L31 cholecystitis students

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  • 1. Cholecystitis Lecture 31

2. Cholecystitis (Greek, -cholecyst, "gallbladder", combined with the suffix -itis, "inflammation") is inflammation of the gallbladder, which occurs most commonly due to obstruction of the cystic duct with gallstones (cholelithiasis). Gall bladder- Cholecyst, Biliary Vesicle, Bile Bladder 3. Classification of Cholecystitis I. Acute Cholecystitis: calculous & acalculous II. Chronic Cholecystitis III. Acute superimposed on chronic 4. Acute Calculous Cholecystitis (90%) Acute Calculous cholecystitis is an acute inflammation of the gallbladder, precipitated 90% of the time by obstruction of the neck or cystic duct (by gallstones). It is the primary complication of gallstones and the most common reason for emergency cholecystectomy. ObstructionDistensionInflammation (due to chemical irritation & Infection) Hartmann's pouch is an out-pouching of the wall of the gallbladder at the junction of the neck of the gallbladder and the cystic duct. The commonest location of impaction of a gallstone is Hartmanns pouch. 5. Acalculous cholecystitis (10%) Cholecystitis without gallstones, called acalculous cholecystitis may occur in severely ill patients and accounts for about 10% of patients with cholecystitis. 6. Pathogenesis- Calculous cholecystitis Acute CALCULOUS cholecystitis results from chemical irritation and inflammation of the obstructed gallbladder. The action of mucosal phospholipases hydrolyzes luminal lecithins (Phospholipids) to toxic LYSOLECITHINS. The normally protective glycoprotein mucus layer is disrupted, exposing the mucosal epithelium to the direct DETERGENT action of bile salts. 7. Prostaglandins released within the wall of the distended gallbladder contribute to mucosal and mural inflammation. Gallbladder dysmotility develops; distention and increased intraluminal pressure compromise blood flow to the mucosa. Acute calculous cholecystitis frequently develops in diabeticpatients who have symptomatic gallstones. 8. Stone Obstruction Distension Inflammation (chemical irritation & infection: E Coli & Streptoccocus fecalis) 9. Pathogenesis- Acalculous cholecystitis Acute ACALCULOUS cholecystitis is thought to result from ISCHEMIA. The cystic artery is an end artery with essentially no collateral circulation. 10. ***Risk factors for acute Acalculous cholecystitis include: (1) Sepsis with hypotension and multisystem organ failure; (2) Immunosuppression; (3) Major trauma and burns; (4) Diabetes mellitus; & (5) Infections. (Salmanellosis & Cholera), Parasitic infestation Major nonbiliary surgery Dehydration, gallbladder stasis and sludging, vascular compromise, and, ultimately, bacterial contamination. Sepsis: The presence of pus-forming bacteria or their toxins in blood or tissues. Recent childbirth, Torsion of GB Cause Ischemia 11. Morphology GROSS: Size: The gallbladder is usually enlarged and tense, Color: bright red or blotchy, violaceous to green- black discoloration, imparted by subserosal hemorrhages. Serosa : The serosal covering is frequently layered by fibrin and, in severe cases, by a definite suppurative, coagulated exudate. Except for the presence or absence of calculi, the two forms of acute cholecystitis are morphologically similar. 12. Morphology Neck & Cystic duct: an obstructing stone is usually present LUMEN: Stones + Bile (cloudy or turbid bile that may contain large amounts of fibrin, pus, & hemorrhage). WALL: Thickened, edematous, and hyperemic. 13. In more severe cases GB is transformed into a green-black necrotic organ, termed Gangrenous cholecystitis, with small-to-large perforations. The invasion of GAS-FORMING ORGANISMS, notably clostridia and coliforms, may cause an acute Emphysematous cholecystitis. Mucosa: Bright Red, swollen. When obstruction of the cystic duct is complete, the lumen is filled with purulent exudate and the condition is known as EMPYEMA of the gallbladder. 14. Microscopy The inflammatory reactions are not distinctive and consist of the usual patterns of acute inflammation: Edema, Leukocytic infiltration, Vascular congestion, Frank abscess formation, or Gangrenous necrosis. 15. Clinical Features PAIN, fever, anorexia, tachycardia, sweating, nausea, vomiting & mild jaundice. The pain may be referred pain that is felt in the right scapula rather than the right upper quadrant or epigastric region (Boas' sign). Phrenic Nerve Boas's sign is hyperaesthesia (increased or altered sensitivity) below the right scapula . The patients of acute cholecystitis of either type have similar clinical features. with features of peritoneal irritation such as guarding and hyperaesthesia. The gallbladder is tender and may be palpable. Leucocytosis with neutrophilia 16. PAIN may also correlate with eating greasy, fatty, or fried foods. CCK The Murphy sign is specific, but not sensitive for cholecystitis. Elderly patients and those with diabetes may have vague symptoms that may not include fever or localized tenderness. Classically Murphy's sign is tested for during an abdominal examination; 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 in contact with the examiner's fingers) and winces with a 'catch' in breath, the test is considered positive. In order for the test to be considered positive, the same maneuver must not elicit pain when performed on the left side. Ultrasound imaging can be used to ensure the hand is properly positioned over the gallbladder 17. Clinical features More severe symptoms such as high fever, shock and jaundice indicate the development of complications such as Abscess formation, Perforation or Ascending cholangitis. 18. Another complication, gallstone ileus, occurs if the gallbladder perforates and forms a fistula with the nearby small bowel, leading to symptoms of intestinal obstruction. Ileus is a disruption of the normal propulsive ability of the gastrointestinal tract . It is caused by failure of peristalsis i.e. non-mechanical obstruction. 19. Clinical symptoms of acute acalculous cholecystitis tend to be more insidious, since symptoms are obscured by the underlying conditions precipitating the attacks. As a result of either delay in diagnosis or the disease itself, the incidence of gangrene and perforation is much higher in acalculous than in calculous cholecystitis. Early cholecystectomy within the first three days has a mortality of less than 0.5% and risk of complications such as perforation, biliary fistula, recurrent attacks and adhesions is avoided. However, medical treatment brings about resolution in a fairly large proportion of cases though chances of recurrence of attack persist. 20. Chronic cholecystitis is the commonest type of clinical gallbladder disease. There is almost constant association of chronic cholecystitis with cholelithiasis. 21. Chronic Cholecystitis Chronic cholecystitis may be a sequel to repeated bouts of mild to severe acute cholecystitis, but in many instances it develops in the apparent absence of antecedent attacks. Since it is associated with cholelithiasis in more than 90% of cases, the patient populations are the same as those for gallstones. 22. Supersaturation of bile predisposes to both chronic inflammation and, in most instances, stone formation. Unlike acute calculous cholecystitis, obstruction of gallbladder outflow is NOT a requisite. The symptoms of calculous chronic cholecystitis are biliary colic to indolent right upper quadrant pain & epigastric distress. 23. Morphology Grossly, the gallbladder is generally CONTRACTED but may be normal or enlarged. 24. Morphology The morphologic changes in chronic cholecystitis are extremely variable & sometimes minimal. The serosa is usually smooth and glistening but may be dulled by subserosal fibrosis. Dense fibrous adhesions On sectioning, the WALL is variably thickened, and has an opaque gray-white APPEARANCE. 25. In the uncomplicated case The LUMEN contains fairly clear, green- yellow, mucoid BILEand usually STONES. The MUCOSAitself is generally preserved?. 26. Microscopy- Chronic cholecystitis In the mildest cases, only scattered LYMPHOCYTES, PLASMA CELLS, & MACROPHAGES are found in the mucosa and in the subserosal fibrous tissue. In more advanced cases there is marked subepithelial and subserosal FIBROSIS, accompanied by MONONUCLEAR CELL INFILTRATION. CHRONIC INFLAMMATION 27. Outpouchings of the mucosal epithelium through the wall (Rokitansky-Aschoff sinuses) may be quite prominent. RokitanskyAschoff sinuses, also entrapped epithelial crypts, are pseudodiverticula or pockets in the wall of the gallbladder.Histologically they are outpouchings of gallbladder mucosa into the gallbladder muscle layer and subserosal tissue. They are not of themselves considered abnormal, but they can be associated with cholecystitis. They form as a result of increased pressure in the gallbladder and recurrent damage to the wall of the gallbladder. They are associated with gallstones (cholelithiasis). Carl Freiherr von Rokitansky and Ludwig Aschoff Germans. 28. Outpouchings of gallbladder mucosa into the gallbladder muscle layer and subserosal tissue Rokitansky-Aschoff sinuses Entrapped epithelial crypts Ppseudodiverticula Pockets in the wall of the gallbladder 29. Chronic cholecystitis, microscopic appearance. There is penetration of epithelium-lined spaces into the gallbladder wall (Rokitansky- Aschoff sinus) in an area. There is subepithelial and subse