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Gallstones & their Effects.pptx
- 2. Objectives • To be familiar with the pathophysiology and management of gallstones • To appreciate the multidisciplinary management of gallstone disease
- 3. Outline • Terminology • Gallstone disease • Basic anatomy • Bile & composition • Functions of Bile • Types of Gallstones • Risk factors for formation of Gallstones • Clinical manifestations: Symptoms & Physical examination • Investigations • Management of Gallstones • Complications of Gallstones • Acute cholecystitis & Management
- 4. Terminology • Choleliths - gallstones • Microlithiasis - biliary sludge • Cholelithiasis - the presence of stones in the gallbladder (GB) • Choledocholithiasis - the presence of gallstones within the common bile duct (CBD) • Gallstone disease - gallstones that cause symptoms* • Uncomplicated gallstone disease - biliary colic in the absence of gallstone-related complications • Complicated gallstone disease - gallstone-related complications that include acute cholecystitis, cholangitis, gallstone pancreatitis, gallstone ileus, and Mirizzi syndrome • Cholecystitis: inflammation of the gallbladder • Cholangitis: inflammation of the bile ducts • Gallbladder empyema: pus in the gallbladder • Cholecystectomy: surgical removal of the gallbladder • Cholecystostomy: inserting a drain into the gallbladder
- 5. Gallstones Disease • Gallstones disease refers to diseases of the gallbladder and biliary tree that are a direct result of gallstones • Gallstones, or Choleliths, are solid masses or concretions or aggregates formed from bile precipitates • ~75-80% patients are asymptomatic • Gallstone obstruction can lead to life- threatening complications, such as acute cholecystitis, acute cholangitis and biliary pancreatitis
- 7. Bile & Composition • Bile is a complex aqueous secretion that originates from hepatocytes and enters the gallbladder where it is concentrated or is delivered directly into the duodenal lumen. • Modified distally by absorptive and secretory transport systems in the bile duct epithelium. • Bile consists of ~95% water and ~5% dissolved organic and inorganic solutes including bile salts, bilirubin, phospholipids, cholesterol, amino acids, steroids, enzymes, porphyrins, vitamins, and heavy metals, as well as exogenous drugs, xenobiotics and environmental toxins • There is an equilibrium between cholesterol and bile acid in bile.
- 8. Functions of Bile • Bile is the major excretory route for potentially harmful exogenous lipophilic substances, as well as other endogenous substrates such as bilirubin and bile salts not readily filtered or excreted by the kidney. • Bile salts in bile emulsify dietary fats and facilitate their digestion and absorption. • Bile is the major route for elimination of cholesterol. • Bile protects from enteric infections by excreting immune globulin A (IgA), inflammatory cytokines, and stimulating the innate immune system in the intestine. • Bile is an essential component of the enterohepatic circulation, and finally, • Hormones and pheromones are excreted in bile, and contribute to growth and development of the intestine in some species and provide attractants for the weaning of nonhuman vertebrates.
- 9. Types of Gallstones • Cholesterol stones are: • yellow-green, hardened cholesterol • Pigment stones: black or brown • Black pigments: pure calcium bilirubinate or complexes of calcium, copper, and mucin glycoproteins • Brown pigment stones: calcium salts of unconjugated bilirubin with small amounts of cholesterol and protein • Types: cholesterol (~90%), pigment, and mixed stones Black Brown Cholesterol
- 10. Formation of Gallstones Five (5) Factors promote formation: • genetic factors; • cholesterol supersaturation in gallbladder bile from liver cholesterol hypersecretion; • accelerated nucleation of cholesterol crystal or the rapid transition from liquid to crystal; • impaired gallbladder motility; • intestinal factors. Admirand's triangular hypothesis/Triangle of solubility
- 12. Factors influencing formation of Gallstones Incidence of gallstones increases with age; becoming 4 -10 times in individuals older than 40years; very low rate among infants and children
- 13. Factors influencing formation of Gallstones Female gender - hormonal effect: 1. Estrogen decreases bile salts secretion and increases cholesterol, whereas progestins act by impairing gallbladder emptying, causing stasis 1. Pregnancy - 30% risk
- 14. Factors influencing formation of Gallstones • Lithogenic genes (ABCB4/B11/G5/G8, etc.) - in hepatocytes and intestinal cells: a) Decreased bile salt secretion b) Increased cholesterol content in the gallbladder. • G6PD/SCD/Thalassemia/ Hereditary spherocytosis: increased bilirubin load
- 15. Factors influencing formation of Gallstones Oral contraceptive use and low-dose estrogen therapy (postmenopausal women) increase risk
- 16. Factors influencing formation of Gallstones • High caloric and carbohydrate intake – most cholesterol found in gallstones is from the diet because de novo hepatic synthesis is only about 20%; • Liver insulin resistance may promote GSD by increasing the diagenesis of bile
- 17. Factors influencing formation of Gallstones When in bile, microorganisms play an important role as nucleating factors, leading to the formation of pigment and cholesterol gallstones
- 18. Factors influencing formation of Gallstones Recent studies have found that GSD is also closely related to the occurrence of cardiovascular disease (CVD), and the presence of GSD increases the incidence of CVD
- 19. Factors influencing formation of Gallstones • Gallstones occur in 25% of morbidly obese patients; • Associated with simple obesity in females, whereas in males it is mostly associated with intraabdominal (central) obesity
- 20. Clinical Manifestation Four stages: • Lithogenic state, in which conditions favor gallstone formation; • Asymptomatic gallstones, in most individuals with gallstones • Symptomatic gallstones, characterized by episodes of biliary colic • Complicated cholelithiasis
- 21. Symptomatic gallstones Biliary colic (‘Gallstone colic’ preferable terminology) • sudden, an intense, dull discomfort or pain in the RUQ, epigastrium, or (less often) substernal area that may radiate to the back (particularly the tip of the right shoulder blade) • despite the name, it’s not a true colic as the pain is usually constant with excruciating exacerbations (it does not remit between exacerbations) • pain has a characteristic pattern and timing: • triggered by a fatty meal; postprandial pain • association with meals is not universal, and in a significant proportion of patients, the pain is nocturnal
- 22. Symptomatic gallstones Biliary colic • typically lasts at least 30 minutes, plateauing within an hour; then starts to subside, with an entire attack usually lasting less than six hours unless acute cholecystitis develops • frequency of recurrent attacks is variable, ranging from hours to years, though most patients do not have symptoms on a daily basis • often associated with diaphoresis, nausea, and vomiting & a history of flatulent dyspepsia • previous episodes of upper abdominal pain is notable
- 23. Atypical symptoms of Gallstone Dx • Belching • Fullness after meals/early satiety • Regurgitation • Abdominal distension/bloating • Epigastric or retrosternal burning • Nausea or vomiting alone • Chest pain • Nonspecific abdominal pain
- 24. Physical Examination General • Frightened, restless patient – due to the intensity of the pain • Mild tachycardia – in the early stages • Fever is absent • Jaundice may be present • Presence of fever, persistent tachycardia, hypotension, or jaundice >>>>>>>>>complications of cholelithiasis (cholecystitis, cholangitis, pancreatitis, or other systemic causes) Abdomen • Extremely tender • Intense guarding in the upper abdomen
- 25. Differential diagnoses • Peptic Ulcer Disease, • Pancreatitis (Acute or Chronic), • Hepatitis, • Gastroesophageal Reflux Disease (GERD), • Esophageal Spasm, • Pneumonia, • Cardiac Chest Pain, • Appendicitis, • Bile Duct Strictures, • Bile Duct Tumors, • Cholangiocarcinoma, • Acute Cholecystitis, • Gallbladder Cancer, • Pancreatic Cancer.
- 26. Laboratory investigations • FBC with differential, • BUE&Cr; • LFT (ALT, AST, ALP, BIL), • Pancreatic enzymes (Amylase & Lipase) Normal in uncomplicated gallstone disease Abnormal blood tests (leukocytosis, elevated liver tests or pancreatic enzymes) suggest complication of gallstone disease.
- 27. Imaging investigations • Transabdominal USG • the most useful test to detect the presence of gallstones; • noninvasive, • readily available, • relatively inexpensive, and • does not subject the patient to ionizing radiation • Abdominal X-ray • Abdominal computed tomography (CT) scan
- 28. USG images of a gallbladder polyp compared with a gallstone
- 29. USG images in a patient with gallbladder sludge
- 30. (A) Ultrasound was obtained from a patient with a gallbladder that contained numerous gallstones. On ultrasound, the stones appear as one large concretion or gas. (B) Multiple stones were found in the gallbladder after cholecystectomy.
- 31. Endoscopic ultrasound (EUS) may identify small stones and microlithiasis missed on abdominal ultrasound EUS also includes an upper endoscopy, which serves to exclude other conditions (e.g., peptic ulcer disease)
- 32. A plain abdominal x-ray showing calcified gallstones in the gallbladder (GB), cystic duct (CD) and common bile duct (CBD) Radiopaque stones are rare (10%)
- 35. Management of gallstones • Asymptomatic gallstones: do not need intervention
- 36. Management of gallstones Symptomatic Gallstone Disease • Biliary colic: • Acute pain management – NSAIDS, Opioids • Cholecystectomy – As an elective, Open or Laparoscopic • Atypical symptoms and gallstones: • Empiric trial of Ursodiol dissolution therapy – takes two or more years • Cholecystectomy - a reasonable alternative if patient wants to discontinue ursodiol therapy
- 39. Introduction • Cholecystitis refers to inflammation of the gallbladder • It predominantly occurs as a complication of gallstone disease (calculous cholecystitis – Obstructive type) and typically develops in patients with a history of symptomatic gallstones • Less often (5 - 10 % of cases), acute cholecystitis may develop without gallstones (acalculous cholecystitis – Nonobstructive type) • More common in females than in males • Complications of acute cholecystitis include gallbladder gangrene or perforation, which can be life-threatening
- 40. Definition • Acute cholecystitis - a syndrome of right upper quadrant pain, fever, and leucocytosis associated with gallbladder inflammation. • Chronic cholecystitis - used to describe chronic inflammatory cell infiltration of the gallbladder seen on histopathology. invariably associated with the presence of gallstones thought to be the result of mechanical irritation or recurrent attacks of acute cholecystitis leading to fibrosis and thickening of the gallbladder wall
- 41. Pathogenesis
- 42. Clinical manifestations History: • Age: commonly 30-60 years, younger patients (SCD who form pigment stones) • Sex: more common in females than males • Symptoms: sudden onset right hypochondrium/RUQ pain, often radiating to the right shoulder or tip of the right scapula in the back; pain is constant, lasting more than 6 hours, exacerbated by movement and breathing; relieved by analgesics; nausea and vomiting; dark urine, pale stools and pruritus/itchy skin if an associated obstructive jaundice • Previous history: dyspepsia, gallstone colic
- 43. Clinical manifestations Examination: • General: patient in pain, lies still, breathing shallowly; tachycardia, pyrexia (temperature often normal in the early stage); +/- jaundice • Abdomen: fullness in the RUQ; RUQ tenderness & guarding; Positive Murphy’s sign; palpable inflammatory mass in the RUQ (Zackary Cope’s sign, often indicates GB empyema); palpable GB (Mucocele); Boas’ sign (hyperesthesia to light touch in the right lower scapular region or the right upper quadrant of the abdomen); Dull percussion beneath the right costal margin; Normal bowel sounds, unless biliary peritonitis following infarction & perforation of GB
- 45. Investigations FBC • Raised WCC (Leucocytosis), with left shift BUE&Cr • Usually normal; alteration reflect severity of vomiting/comorbidity LFT • Elevated bilirubin and ALP (alkaline phosphatase) concentrations not common in uncomplicated acute cholecystitis since obstruction is limited to the gallbladder if present, should raise concerns about biliary obstruction and conditions such as cholangitis, choledocholithiasis, or Mirizzi syndrome (a gallstone impacted in the distal cystic duct causing extrinsic compression of the common hepatic duct)
- 46. Investigations • Ultrasound scanning is the investigation of choice • Sonograms show pericholecystic fluid (fluid around the gall bladder), distended GB, oedematous gallbladder wall, and gallstones, and Murphy’s sign can be elicited on ultrasound examination. • Colour flow Doppler ultrasound shows hyperaemic, pericholecystic blood flow and acute inflammation.
- 47. Investigations • Plain abdominal radiographs show radio-opaque gallstones in about 10% of cases of acute cholecystitis and gas within the gallbladder wall in emphysematous cholecystitis
- 48. • Biliary scintigraphy (hepatic iminodiacetic acid (HIDA) scan) is the gold standard investigation when the diagnosis remains in doubt after ultrasound scanning in acute cholecystitis. • Abdominal CT scan & MRCP (magnetic resonance cholangiopancreatography) not usually required but may be performed in patients with suspected complications or to rule out alternate diagnoses Investigations
- 49. Common: • Appendicitis • Perforated Peptic ulcer • Acute pancreatitis • Acute cholangitis Rare: • Acute pyelonephritis • Myocardial infarction • Pneumonia – right lower lobe • Fitz-Hugh-Curtis syndrome Differential diagnosis
- 50. Conservative/Non-operative mgt: Patients diagnosed with acute calculous cholecystitis (ACC) should be: • Admitted; • Kept NPO, those vomiting should have NG tube placed; • Intravenous hydration; • Correction of any electrolyte abnormalities; • Pain control; • Intravenous antibiotics; However, an interval cholecystectomy (after 6 weeks) will be required once the patient’s condition has stabilised and inflammation completely resolved. Treatment
- 51. Surgical/operative mgt: • Cholecystectomy is the mainstay of treatment • Laparoscopic / Open • Poor surgical candidates may benefit from initial nonoperative management with antibiotics and a gallbladder drainage procedure • Those whose surgical risk improves after resolution of the acute inflammation - interval cholecystectomy (…usually after 6 weeks) to prevent recurrent symptoms. Treatment
- 52. Acalculous cholecystitis • A life threatening condition that occurs in critically ill patients; it accounts for 5-14% of all cases of cholecystitis • Diagnosis is often elusive and is associated with high mortality (up to 50%) • Results from sludge and gallbladder disuse and biliary stasis, perhaps secondary to absence of cholecystokinin stimulation (decreased contraction of gallbladder)
- 53. Acalculous cholecystitis • The diagnosis of acute acalculous cholecystitis may be hindered by obtundation of the patient, pre-existing disease, or recent abdominal surgery, and it needs a high index of suspicion. • Ultrasound scanning is the investigation of choice - it can detect concomitant lesions, it can be performed in intensive care units, and therapeutic interventions (such as percutaneous drainage) can be done simultaneously. • Early cholecystectomy may be appropriate, depending on the patient’s clinical condition. • Percutaneous cholecystostomy is an accepted alternative to cholecystectomy if the patient is unstable (placed percutaneously by radiology or open surgery).
- 54. Complications of cholecystitis • Empyema of the gallbladder – GB lumen filled with pus; • Perforation (5-10%) – generalised peritonitis, localised pericholecystic abscess; • Fistula formation with CBD, duodenum, colon, and stomach; • Mirizzi syndrome; • Cholangitis and sepsis; • Gallstone ileus (at the terminal ileum); • Gangrenous gallbladder • Empyema necessitatis > cholecystocutaneous fistula – spontaneous drainage of the gallbladder through the abdominal wall, occurs in neglected cases
- 55. Complications of cholecystectomy • Haemorrhage > due to injury to cystic artery, right hepatic artery • Bile leak > Biloma > due to injury to CBD, or slippage of ligature/clips from cystic duct • Injury to surrounding structure > intestines or liver • Intraabdominal sepsis - from stones and concretions lost in the peritoneal cavity during cholecystectomy • Post-cholecystectomy syndrome > persistent pain due to retained stones or chronic diarrhoea due to excess bile acid • Anaesthesia complications
- 56. Differentiating Acute cholecystitis from Biliary colic Acute cholecystitis Features Biliary colic Somatic Nature of pain Visceral Right hypochondrium Location of pain Epigastric > 3 hours Duration of pain < 3 hours Positive Murphy’s sign Negative Present Fever Absent Present Leucocytosis Absent Gallstones + thickened GB wall >3mm; pericholecystic fluid collection USG Gallstones
- 58. References • BAJA, 5th Edition • UpToDate (https://www.uptodate.com/) • https://emedicine.medscape.com/article/197206-overview#showall • Cope’s Early Diagnosis of the Acute Abdomen, 22nd Edition (2010) • Browse's Introduction to the Symptoms & Signs of Surgical Disease, 6th Edition (2021) • Bailey & Love's SHORT PRACTICE of SURGERY, 28th Edition (2023) • Indar A. A., Beckingham I. J.; Acute cholecystitis; Clinical review, BMJ 2002;325:639–43 • James Lorenzen Boyer, Carol Jean Soroka, Bile formation and secretion: An update, Journal of Hepatology, 2021;75:190-201, ISSN 0168-8278. https://doi.org/10.1016/j.jhep.2021.02.011 • Gutt C, Schläfer S, Lammert F: The treatment of gallstone disease. Dtsch Arztebl Int 2020; 117: 148–58. DOI: 10.3238/arztebl.2020.0148
Editor's Notes
- Gallstone disease and Cholecystitis
- The presence of stones in the gallbladder is not considered to be a disease unless they cause symptoms.
- The right hepatic duct and left hepatic duct leave the liver and join together to become the common hepatic duct. The cystic duct from the gallbladder joins the common hepatic duct halfway along to form the common bile duct. The pancreatic duct from the pancreas joins with the common bile duct further along to become the ampulla of Vater distally, which then opens into the duodenum. The sphincter of Oddi is a ring of muscle surrounding the ampulla of Vater that controls the flow of bile and pancreatic secretions into the duodenum.
- A xenobiotic is a chemical substance found within an organism that is not naturally produced or expected to be present within the organism. It can also cover substances that are present in much higher concentrations than are usual. Natural compounds can also become xenobiotics if they are taken up by another organism, such as the uptake of natural human hormones by fish found downstream of sewage treatment plant outfalls, or the chemical defenses produced by some organisms as protection against predators.
- A pheromone is a secreted or excreted chemical factor that triggers a social response in members of the same species. Pheromones are chemicals capable of acting like hormones outside the body of the secreting individual, to affect the behaviour of the receiving individuals.
- Bacterial infection and increase in bilirubin load play a role in the development of black and brown gallstones. These gallstones typically form in conditions of stasis (e.g., parenteral nutrition) or excess unconjugated bilirubin (e.g., hemolysis or cirrhosis).
- The Physicochemical Basis of Cholesterol Gallstone Admirand's triangular hypothesis/Triangle of solubility: Normal ratio of bile salt and lecithin to cholesterol is 25:1. Ratio below 13:1 leads to precipitation of cholesterol. Insoluble cholesterol is within the soluble micelle which is formed by lecithin and bile salts. If cholesterol component increases, bile gets supersaturated and inadequate micelle makes insoluble cholesterol to undergo crystallisation and cholesterol monohydrate stone formation.
- Factors associated with gallstone formation Remember The “Big 5” risk factors.
- Age: incidence of gallstones increases with age across all ethnic groups; becoming 4-10 times in > 40years; very low rate among infants and children.
- Female gender is a risk factor for developing gallstones, surpassing males in the incidence of gallstones and the chance of having surgery by 2:1 or 3:1; explained in part by hormonal effect: estrogen decreases bile salts secretion and increases cholesterol, whereas progestins act by impairing gallbladder emptying, causing stasis Oral contraceptive use and low-dose estrogen therapy for postmenopausal women increase risk)
- Lithogenic genes (ATP Binding Cassette Subfamily G Member 5/8; ABCG5/G8 in human) in hepatocytes and intestinal cells may play a role in gallstone formation. Overexpression of ABCG5/G8 protein increases cholesterol content in the gallbladder, thus increasing the likelihood of cholesterol crystal precipitation. Subsequently, ABCG5/G8 was found to be associated with cholesterol gallstone disease in patients, and two gallstone associated variants in ABCG5/G8 (ABCG5-R50C and ABCG8-D19H) were identified in Germans, Chileans, Chinese, and Indians. Taking this information into account, these may be the primary promoter genes of gallstones.
- In times of increased blood estrogen concentration, synthesis of cholesterol increases mainly by estrogen-induced stimulation of sterol regulatory element binding protein-2 (SREBP-2). These changes lead to excessive secretion of newly synthesized cholesterol, supersaturation of bile, and easily lead to cholesterol precipitation and gallstone formation.
- GSD – Gallstone disease Diagenesis – biotransformation; physical and chemical changes in bile leading to sludge and stone formation
- Microorganisms can enter the biliary system from the duodenum by migrating through the sphincter of Oddi. They can also spread hematogenously to the liver and from there into bile. When in bile, microorganisms play an important role as nucleating factors, leading to the formation of pigment and cholesterol gallstones
- Cholesterol accumulation is a major cause of atherosclerotic CVD and GSD. In the cardiovascular system, such metabolic abnormalities usually lead to the accumulation of excessive cholesterol esters in the arterial wall, leading to clinical atherosclerosis, which mainly occurs in the heart and brain, leading to cardiovascular and cerebrovascular diseases. If excess cholesterol cannot be dissolved in bile by the bile salts and/or phospholipids, it precipitates, thus leading to the formation of cholesterol gallstones in the gallbladder and/or the bile duct.
- Nonalcoholic fatty liver disease (NAFLD) is an important risk factor for gallstone formation. Other risk factors: certain medical conditions and medications: - Cirrhosis – decreased bile salts synthesis and malabsorption, chronic hemolysis, and a hyperestrogenic state - Inflammatory bowel disease, ileal resection, and cystic fibrosis – impair bile salt absorption, leading to cholesterol supersaturation; - estrogen and thiazide diuretics – increase biliary cholesterol secretion; - Progesterone – impair GB motility - Octreotide – GB hypomotility, increases deoxycholic acid reabsorption, leading to cholesterol supersaturation - Ceftriaxone – excreted in bile, cause biliary pseudolithiasis and sludge (disappear after antibiotic therapy is discontinued
- Gallstone disease may be thought of as having the following four stages Nearly 75% - 80% (depending on source of literature) of patients with gallstones have no obvious symptoms in the initial stages; As the gallstones progress in development, they may trigger symptoms and complications resulting from effects occurring within the gallbladder or from stones that escape the gallbladder to lodge in the CBD. Asymptomatic gallstones: - detected incidentally on abdominal imaging - majority will remain asymptomatic - Patients who develop symptoms typically report biliary colic
- Biliary colic is visceral pain, and there are no peritoneal signs because the gallbladder is not inflamed. However, voluntary guarding may be encountered depending upon the severity of the pain. ‘Gallstone colic’ is a preferable term to ‘Biliary colic’ because the pain is usually caused by spasm of the gallbladder in response to hormonal or neural stimulation, forcing a gallstone (or possibly sludge) down the gallbladder outlet or cystic duct, leading to increased intra-gallbladder pressure. This increase in pressure then results in pain. As the gallbladder relaxes, the stones often fall back from the cystic duct, and the pain slowly subsides. Not exacerbated by movement, not relieved by squatting, bowel movements, or passage of flatus
- Once a patient develops symptoms, it’s likely to recur and the patient is at increased risk for the development of complications There is an overlap between gallstone colic and acute cholecystitis. ~ a fifth of patients who present with biliary colic become jaundiced. Many cases of gallstone colic progress to acute cholecystitis.
- Symptoms other than biliary colic have been reported in patients with gallstones, but their predictive value for the presence of gallstone disease is poor. In many cases, they may coexist with biliary colic but may or may not be related to the gallstones.
- Since the gallbladder is not inflamed in uncomplicated biliary colic, the pain is poorly localized and visceral in origin; the patient has an essentially benign abdominal examination without rebound or guarding. Fever is absent. Presence of fever, persistent tachycardia, hypotension, or jaundice necessitate a search for complications of cholelithiasis, including cholecystitis, cholangitis, pancreatitis, or other systemic causes
- Diagnostic considerations include both intra-abdominal and extra-abdominal pathology that can present as upper abdominal pain, and that these conditions may coexist with cholelithiasis. A careful history and physical examination should guide further workup.
- Raise WCC – Leucocytosis: acute cholecystitis/choledocholithiasis/cholangitis
- Abdominal radiography and abdominal computed tomography (CT) scan, are less sensitive as compared with ultrasound for the detection of gallstones. Only 10 percent of gallstones contain enough calcium to make them sufficiently radio-opaque to be visible on a plain radiograph
- Ultrasound images of a gallbladder adenomatous polyp (arrow) (A) compared with a gallstone (arrowhead) (B). Note the shadow cast by the stone (dashed arrow) compared with the absence of a shadow behind the polyp
- Ultrasonographic images (Panel A) A large amorphous collection of sludge within the gallbladder (arrow) that does not cast an acoustic shadow. (Panel B) When the patient was turned onto one side, the gallbladder sludge formed a layer along the dependent portion of the gallbladder (arrows).
- Misleading ultrasound in a patient with gallstones
- During EUS, an ultrasound transducer on the tip of an endoscope is placed into contact with the gastric antrum, which is in close proximity to the gallbladder. This permits gallbladder visualization without interference from bowel gas, subcutaneous tissue, or the liver. As a result, EUS is more sensitive than transabdominal ultrasound for the detection of gallstones, particularly in patients who are obese or have other anatomic considerations that limit gallbladder visualization with transabdominal ultrasound
- Oral cholecystography – Oral cholecystography can diagnose gallstones, but it has largely been replaced by transabdominal ultrasound, which has higher sensitivity and specificity. Oral cholecystography is occasionally used in patients in whom a high-quality ultrasound examination cannot be performed (e.g., patients who are obese), and to evaluate patients who are being considered for medical dissolution therapy for gallstones. Cholescintigraphy (HIDA scan) – Cholescintigraphy (99mTc-heapto-iminodiacetic acid [HIDA] scanning) is not used in the diagnosis of gallstones, but is useful in excluding acute cholecystitis in patients who present with acute biliary colic.
- Endoscopic retrograde cholangiopancreatography (ERCP) is a technique that uses a combination of luminal endoscopy and fluoroscopic imaging to diagnose (diagnostic) and treat (therapeutic) conditions associated with the pancreatobiliary system. This technique is now used only as a therapeutic modality (sphincterotomy, stone extraction, stent insertion) in patients with obstructive jaundice; USG and MRCP have taken over the diagnostic aspect. The endoscopic portion of the examination uses a side-viewing endoscope that is passed through the esophagus and stomach and into the second portion of the duodenum. SE: haemorrhage, cholangitis, pancreatitis
- Magnetic resonance cholangiopancreatography (MRCP) showing 5 gallstones in the common bile duct (arrows). In this image, bile in the duct appears white; stones appear as dark-filling defects. Magnetic resonance cholangiopancreatography (MRCP) is a non-invasive modality that provides excellent images of the gallbladder and biliary system. These images are comparable to those obtained at endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous transhepatic cholangiography (PTC) without the potential complications of the latter; they can demonstrate ductal abnormalities, including obstruction/stricture, stones and tumours.
- Medical management is more effective in patients with good gallbladder function who have small stones (< 1 cm) with a high cholesterol content. Bile salt therapy (ursodeoxycholic acid) may be required for more than 6 months and has a success rate of less than 50%. A relative indication for Prophylactic cholecystectomy is before or during renal transplantation or during bariatric surgery. Patients with risk factors for complications of gallstones may be offered elective cholecystectomy, even if they have asymptomatic gallstones. These groups include persons with the following conditions and demographics: Cirrhosis Portal hypertension Children Transplant candidates Diabetes with minor symptoms Patients with a calcified or porcelain gallbladder should consider elective cholecystectomy due to the possibly increased risk of carcinoma (25%).
- Saint's triad is characterized by the concomitant occurrence of cholelithiasis, hiatal hernia, and colonic diverticulosis Cholecystectomy is a reasonable alternative if a thorough evaluation for other causes of the patient's symptoms is negative and if the patient has a symptomatic response to dissolution therapy, especially in patients who want to discontinue ursodiol therapy
- Acute cholecystitis refers to inflammation of the gallbladder or a syndrome of right upper quadrant pain, fever, and leukocytosis associated with gallbladder inflammation that is usually related to gallstone disease. CBD stones +/- Patients with acute cholangitis often present with Charcot's triad (fever, right upper quadrant pain, and jaundice) and leucocytosis. In severe cases, bacteraemia and sepsis may lead to hypotension and altered mental status (Reynolds' pentad). Obstructive stones in the biliary tract or ampulla of Vater can cause persistent biliary and pancreatic duct obstruction leading to acute pancreatitis and cholangitis. Mirizzi syndrome: An impacted stone in the cystic duct or Hartmann's pouch of the gallbladder obstructs the common hepatic duct both by extrinsic compression and associated inflammation. Mirizzi syndrome has been classified based on the presence and extent of a cholecystobiliary fistula: ●Type I (11 percent of Mirizzi syndrome): External compression of the common hepatic duct due to a stone impacted at the neck/infundibulum of the gallbladder or at the cystic duct. ●Type II (41 percent of Mirizzi syndrome): The fistula involves less than one-third of the circumference of the common bile duct. ●Type III (44 percent of Mirizzi syndrome): Involvement of between one-third and two-thirds of the circumference of the common bile duct. ●Type IV (4 percent of Mirizzi syndrome): Destruction of the entire wall of the common bile duct. Bouveret syndrome (impaction of a large gallstone within the pyloric channel) usually requires surgery to remove the impacted stone, repair the fistula, and remove the gallbladder. For patients who are unable or unwilling to undergo surgery, options include endoscopic removal of the obstructing stone and electrohydraulic lithotripsy of obstructing stones. Gallbladder cancer - hypothesized to be predisposed to by the recurrent inflammation and biliary stasis from gallstones.
- Cystic duct obstruction, if it persists for more than a few hours, may lead to acute gallbladder inflammation (acute cholecystitis)
- Chronic inflammatory cells - The cell types that characterize what pathologists term chronic inflammation primarily including lymphocytes, macrophages, and plasma cells. These leukocytes mediate innate as well as adaptive immunity. For historical reasons, pathologists continue to refer to macrophages as histiocytes.
- Over 90% of cases of acute cholecystitis result from obstruction of the cystic duct by gall stones or by biliary sludge that has become impacted at the neck of the gall bladder. Histologic changes of the gallbladder in acute cholecystitis can range from mild edema and acute inflammation to necrosis and gangrene. Occasionally, prolonged impaction of a stone in the cystic duct can lead to a distended gallbladder that is filled with colorless, mucoid fluid. This condition, known as a mucocele with white bile (hydrops), is due to the absence of bile entry into the gallbladder and absorption of all the bilirubin within the gallbladder
- Hemoglobinopathy Associated complaints may include fever, nausea, vomiting, and anorexia. There is often a history of fatty food ingestion one hour or more before the initial onset of pain
- Patients with acute cholecystitis are usually ill-appearing, febrile, tachycardic, and lie still on the examining table because cholecystitis is associated with true local parietal peritoneal inflammation that is aggravated by movement. Patients with complications may have signs of sepsis (gangrene), generalized peritonitis (perforation), abdominal crepitus (emphysematous cholecystitis), or bowel obstruction (gallstone ileus).
- Acute cholecystitis should be differentiated from biliary colic by the constant pain in the right upper quadrant and Murphy’s sign (in which inspiration is inhibited by pain on palpation)
- Mild elevations in serum aminotransferases and amylase, along with hyperbilirubinemia and jaundice, have been reported even in the absence of these complications and may be due to the passage of sludge, or pus In addition to a complete blood count, we evaluate levels of serum lipase and amylase, electrolytes, alanine aminotransferase, aspartate aminotransferase, bilirubin, calcium, and albumin to rule out other causes of acute abdominal pain or complications of acute cholecystitis. A pregnancy test should be performed in all women of childbearing age.
- Ultrasound scanning is the investigation of choice in patients suspected of having acute cholecystitis. Color flow Doppler is used frequently in sonography to semiquantitate overall blood flow to a region of interest.
- We perform Cholescintigraphy if the diagnosis remains unclear despite ultrasonography After intravenous injection, IDA radiotracers (Technetium-99m (99mTc)-labelled derivatives of iminodiacetic acid (hepatobiliary iminodiacetic acid [HIDA]) are taken up by hepatocytes and then excreted into the biliary system and then the abdomen is scanned; in patients with acute cholecystitis, the gallbladder lumen will not take up any radioactive isotope one to two hours after injection and therefore the gall bladder will not be visible on the scan. Magnetic resonance cholangiopancreatography or endoscopic ultrasound — Choledocholithiasis should be suspected in patients with acute cholecystitis and elevations of liver transaminases, total bilirubin, or evidence of common bile duct dilatation on ultrasound.
- Pain arising from a stone in the cystic duct or CBD is essentially the same because of identical segmental innervation of these structures. Consequently, during the acute painful attack itself, the surgeon is rarely, if ever, able to predict which course of events outlined above will ensue. Occasionally acute cholecystitis occurs in the absence of gallstones or obstruction of the cystic duct, but this accounts for only about 5 percent of cases. Acalculous cholecystitis is most often observed in an otherwise seriously ill patient who is being given intravenous hyperalimentation!
- The gall stone disimpacts and falls back into the gall bladder, which allows the cystic duct to empty. If the gall stone does not disimpact, complications - such as advanced cholecystitis (gangrenous cholecystitis or empyema of the gall bladder) or perforation—may result.
- The timing of surgery in acute cholecystitis remains controversial. Early cholecystectomy, undertaken by an experienced surgeon with excellent operating facilities within 5–7 days of the onset of the attack, is safe and shortens total hospital stay. Nevertheless, the conversion rate in laparoscopic cholecystectomy is higher in acute than in elective surgery. If early operation is not indicated, one should wait approximately 6 weeks for the inflammation to completely subside before operating. Percutaneous cholecystostomy is a safe alternative to cholecystectomy for very ill patients or those unfit to undergo surgery
- Risk factors include severe trauma or burns, major surgery (such as cardiopulmonary bypass), long term fasting, total parenteral nutrition, sepsis, diabetes mellitus, atherosclerotic disease, systemic vasculitis, acute renal failure, and AIDS. Over 70% of patients have atherosclerotic disease; this might explain the high prevalence of the condition in elderly men
- Bacteria inside gallstones have long been thought to be dead, as is explicit in the well known aphorism of Lord Moynihan: Gallstone is a ‘Tombstone erected to the memory of organisms which lie dead within them’. Anaesthesia complications: reaction to anaesthesia, PONV, lung/pulmonary complications, malignant hyperthermia