Figure 1 displays an acutely inflamed gall bladder (Cholecystitis) specimen. There are several gross features associated with acute cholecystitis; most apparent is the cholesterol stones filling the fundus and neck regions of the gallbladder (Cholelithiasis). The stones’ sizes suggest the chronic nature of pathogenesis, and their off-white colour indicates high proportions of calcium and phosphate salts (1). Further morphology relevant to the pathology is that the gallbladder is enlarged, with thick walls. This specimen is 15cm long, 5 cm wide, and its walls are about 1cm thick (compared to the usual dimensions of 7-10cm, 2.5cm, and 3mm respectively (2)). This owes to both the effects of acute and chronic inflammation; the thick, fibrous wall is indicative of a history of previous inflammatory episodes (due to intermittent oedema, fibrosis and leukocyte infiltration of the tissue layers). There are also the acute signs of red-grey “blotchy” discolouration due to a mixture of necrosis and haemorrhage, in the mucosal and submucosal layers (1).
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Expected Microscopic Appearance:
A biopsy of the specimen would include all the signs of acute (and chronic to a lesser extent) inflammation. Extensive fibrosis (formation of collagen fibres) will be the key visible feature, as well as amounts of fibrous scar tissue from previous healing. Leukocytes (mostly neutrophils and lymphocytes) will be seen infiltrating the mucosal and sub-serosal layers, as well as a small amount of monocytes. The mucosa will be atrophic (flattened) as a result of the inflammation, but there will also be proliferation of the epithelial cells in an attempt to repair itself. Some sections of mucosal folds may even fuse to form distinctive “buried crypts of epithelium” which lie below the mucosa, called Rokitansky Aschoff sinuses. Dilation of blood vessels and some haemorrhage (scattered erythrocytes) should also be visible (1).
Cholecystitis is intimately linked with gallstone (cholelith) formation (an estimated 90% of cases occur due to cystic duct/gallbladder neck obstruction by cholelithiasis (2)) and thus an understanding of the pathogenesis for cholelith formation is relevant.
Figure 2: General risk factors contributing to gallstones 1 recent discovery; gene for ATP-binding cassette (ABC) transporters (1) (see text)The major prerequisite for cholesterol gallstones is an imbalance of cholesterol and bile salt levels in the biliary secretions – specifically, excess cholesterol (1). Figure 2 mentions some of the main risk factors that contribute to this. Oestrogens increase cholesterol uptake in liver as well as synthesis by increasing the amount of hepatic lipoprotein receptors and by increasing activity of HMG-CoA reductase enzymes (key regulators of cholesterol biosynthesis). Blood cholesterol lowering drugs have a similar effect on these enzymes, in addition to reducing cholesterol conversion to bile. Recent studies have shown that having a certain variant (D19H) of ABCG5 and ABG2 genes coding for ATP-binding cassette transporters adds further risk for gallstones, because it biosynthesises more cholesterol (1).
Once cholesterol concentrations are too high for bile salts and phospholipids to accommodate (supersaturation), the cholesterol nucleates into solid “plate-like” crystals (cholesterol monohydrate). These are formed more frequently when there is decreased contractility or movement of the gall bladder (gallbladder stasis) as well as high secretions of mucus. Finally, the prolonged simultaneous occurrence of all of these conditions causes the crystals to aggregate further into macroscopic cholesterol stones, such as in Figure 1 (3).
Figure 3: Key events leading up to inflammation of the gallbladder. Note: Red arrows showing secondary events that occur later on.Acute cholecystitis nearly always results from gallstone obstruction of the cystic duct (1, 4). Obstruction at the neck raises the pressure within the lumen, resulting in three things; venous congestion, reduced lymphatic drainage, and decreased blood supply. The walls of the gallbladder then release prostaglandins (E2 and I2) to bring on inflammation. Lysosomic phospholipases released from cell injury hydrolyse biliary lecithins to lysolecithins (toxic) – these create further injury by disrupting the mucosal protective glycoprotein barrier and allowing bile salt damage at exposed areas (1). Figure 3 summarises these events. Note that bacterial infection can occur later on (4).
Symptoms and Signs:
Most patients present with sudden onset of right upper quadrant (RUQ) or epigastric pain, as well as a history of previous episodes of pain (4). Intolerance for fatty foods, anorexia, vomiting, and tachycardia are the usual signs associated with acute cholecystitis. Leukocytosis may be present, and hyperbilirubinemia indicates obstruction of the common bile duct (1). Palpable tenderness and a positive ‘Murphy sign’ (during inspiration gallbladder is palpable and patient winces from pain) confirms cholecystitis (3).
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Methods of investigating patient:
Ultrasound (US) is the ideal and preferred imaging technique for diagnosing acute calculous (presence of gallstones) cholecystitis, owing to its sensitivity of 80-100%. However, US is less effective for obese patients, and new studies show that recent advances in magnetic resonance imaging (hardware, software, and contrast media) have made it the most accurate imaging technique for the gallbladder (with a sensitivity of 95% (2)).
General approaches to treatment:
Upon confirmed diagnosis, patients will firstly be given fluid resuscitation, analgesics, and broad-spectrum antibiotics. Laparoscopic Cholecystectomy is the “standard definitive management” for acute calculous cholecystitis, and is proven to be effective (4). This is now performed preferably within 12-24 hours (decreasing risk of complications), rather than the previous practise of waiting up to 3 days for inflammation to subside before surgery (2). Often, surgeons will need to change their procedure to an open cholecystectomy; especially when there is uncertainty of the anatomical variants of a patient (4).
Features bearing on prognosis:
The work of Gurusamy K. et al.  has found that laparoscopic cholecystectomy is generally very safe. Potential complications include bile duct injury (potentially fatal), infection, and bile leakage, but this affected only 1 of 222 study participants (0.5%). The average hospital stay was 4-7 days, and time needed for full recovery ranged from 15-26 days. Apart from this, quality of life is not reduced .
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