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Gallbladder, The Big Picture


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The gall bladder is located in the junction of the right ninth costal cartilage and lateral border of the rectus abdominis.
It is a pear shaped sac lying on the inferior surface of the liver in a fossa between the right and quadrate lobes with a capacity of about 30 to 50 mL.

Published in: Health & Medicine

Gallbladder, The Big Picture

  1. 1. GallbladderBy: Krystle Rolle Bobby Korah & Oladapo Samson
  2. 2. Anatomy of Gallbladder The gall bladder is located in the junction of the right ninth costal cartilage and lateral border of the rectus abdominis . It is a pear shaped sac lying on the inferior surface of the liver in a fossa between the right and quadrate lobes with a capacity of about 30 to 50 mL.
  3. 3. Anatomy of Gallbladder The gallbladder is in direct contact to the superior part of the duodenum and transverse colon. The gall bladder has three parts the neck which tapers into the narrow cystic duct which connects with the common duct. Body: contacts the visceral surface of the liver the transverse colon and superior part of the duodenum Fundus: The wide end of the organ projects 1-2 cm from the inferior border of
  4. 4. Anatomy of Gallbladder The cystic duct (3-4 cm long) connects the neck of the gallbladder to the common hepatic duct . The spiral fold helps keep the cystic duct open ;thus bile can easily be diverted into the gallbladder when the distal end of the bile duct is closed by the sphincter of the bile duct. The spiral fold also offers additional resistance to sudden dumping of bile when the sphincters are closed, and intra-abdominal pressure is suddenly increased, as during a sneeze or cough. The cystic duct passes between the layers of the lesser omentum, usually parallel to the common hepatic duct, which it joins to form the bile duct.
  5. 5. Blood Supply of the Gall Bladder The cystic artery, supplying the gallbladder and cystic duct commonly arises from the right hepatic artery.
  6. 6. CYSTOHEPATIC TRIANGLE OF CALOTIn the angle between thecommon hepatic duct and thecystic duct cystohepatic triangle(of Calot) which is formed bythe visceral surface of the liversuperiorly, the cystic ductinferior-laterally and thecommon hepatic duct medially.
  7. 7. Variations to the Cystic Artery Variations occur in the origin and course of the cystic artery . In approximately 12% of cases, the right hepatic artery arises from the superior mesenteric artery. The cystic artery usually arises from the right hepatic artery, but other origins are possible. The cystic artery may pass posterior (75%) or anterior
  8. 8. Venous Drainage of the Gallbladder The cystic veins, draining the neck of the gallbladder and cystic duct, enter the liver directly or drain through the portal vein to the liver, after joining the veins draining the hepatic ducts and upper bile duct. The veins from the fundus and body of the gallbladder pass directly into the visceral surface of the liver and drain into the hepatic sinusoids. Because this is drainage from one capillary (sinusoidal) bed to another, it constitutes an addition (parallel) portal system.
  9. 9. Lymphatic Drainage of Gallbladder The lymphatic drainage of the gallbladder is to the hepatic lymph nodes often through cystic lymph nodes located near the neck of the gallbladder. Efferent lymphatic vessels from these nodes pass to the celiac lymph nodes.
  10. 10. Nerve Supply The nerves to the gallbladder and cystic duct pass along the cystic artery from the celiac nerve plexus (sympathetic and visceral afferent [pain] fibers), the vagus nerve (parasympathetic), and the right phrenic nerve (actually somatic afferent fibers). Parasympathetic stimulation causes contractions of the gallbladder and relaxation of the sphincters at the hepatopancreatic ampulla. However, these responses are generally stimulated by the hormone cholecystokinin (CCK), produced by the duodenal walls (in response to the arrival of a fatty meal) and circulated through the blood stream
  11. 11. Functions Gall bladder  It stores Bile  It concentrates bile  Ejects bile into lumen Bile  Emulsify dietary lipids  Formation of micelles with products of lipid digestion.
  12. 12. BILE Bile is produced at a rate of 500–1500 mL/d by the hepatocytes and the cells of the ducts The organic constituents of bile are bile salts (50%), bile pigments such as phospholipids (40%), cholesterol (4%), and bilirubin (2%) Bile also contains electrolytes and water. Bile acids are conjugated with amino acids , glycine or taurine to form bile salts. Bilirubin , a yellow- colored byproduct is the major bile pigment.
  13. 13. Secretion and enterohepatic circulationof bile salts
  14. 14. CHOLELITHIASIS Presence of one or more calculi (gallstones) in the gallbladder.
  15. 15. Incidence and Epidemiology In the United States, about 20 million people (10- 20% of adults) have gallstones. Every year 1-3% of people develop gallstones and about 1-3% of people become symptomatic. Prevalence of cholesterol cholelithiasis in other Western cultures is similar to that of the United States, but it appears to be somewhat lower in Asia and Africa. Prevalence is highest in people of northern European descent and in Hispanic populations Women are more likely to develop cholesterol gallstones than men, especially during their reproductive years, when the incidence is 2-3 times than that in men.
  16. 16. Risk factors Cholesterol stones:  Obesity, age <50  Estrogens: female, multiparity, OCPs  Ethnicity: Caucasian > black  Terminal ileal resection or disease (Crohn’s Disease)  Impaired gallbladder emptying: starvation, DM type 1  Rapid weight loss: rapid cholesterol mobilization and biliary stasis Pigment stones :  Chronic (contains calcium bilirubinate):  Cirrhosis  Chronic hemolysis  Biliary stasis (strictures, dilation, biliary infection)
  17. 17. Pathophysiology Biliary sludge is often a precursor of gallstones. It consists of Ca++ bilirubinate (a polymer of bilirubin), cholesterol microcrystals, and mucin. Sludge develops during gallbladder stasis, as occurs during pregnancy. Most sludge is asymptomatic or disappears when the primary condition resolves. Alternatively, sludge can evolve into gallstones and migrate into the biliary tract, obstructing the ducts and leading to biliary colic, cholangitis, or pancreatitis.
  18. 18. Pathophysiology Three types of stones, cholesterol, pigment, mixed. Formation of each types is caused by crystallization of bile. Cholesterol stones most common. Impaired motility can predispose to stones. Pigment stones (15%) are from calcium bilirubinate. Diseases that increase RBC destruction will cause these. Also in cirrhotic patients, parasitic infections.
  19. 19. Pathophysiology Cholesterol stones – vary in color from light yellow to dark green or brown and are oval in shape, 2-3 cm in length, often having a tiny dark central spot. Pigmented stones – are small dark stones made of bilirubin and calcium salts that are found in the bile Mixed stones – calcium carbonate, palmitate phosphate, bilirubin and other bile pigments. Because of their calcium content, they are often radiographically visible.
  20. 20. 4 Stages of Cholelithiasis 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
  21. 21. Symptoms and signs 80% of gallstones are asymptomatic. The remainder have symptoms ranging from biliary- type pain (biliary colic) to cholecytitis to life- threatening cholangitis. Biliary colic is the most common symptom. RUQ (Right Upper Quadrant) pain which may radiate to the back – described as colicky, but more often is dull and constant. Nausea & Vomiting, fever and chills do not occur. Other symptoms include dyspepsia, flatulence, food intolerance, particularly to fats, and some alteration in bowel frequency. Restlessness
  22. 22. Biliary colic Biliary colic is pain associated with irritation of the viscera secondary to cholecystitis and gallstones. Unlike renal colic, the phrase biliary colic refers to the actual cholelithiasis. Although it is frequently described as a colic, the pain is steady, starts rapidly, becomes intense and lasts at least 30 minutes and up to several hours.
  23. 23. CHOLECYCTITISA common condition that results from inflammatory, infections, metabolic, neoplastic and congenital disorders It is the inflammation of gallbladder that occurs most commonly because of an obstruction of the cystic duct from cholelithiasis. Acute acalculous cholecystitis – cholecystitis without stones. It accounts for 5-10% of cholecystectomies done for acute cholecystitis Acute calculous cholecystitis – cholecystitis with stones. It accounts for 90-95%.
  24. 24. CHOLECYCTITIS Acute cholecystitis is inflammation of the gallbladder that develops over hours, usually because a gallstone obstucts the cystic duct. Symptoms include RUQ pain and tenderness, sometimes accompanied by fever (usually low grade), chills, nausea, and vomiting. Most patients have had prior attacks of biliary colic or acute cholecystitis. Pain lasts longer (i.e. >6hr) than in biliary colic and more severe. Acute cholecystitis begins to subside in 2 to 3 days and resolves within 1 week in 85% of patients.
  25. 25. CHOLECYCTITIS Chronic cholecystitis is long-standing gallbladder inflammation almost always due to gallstones. Chronic cholecystitis almost always results from gallstones and prior episodes of acute cholecystitis (even if mild). Damage ranges from a modest infiltrate of chronic inflammatory cells to a fibrotic, shrunken gallbladder. Extensive calcification due to fibrosis is called porcelain gallbladder. Gallstones intermittently obstruct the cystic duct and so cause recurrent biliary colic. Such episodes of pain are not necessarily accompanied by overt gallbladder inflammation; the extent of inflammation does not correlate with the intensity or frequency of biliary colic. Upper abdominal
  26. 26. Physical findings: Fever, tachycardia, and hypotension; alert you to more serious infections, including cholangitis, cholecystitis. Murphy’s sign - it is performed by asking the patient to breathe out and then gently placing the hand below the costal margin on the right side at the mid- clavicular line (the approximate location of the gallbladder). The patient is then instructed to inspire (breathe in). Normally, during inspiration, the abdominal contents are pushed downward as the diaphragm moves down (and lungs expand). If the patient stops breathing in (as the gallbladder is tender and, in moving downward, comes
  27. 27. Physical findings: Lepenet’s symptom – tenderness is revealed by a light tapping of the right hypochondrium with flexed fingers on inspiration. Kehr’s symptom – tenderness in the zone of gallbladder (Kehr’s point) especially evident on inspiration) Mussi’s sign – detects pain by pressing a point of the phrenic nerve between peduncles of the right sternocleidomastoid muscle. Gausman’s symptom – light tapping of the right hypochondrium with breath holding on deep inspiration (inflated abdomen) – tenderness on inspiration suggests chronic cholecystitis, and on expiration – a likelihood of pyloro-duodenal pathology.
  28. 28. Differentials Abdominal Aorta Aneurysm Appendicitis Cholangitis, cholelithiasis Diverticulitis Gastroenteritis Hepatitis Inflammatory Bowel Disease Myocardial Infarction Pancreatitis, renal colic, pneumonia
  29. 29. CHOLECYCTITIS - complication Perforation Empyema – pus in the gallbladder Gangrene Mirizzi’s syndrome – rarely, a gallstone becomes impacted in the cystic duct or Hartman’s pouch and compresses and obstructs the common bile duct, causing cholestasis. Gallstone pancreatitis: Gallstones pass from the gallbladder into the biliary tract and block the pancreatic duct. Cholecystoenteric fistula: Infrequently, a large stone erodes the gallbladder wall, creating a fistula into the small bowel (or elsewhere in the
  30. 30. CHOLEDOCHOLITHIASIS Is the presence of stones in bile ducts; the stones can form in the gallbladder or in the ducts themselves. These stones cause biliary colic, biliary obstruction, gallstone pancreatitis, or cholangitis (bile duct infection and inflammation). Stones may be described as:  Primary stones (usually brown pigment stones), which form in the bile ducts  Secondary stones (usually cholesterol), which form in the gallbladder but migrate to the bile ducts  Residual stones, which are missed at the time of cholecystectomy (evident < 3 years later)  Recurrent stones, which develop in the ducts > 3 years after surgery.
  31. 31. CHOLEDOCHOLITHIASIS Essentials for diagnosis:  Biliary pain  Jaundice  Episodic cholangitis  Gallstones in gallbladder or previous cholecystectomy Signs:  Patient may be icteric and toxic, with high fever and chills, or may appear to be perfectly healthy.  A palpable gallbladder is unusual in patients with obstructive jaundice.  Dark-tea coloured urine.
  32. 32. Acute Biliary Pancreatitis Gallstones are the most common cause of acute pancreatitis (AP), a potentially life- threatening condition, worldwide. accounting for at least one half of the 4.8-24.2 cases of pancreatitis per 100,000 people that occur in Western countries. About 80,000 cases occur in the USA;
  33. 33. Etiology ? ?Unknown ?? - But Gender and Stone size may be risk factors. Suggested possible initiating events in gallstone pancreatitis include the reflux of bile into the pancreatic duct due to transient obstruction of the ampulla during passage of gallstones. The risk of developing acute pancreatitis in patients with gallstones is greater in men; however, more women develop this disorder since gallstones occur with increased frequency in women.
  34. 34. Prevailing Theory of Pathogenesis Common Channel Theory  sterile bile does not result in pancreatitis. However, infected bile is capable of activating pancreatic enzymes leading to auto digestion of the gland.  reflux of infected bile into the pancreas activating a cascade of proteolytic enzymes, and obstruction of pancreatic duct causing acinar disruption from raised pressure.
  35. 35. History/PE Severe epigastric pain  radiating to the back Grey Turner’s sign  Flank discoloration Cullen’s sign  Periumbilical discoloration Nausea, vomiting, weakness, fever, shock
  36. 36. Clues for Differentials Prior History of Biliary Colic Rule out other causes of acute Pancreatitis  Heavy alcohol consumption  Medications  Genetic diseases  Infectious agents  Postoperative states  Endoscopic procedure involving pancreatic and bile ducts and other types of injury to pancreas.
  37. 37. Investigations In patients with suspected gallstone complications, blood work should include:  CBC with differentials  LFT – Liver Function Test  Amylase and lipase. Abdominal Ultra Sound – sensitivity and specificity are 95%. It also accurately detects sludge. Endoscopic Ultra Sound accurately detects small stones (<3mm) and may be needed if other tests are ambiguous. CT, MRI – though accurate but are not cost effective.
  38. 38. Labs Serological inflammatory markers  Serum amylase  elevated in at least 75% of cases of acute pancreatitis and remains elevated for 5-10 days in most patients.  However, amylase lacks specificity.  Serum lipase  Serum lipase has a longer half life than amylase and therefore tends to remain elevated for longer.  Using a cut-off of three times the upper limit of normal, the sensitivity of serum lipase for pancreatitis approaches 90% in patients presenting with abdominal pain. Calcium
  39. 39. Investigations Ultra Sound  Should be considered for initial investigation  Can show enlarged pancreas with  Stranding  Abscess  Hemorrhage  Necrosis  Pseudocyst  The sensitivity of this study in detecting pancreatitis is 62 to 95 percent. However, in 35 percent of cases, the pancreas is obscured secondary to bowel gas.
  40. 40. Imaging studies: Ultra Sound  → denotes gallstones → →  denotes the ► acoustic shadow due to absence of reflected sound waves behind the gallstone
  41. 41. Investigations cont. Computed Tomography (CT) scan  provides the best imaging of the pancreas and surrounding structures.  useful when other diagnostic studies are:  Inconclusive  when the patient has severe symptoms  when fever is present  in the face of persistent leukocytosis that suggests secondary infection.  findings in pancreatitis may show inflammation characterized by diffuse or segmental enlargement of the pancreas, with irregular contour and obliteration of peri-pancreatic fat, necrosis or a pseudocyst.
  42. 42. CT scan  Contrast-enhanced axial computed tomographic section of the upper abdomen showing peri- pancreatic and retroperitoneal edema (large arrows) and stranding. The pancreas itself (small rrow) appears relatively normal.
  43. 43. CT  Contrast-enhanced axial computed tomographic section of the upper abdomen showing peripancreatic and retroperitoneal edema. Large non- enhancing areas of necrosis are visible in the body and neck of the pancreas (arrows).
  44. 44. CT  Contrast-enhanced axial computed tomographic section of the upper abdomen showing a well- defined fluid collection in the retroperitoneum (arrow) just below the level of the pancreas.
  45. 45. Investigations cont. Early Endoscopic Retrograde Cholangiopancreatography (ERCP) It is primarily indicated in patients with severe disease who are suspected of having biliary obstruction.  The endoscope travels orally into the stomach, through the pylorus into the duodenum where the ampulla of Vater (the opening of the common bile duct and pancreatic duct) exists.  The sphincter of Oddi is a muscular valve that controls the opening of the ampulla.  Through the endoscope, the surgeon can see the inside of the stomach and duodenum, and inject dyes into the ducts in the biliary tree and pancreas so they can be further visualized on X-rays.
  46. 46. ERCP  Fluoroscopic image of common bile duct stone seen at the time of ERCP.  The stone is impacted in the distal common bile duct.  A nasobiliary tube has been inserted.
  47. 47. ERCP  Fluoroscopic image showing dilatation of the pancreatic duct during ERCP investigation.  Endoscope is visible
  48. 48. HIDA SCAN A HIDA scan (hepatobiliary iminodiacetic acid scan) is radiodiagnostic procedure that helps track the production and flow of bile from the liver to the small intestine. It uses a radioactive chemical, or tracer, that helps highlight certain organs on the scan. The gallbladder should be visualized between 1 – 4 hours.
  49. 49. HIDA SCANNormal Abnormal
  50. 50. Treatment Laparoscopic cholecystectomy with preoperative endoscopic common bile duct clearance is recommended as a treatment of choice for acute biliary pancreatitis. Supportive care:  IV fluids/electrolyte replacement  Analgesia  Bowel rest  NG suction  Nutritional support  Oxygen
  51. 51. Treatment Symptomatic  Laparoscopic cholecystectomy for symptomatic stones  Open cholecystectomy, which involves a large abdominal incision and direct exploration, is safe and effective. Its overall mortality rate is about 0.1% when done electively during a period free of complications. Asymptomatic  For patients who decline surgery, or are at high risk of surgical complications, but want to remove asymptomatic stones; these gallstones can sometimes be dissolved by ingesting bile acids orally for many months.
  52. 52. Prognosis 85-90% are mild and self-limiting 10-15% are severe  Which require ICU admission  Mortality may approach 50% in severe cases Acute pancreatitis is a potentially fatal disease with an overall mortality of 2 - 7% despite aggressive intervention. The outcome of acute pancreatitis is determined by two factors which reflect the severity of the illness: organ failure and pancreatic necrosis. About half of the deaths in patients with acute pancreatitis occur within the first one/two weeks and are mainly attributable to multiple organ dysfunction syndromes. When not treated, the risk of recurrence in gallstone pancreatitis ranges from 32 to 61%. At least one study has shown that patients with severe biliary
  53. 53. Case 1 : 46 year old female patient presents with RUQ pain, jaundice, acholic stools, dark tea-colored urine, no fevers Known history of cholelithiasis Exam: unremarkable WBC 8,000 per μl; Total Bilirubin is 8mg/dl, increased AST/ALT , negative for Hepatitis B & C Ultrasound: Gallstones, Common Bile Duct stone, dilated Common Bile Duct > 1cm CHOLEDOCHOLITHIASIS
  54. 54. Case 2A 47-year-old man presents to the emergency room with sudden onset of severe upper abdominal pain with vomiting. The pain is focused in the epigastrium with radiation to the back. Serum amylase levels are 2000 U/L. Which of the following are the most commonly encountered predisposing factors for this patient‘s condition?  A. Alcohol use and gallstones  B. Helicobacter pylori infection and excess gastric acid secretion  C. Hepatitis B infection and iron overload  D. Obesity and high serum cholesterol  E. Stress and cigarette use The correct answer is A. The clinical scenario is typical of acute pancreatitis. The overwhelmingly most important contributing factors for development of acute pancreatitis are gallstones (particularly small ones) and alcohol abuse.