are uncommonly treated with medical therapy alone. Ursodiol: may have a role to enhance gallstone dissolution and perhaps reduce symptoms in patients with mild symptoms or those who are not candidates for laparoscopic surgery (grade 2 B). ESWL and contact lithotripsy will likely be limited to specialized centers with experience in these techniques and in the majority of cases as an adjunct to endoscopic or other invasive treatments. In patients with stones too large for dissolution therapy, lithotripsy (plus bile salts) provided that patients have fewer than three noncalcified stones (Grade 2B).
Syndrome of right upper quadrant pain, fever, and leukocytosis associated with gallbladder inflammation. Usually related to gallstone disease. Pain may radiate to the right shoulder or back. Characteristically, acute cholecystitis pain is steady and severe. Associated complaints may include nausea, vomiting, and anorexia. Should be suspected when a patient presenting with the clinical manifestations outlined above is found to have gallstones on an imaging study. Left untreated, symptoms of cholecystitis may abate within 7 to 10 days. However, complications can occur at high rates. Most common complication is the development of GB gangrene (up to 20 % of cases) with subsequent perforation (2 % of cases).
Radionuclide imaging/ Scintigraphy • IV administered Technetium-99m hepatic iminodiacetic acid (Tc-99m HIDA) is secreted from liver in to hepatic bile ducts, but unable to enter GB if cystic duct is obstructed. • If GB is not seen in 60 min: do delayed imaging at 4 hrs or administration of morphine. • Morphine increases pressure at sphincter of oddi and forces bile in to GB if cystic duct is patent. • Complications of acalculous cholecystitis (gangrene and perforation) can be identified by spill of radionuclide into peritoneal cavity.
Ultrasound of the right upper quadrant in a patient with acute cholecystitis reveals marked thickening of the gallbladder wall (arrow) with fluid surrounding the distended gallbladder (arrowhead).
Treatment of acute cholecystitis Admit Analgesia (opioids) Antibiotics (unasyn/ zosyn/ rocephin + flagyl) (grade 2C)
Clinical syndrome characterized by fever, jaundice, and abdominal pain that develops as a result of stasis and infection in the biliary tract. The classic triad of Charcot — fever, right upper quadrant pain, and jaundice — occurs in only 50 to 75 % of patients . Confusion and hypotension can occur in patients with suppurative cholangitis, producing Reynold's pentad, which is associated with significant morbidity and mortality.
Differential diagnosis Biliary leaks Liver abscess Infected choledochal cysts Cholecystitis Mirizzi syndrome (chronic cholecystitis and large gall stones resulting in compression of common hepatic duct) Right lower lobe pneumonia/empyema
Treatment Antibiotics (unasyn/ zosyn/ meropenem/ rocephin + flagyl) Establishment of biliary drainage (ERCP/ open surgical decompression) IV fluids Correction of coagulopathy Monitoring
80 % of patients with acute cholangitis will respond to conservative management and antibiotic therapy. • Biliary drainage can be performed on an elective basis. • In 15- 20 % of cases, cholangitis fails to settle over the first 24 hours with conservative therapy alone, requiring urgent biliary decompression. • Indications for urgent biliary decompression include: • Persistent abdominal pain • Hypotension despite adequate resuscitation • Fever greater than 39ºC (102ºF) • Mental confusion, which is a predictor of poor outcome
Diagnosis and treatment of acute cholangitis with ERCP. Left: Multiple small stones in the lower common bile duct (arrow). Ultrasonography had shown borderline dilatation of the common bile duct but no stones. Right : After sphincterotomy and stone extraction, the common bile duct is free of stones.
Following cannulation of the distal common bile duct during an ERCP examination (black arrow indicates cannula), contrast material was injected, outlining a large stone producing complete obstruction of the distal duct (white arrow).
Acalculous cholecystitis / Biliary dyskinesia F>M Associated with systemic infection / surgery / trauma. Risk factors: prolonged fasting, PN, sepsis. Abdominal pain : RUQ, worse after eating. Examination and routine workup is generally normal. USG shows GB wall thickness > 3.5 mm. Hepatobiliary scintigraphy scan is usually diagnostic (ejection fraction <35%). Cholecystectomy is usually helpful.
Sphincter of oddi dysfunction There is effectively an obstruction at the level of sphincter that may be caused by fibrosis / inflammation / elevated sphincter tone. Symptoms usually similar to GB dyskinesia. ERCP with Manometry is usually diagnostic. Sphincterotomy is the treatment of choice. Cholecystectomy does not provide relief.
Benign masses of gall bladder • Usually polyps: primary or secondary • Primary polyps include: -Cholesterol polyps -Inflammatory polyps -hyperplastic adenomyoma -Adenoma -Heterotopic gastric and pancreatic tissue • Can present with sign and symptoms of biliary colic • USG usually diagnostic
