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ANATOMY OF GALLBLADDER The gallbladder is a thin, green, saclike structure located on the inferior portion of the liver that stores and modifies bile not immediately needed for digestion. It is ~8 cm long and 4 cm wide and has three layers: the inner mucosa, muscularis, and serosa. The inner mucosa is folded to allow for expansion. The muscularis contains smooth muscle that allows for contraction. The serosa is the outer covering. The regions of the gallbladder itself include the fundus, body, and neck. It is connected to the common bile duct via the cystic duct. Arterial supply of gallbladder-- The gallbladder is supplied by the cystic artery (a branch of right hepatic artery that passes behind the cystic duct ), an accessory cystic artery arises the, from the gastroduodenal artery. Venous return is via cystic veins to the portal vein and small veins that drain directly into the liver. Lymphatic drainage from gallbladder goes both to the liver and to hilar nodes. Innervation is from the celiac plexus. Motor parasympathetic innervation from celiac ganglia, sympathetic ganglia level T8- T9.Sensory sympathetic innervation to celiac plexus (right posterior root ganglion level T8-T9. Physiology Bile is produced by the liver and transported via extrahepatic ducts to gallbladder where it is concentrated and released in response to humoral and neural control. Increase bile flow by: Vagal & splanchnic stimulation, theophylline, phenobarbital, and steroids. The liver excretes bile 40 ml/hour. Approximately 600 ml of bile produced daily (normal range: 250—1000 ml/day). Bile is composed of: (1) Electrolytes & water (97 %) (2) Bile pigments (1 %)

ReFarat CholeCystitis

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Page 1: ReFarat CholeCystitis

ANATOMY OF GALLBLADDER

The gallbladder is a thin, green, saclike structure located on the inferior portion of the liver that stores and modifies bile not immediately needed for digestion. It is ~8 cm long and 4 cm wide and has three layers: the inner mucosa, muscularis, and serosa. The inner mucosa is folded to allow for expansion. The muscularis contains smooth muscle that allows for contraction. The serosa is the outer covering. The regions of the gallbladder itself include the fundus, body, and neck. It is connected to the common bile duct via the cystic duct.

Arterial supply of gallbladder-- The gallbladder is supplied by the cystic artery (a branch of right hepatic artery that passes behind the cystic duct ), an accessory cystic artery arises the, from the gastroduodenal artery. Venous return is via cystic veins to the portal vein and small veins that drain directly into the liver. Lymphatic drainage from gallbladder goes both to the liver and to hilar nodes. Innervation is from the celiac plexus. Motor parasympathetic innervation from celiac ganglia, sympathetic ganglia level T8-T9.Sensory sympathetic innervation to celiac plexus (right posterior root ganglion level T8-T9.

PhysiologyBile is produced by the liver and transported via extrahepatic ducts to gallbladder where it is

concentrated and released in response to humoral and neural control. Increase bile flow by: Vagal & splanchnic stimulation, theophylline, phenobarbital, and steroids.

The liver excretes bile 40 ml/hour. Approximately 600 ml of bile produced daily (normalrange: 250—1000 ml/day). Bile is composed of:(1) Electrolytes & water (97 %)(2) Bile pigments (1 %)(3) Protein(4) Lipids

(a) Phospholipids, primarily lecithin(b) Cholesterol(c) Bile acids (bile salts); chenodeoxycholic acid and cholic acid conjugated with taurine

Functions of the gallbladder include:(1) Storage of bile(2) Release of bile (via cholecystokinin)(3) Concentration of bile

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N.B.: Concentration of bile by absorption of water & electrolytes results in a 10-fold increased concentration of lipids, bile salts, and bile pigments. The secretion of mucus (white bile) protects the gallbladder mucosa from the irritant effects of bile and facilitates the passage of bile through the cystic duct.

After meals, the gallbladder is empty and flat, like a deflated balloon. Before a meal, the gallbladder may be full of bile and about the size of a small pear. In response to signals, the gallbladder squeezes stored bile into the small intestine through a series of tubes called ducts. Bile helps digest fats, but the gallbladder itself is not essential.

HISTOLOGY

Has mucosa, muscularis propria and serosa on free surface; no muscularis mucosa or submucosa is presentMucosa: variable branching folds, more prominent if gallbladder not distendedSurface epithelium: composed of single layer of uniform, tall columnar cells with basal nuclei, indistinct nucleoli, pale cytoplasm due to sulfomucins; also pencil cells (small, darkly staining columnar cells), inconspicuous basal epithelial cells, T lymphocytes; no goblet cells, myoepithelial cells or melanocytes; neck region has tubuloalveolar mucus glands that secrete sulfo-, sialo- and neutral mucin and contain neuroendocrine cells; true glands are not present outside the neckLamina propria: loose connective tissue with blood vessels, lymphatics, occasional chronic inflammatory cells (IgA secreting plasma cells), no neutrophilsMuscular layer: circular, longitudinal and oblique smooth muscle fibers without distinct layers, resembles muscularis mucosa; adjacent to lamina propria without an intervening submucosaAdventitia: perimuscular connective tissue composed of collagen, elastic tissue, fat, vessels, lymphatics, nerves, paragangliaPeritoneum: lines gallbladder that is not directly attached to liver, is continuous with that of liverAberrant bile ducts (ducts of Lushka): present in 10% of cholecystectomy specimens, often buried in gallbladder wall adjacent to liver, may contain collar of fibrous tissue, may communicate with intrahepatic bile ducts

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Larger accessory bile ducts: join with cystic or hepatic ducts, may be present within gallbladder bedMucin-secreting accessory glands: prominent near terminus of common bile duct

The walls of the gall-bladder are about 2 mm. thick, and are composed of three coats : an internal, mucous and muscular ; a middle, of connective tissue ; and an external, the serous.The internal coat is 0.4 to 0.5 mm. thick, and is composed of alternating layers of connectivetissue and smooth muscle fibres, the most internal being a layer of connective tissue whichcontains a fine meshed capillary net work.

The connective tissue is dense and the muscle fibres are arranged in the form of interlacing bands. The internal surface is lined by a layer of cylindrical cells bearing a thickened, striated edge, and the surface is traversed by a network of small intersecting ridges, forming, as it were, a sort of lattice work. The middle coat, 0.5 to 1 mm. Thick, is formed of connectivetissue, the meshes of which are wider on the internal than at the external surface. This coatcontains the larger vessels and nerves. The external, or serous coat is thin, and consists of alayer of dense connective tissue and peritoneum.

A few mucous glands are found scattered here and there in the walls of the gall-bladder.Sections from this organ, hardened in alcohol, may be stained with the carmine or picro-carmine solution and mounted in glycerine or balsam.

The cystic and common ducts resemble in structure the hepatic duct. The inner surface of the former is thrown into crescentic ridges, and in the region of the neck of the gall bladder the connective tissue of the internal coat shows a circular arrangement. The ducts contain nomuscle fibres.

FUNCTIONS

The adult human gallbladder stores about 50 millilitres (1.8 imp fl oz; 1.7 US fl oz) of bile, which is released when food containing fat enters the digestive tract, stimulating the secretion of cholecystokinin (CCK). The bile, produced in the liver, emulsifies fats in partly digested food. After being stored in the gallbladder, the bile becomes more concentrated than when it left the liver, increasing its potency and intensifying its effect on fats.

Its main function is to store the bile that comes from the liver. Bile is a substance that helps in the digestion of fat. Fat does not dissolve in water, so in order to emulsify fat something special is needed. The liver produces the bile and then stores it in the gallbladder until the body needs to digest fats. When this moment comes, the gallbladder starts to let the bile flow down into the intestine, inside the duodenum, where fat is digested with its help and then absorbed by the organism. While bile sits in the gallbladder, the water from it pours out through the gallbladder's walls, making the bile more concentrated and therefore more effective. Bile also neutralizes some of the acids that are found in certain types of food.

The bile has two major functions in the body. Firstly, it breaks down the fats that you eat so that your body can utilize them. Without adequate bile you do not metabolize your fats well which can result in a deficiency of the fat-soluble vitamins (A, D, E and K). You may also have problems digesting the essential fatty acids. Amongst other symptoms you could have trouble utilizing calcium, have dry skin, peeling on the soles of your feet, etc. One way you can tell you have trouble digesting fats is if you have excessive burping that starts shortly after eating a meal that has fat in it. You might feel nauseous or experience gas and bloating.

Secondly, bile is a very powerful antioxidant which helps to remove toxins from the liver. The liver filters toxins (bacteria, viruses, drugs or other foreign substances the body doesn't want) and sends them out via the bile, which is made in the liver. The pathway of departure is from the liver through the bile ducts and into the gallbladder or directly into the small intestine where it joins waste matter and leaves through the colon with the feces. A healthy liver produces about a quart to a quart and a half of bile daily.

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ACUTE CHOLECYSTITIS

Cholecystitis is often caused by cholelithiasis (the presence of choleliths, or gallstones, in the gallbladder), with choleliths most commonly blocking the cystic duct directly. This leads to inspissation (thickening) of bile, bile stasis, and secondary infection by gut organisms, predominantly E. coli and Bacteroides species.

The gallbladder's wall becomes inflamed. Extreme cases may result in necrosis and rupture. Inflammation often spreads to its outer covering, thus irritating surrounding structures such as the diaphragm and bowel.

Less commonly, in debilitated and trauma patients, the gallbladder may become inflamed and infected in the absence of cholelithiasis, and is known as acute acalculous cholecystitis.

Stones in the gallbladder may cause obstruction and the accompanying acute attack. The patient might develop a chronic, low-level inflammation which leads to a chronic cholecystitis, where the gallbladder is fibrotic and calcified.

PATHOGENESIS OF CALCULOUS CHOLECYSTITIS

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. Obstruction of the cystic

CLASSIFICATION OF CHOLECYSTITIS

Calculous Acalculous

Catarrhal Gangrenous Phlegmonous

Biliary colic Dyspeptic Recurrent Residual

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duct causes the intraluminal pressure within the gall bladder to increase and, together with cholesterol supersaturated bile, triggers an acute inflammatory response. The trauma caused by the gall stones stimulates the synthesis of prostaglandins I2 and E2, which mediate the inflammatory response. Secondary bacterial infection with enteric organisms (most commonlyEscherichia coli, Klebsiella, and Streptococcus faecalis) occur in about 20% of cases.

Pathogenesis of calculous cholecystitis

Biliary sludge is a mixture of particulate matter and bile, and it may stimulate microlithiasis. If the sludge persists—for example, because the patient has already had several pregnancies or is receiving total parenteral nutrition—gall stones can form. Most patients with biliary sludge have no symptoms, but the sludge itself can cause acute cholecystitis.

Stage 1The gallbladder is stimulated by certain foods to contract -- passage of stone into the cystic duct-- sudden tension on the wall & stimulation of stretch receptors--Epigastric Pain (as the gallbladder is derived from foregut)—Reflex vomiting.

Clinical picture: Pain of sudden onset, colicky, and occurs within 15 to 30 minutes of eating. Severe nausea and vomiting. Tenderness & rigidity are found in the right hypochondrtum. Positive Roan’s sign--there is an area of hyperaesthesia between 9th & 11th ribs posteriorly on

the right side.Prognosis: is excellent at this stage. There are no systemic sequelae, and the majority of patients are

relieved after several hours. No specific treatment is indicated. With rest, the stone will drop back into the gallbladder, tension is relieved, and the attack is over.

Stage 2The gallstone is impacted in the cystic duct, and gallbladder cannot be emptied. Mucous

secretion occurs, with bacterial growth & chemical irritation of gallbladder wall. As the full thickness of the gallbladder wall becomes inflamed, the pain moves to the right upper quadrant.

Clinical picture: Pain character changes from colic to continuous, dull, or aching.

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Right Shoulder pain or subscapular (due to somatic innervation of the gallbladder by a branch of the right phrenic nerve via the hepatic plexus).

Systemic signs such as low-grade fever and leukocytosis may occur. Right upper quadrant tenderness. Gallbladder may be palpable.Prognosis: Cholecystitis may subside by the release of impacted stone or may develop to 3 rd stage.

Mild frank peritonitis may occurs late in this stage.

Stage 3Continued distention of the gallbladder occurs due to persistent cystic duct obstruction.

Bacterial invasion accompanies this stage, and peritonitis develops.Clinical picture:

Acutely tender right upper quadrant. Guarding rigidity with marked rebound tenderness. Fever associated with leukocytosis.Prognosis: condition (1) may subside or (2) may go on to perforation (Stage 4).

Stage 4 (Perforation of the gallbladder)Gallbladder wall vessels are end arteries. As the gallbladder distends, the tension on the wall

increases markedly --critical closing pressure of the arterioles is exceeded –gallbladder blood supply diminishes --Patchy areas of gangrene develop through which bile, pus & bacteria leaks (i.e. gallbladder perforation).

Site of perforation: (in bile system) Fundus commonest (away from the blood supply) Neck less commonly (from pressure necrosis of an impacted calculus)Sequelae of perforation: Perforation into peritoneal cavity (in which case peritoneal signs will develop in the associated

involved quadrants) Perforation may be partly sealed by the omentum, liver, or intestine Intrahepatic perforation may lead to abscess formation.

N.B. Perforation occurs in 48 to 72 hours in the usual patient, with progressive distention ofthe gallbladder.

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PATHOGENESIS OF ACALCULOUS CHOLECYSTITIS

Acalculous cholecystitis tends to occur in patients hospitalised for multiple trauma or acute non-biliary illness. 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.

RISK FACTORS

Risk factors for calculous cholecystitis mirror those for cholelithiasis and include the following:o Female sexo Certain ethnic groups o Obesity or rapid weight losso Drugs (especially hormonal therapy in women)o Pregnancyo Increasing age

Acalculous cholecystitis is related to conditions associated with biliary stasis, to include the following:

o Critical illnesso Major surgery or severe trauma/burnso Sepsiso Prolonged fasting

Other causes of acalculous cholecystitis include the following:o Cardiac events, including myocardial infarctiono Sickle cell diseaseo Diabetes mellituso Patients with AIDS with cytomegalovirus, cryptosporidiosis, or microsporidiosis

SYMPTOMS

The main symptom is abdominal pain that is located on the upper right side or upper middle of the abdomen. The pain may:• Be sharp, cramping, or dull• Come and go• Spread to the back or below the right shoulder blade• Occur within minutes of a meal

Nausea and vomiting are generally present, and patients may report fever.

In elderly patients, pain and fever may be absent, and localized tenderness may be the only presenting sign. Patients with acalculous cholecystitis may present similarly to patients with calculous cholecystitis, but acalculous cholecystitis frequently occurs suddenly in severely ill patients without a prior history of biliary colic. Often, patients with acalculous cholecystitis may present with fever and sepsis alone, without history or physical examination findings consistent with acute cholecystitis.

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Cholecystitis is differentiated from biliary colic by the persistence of constant severe pain for more than 6 hours.

Physical examination may reveal :

Fever Tachycardia Tenderness in the RUQ or epigastric region, often with guarding or rebound. A palpable gallbladder or fullness of the RUQ is present in 30-40% of cases. Jaundice may be noted in approximately 15% of patients. Tender right upper quadrant +/- Murphy's sign Ortner's sign - tenderness when hand taps the edge of right costal arch. Georgievskiy-Myussi's sign (phrenic nerve sign) - pain when press between edges of sternocleidomastoid muscle.

The absence of physical findings does not rule out the diagnosis of cholecystitis. Many patients present with diffuse epigastric pain without localization to the RUQ. Patients with chronic cholecystitis frequently do not have a palpable RUQ mass secondary to fibrosis involving the gallbladder.

Elderly patients and patients with diabetes frequently have atypical presentations, including absence of fever and localized tenderness with only vague symptoms.

If he has jaundice, swinging fever, chills and rigors, suspect that his cholecystitis is complicated by cholangitis.

DIAGNOSIS1) Clinical pictures and anamnesia

Clinical features of acute cholecystitis: diagnosis is made when features from all three points of diagnostic triangle are present

2) Laboratory test Leukocytosis with a left shift may be observed in cholecystitis.

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Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels are used to evaluate the presence of hepatitis and may be elevated in cholecystitis or with common bile duct obstruction. Bilirubin and alkaline phosphatase assays are used to evaluate evidence of common duct obstruction. Amylase/lipase assays are used to evaluate the presence of pancreatitis. Amylase may also be elevated mildly in cholecystitis. An elevated alkaline phosphatase level is observed in 25% of patients with cholecystitis. Urinalysis is used to rule out pyelonephritis and renal calculi.

3) Imaging studies(a) Radiography (without contrast)

Gallstones may be visualized in 10-15% of cases. This finding only indicates cholelithiasis, with or without active cholecystitis. Gas limited to the gallbladder wall or lumen represents emphysematous cholecystitis, usually because of gas-forming bacteria, such as Escherichia coli and clostridial and anaerobic streptococci species. Emphysematous cholecystitis is associated with an increased mortality rate and occurs most commonly in males with diabetes and with acalculous cholecystitis. A diffusely calcified gallbladder (ie, porcelainized) most commonly is associated with carcinoma.

(b) Ultrasonography

Ultrasonography provides greater than 95% sensitivity and specificity for the diagnosis of gallstones more than 2 mm in diameter. Ultrasonography is 90-95% sensitive for cholecystitis and is 78-80% specific. Studies indicate that emergency clinicians require minimal training in order to use right upper quadrant ultrasonography in their practice.

Ultrasonographic findings that are suggestive of acute cholecystitis include the following: pericholecystic fluid, gallbladder wall thickening greater than 4 mm, and sonographic Murphy sign. The presence of gallstones also helps to confirm the diagnosis.

Ultrasonography is performed best following a fast of at least 8 hours because gallstones are visualized best in a distended bile-filled gallbladder.

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Grossly thickened gallbladder wall (12.8mm measured between callipers, normally up to 2-3mm) with calculi (arrow) within the gallbladder and pericholecystic fluid.

c) Hepatobiliary scintigraphy (hepatoiminodiacetic acid [HIDA]/diisopropyl iminodiacetic acid [DISIDA])

HBS has been found to be up to 95% accurate in diagnosing acute cholecystitis. The reported sensitivities and specificities of biliary scintigraphy are in the range of 90-100% and 85-95%. Biliary scintigraphy is the gold standard investigation when the diagnosis remains in doubt after ultrasound scanning. The patient is given an intravenous injection of radiolabelled hydroxyiminodiacetic acid 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. Occasionally, an acutely inflamed gall bladder may have delayed filling, leading to a false positive result, but augmentation with morphine reduces this.

(c) CT scan

This is a CT scan of the upper abdomen showing cholecystitis (gall stones).

DIFFERENTIAL DIAGNOSIS Acute gastritis Amoebic hepatic abcess

Appendicitis Biliary colic Cholangitis Cholangiocarcinoma

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Acute pancreatitis Nephrolithiasis Gastric ulcer Peptic ulcer disease

MANAGEMENTPatients should be fasted, rehydrated with intravenous fluids, and given oxygen therapy and

adequate analgesia. Indometacin (25 mg three times daily for a week) can reverse the inflammation of the gall bladder and the contractile dysfunction seen in the early stages (first 24 hours) of cholecystitis. The prokinetic action of indometacin will also improve postprandial emptying of the gall bladder in patients with gallbladder disease. A single intramuscular dose of diclofenac (75 mg) may substantially decrease the rate of progression to acute cholecystitis in patients with symptomatic gall stones. Because of the risk of superimposed infection, intravenous antibiotics should be started empirically if the patient has systemic signs or if no improvement is seen after 12-24 hours. A second generation or newer cephalosporin should be used (for example, cefuroxime 1.5 g every 6-8 hours) with metronidazole (500 mg every 8 hours). Non-operative management—solvent dissolution therapy or extracorporeal shockwave lithotripsy—has been used with variable results to treat chronic cholecystitis in patients unfit for surgery, but it has no place in the management of acute cholecystitis.

SURGICAL TREATMENTAbout 20% of patients with acute cholecystitis need emergency surgery. Such surgery is

indicated if the patient's condition deteriorates or when generalised peritonitis or emphysematous cholecystitis is present. These features suggest gangrene or perforation of the gall bladder.

Cholecystectomy

The timing of surgery for the 80% of patients without evidence of gangrene or perforation is under debate. Open cholecystectomy traditionally has been performed 6-12 weeks after the acute episode to allow the inflammatory process to resolve before the procedure (interval surgery). Patients with acute cholecystitis who undergo early laparoscopic cholecystectomy (before symptoms have lasted 72-96 hours) have lower complication rates and lower conversion rates than open cholecystectomy and shorter hospital stays than those undergoing interval surgery. Early surgery for acute cholecystitis also has a lower conversion rate than delayed surgery (which is performed during the index admission after conservative management and after symptoms have lasted 3-5 days). Early surgery also avoids complications when conservative treatment fails. A long time between onset of symptoms and presentation is associated with advanced disease.

Early laparoscopic surgery is safe and feasible in patients with acute cholecystitis. If early intervention—less than 72 hours after symptoms started—can be achieved, “oedema planes” present during this period allow the gall bladder to be dissected laparoscopically. Although it is desirable to operate within this time period, it is often difficult to do so in clinical practice. By the time inflammation has been present for more than 72 hours, features of chronic inflammation (such as fibrosis) predominate and make it more difficult to dissect the gall bladder. The optimal treatment for patients presenting with acute cholecystitis should be resuscitation followed by laparoscopic cholecystectomy on the next available surgical list.

Patients with fever, serum bilirubin >170 μmol/l, male sex, body temperature >38°C, and advanced cholecystitis are more likely to have complications.

Contraindications for laparoscopic cholecystectomy include the following:

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High risk for general anesthesia Morbid obesity Signs of gallbladder perforation, such as abscess, peritonitis, or fistula Giant gallstones or suspected malignancy End-stage liver disease with portal hypertension and severe coagulopathy

Percutaneous cholecystostomyPercutaneous cholecystostomy is a minimally invasive procedure that can benefit patients with

serious comorbidity who are at high risk from major surgery. Percutaneous cholecystostomy can be performed at the bedside under local anaesthetic and is suitable for patients in intensive care units and those with burns. It is the definitive treatment in patients with acalculous cholecystitis or it may be used as a temporising measure—to drain infected bile and delay the need for definitive treatment.

Percutaneous cholecystostomy gives clinical improvement in about three quarters of patients. Mortality after this procedure is related to comorbidity (for example, pneumonia or myocardial infarction) or pre-existing sepsis. An incomplete or poor response to cholecystostomy within the first 48 hours may indicate causes of sepsis other than cholecystitis, inadequate antibiotic coverage, possible complications (such as dislodgement of the drainage tube), or necrosis of the wall of the gall bladder.

Patients can undergo cholecystectomy after percutaneous cholecystostomy. In patients unfit to be given a general anaesthetic, the drain can be left in place for more than six weeks to allow radiological extraction of calculi at a later date.

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Complications

(1) Gangrenous cholecystitis

Gangrenous cholecystitis occurs in 2-30% of cases of acute cholecystitis. Men aged over 50 with a history of cardiovascular disease and leucocytosis (>17 000 leucocytes/ml) have the highest risk of gangrene of the gall bladder.Gangrene occurs most commonly at the fundus because the vascular supply often becomes compromised. Urgent laparoscopic cholecystectomy should be considered in patients at high risk of gangrene, and the surgeon should have a low threshold for conversion to open cholecystectomy during the procedure.

(2) Gallbladder perforation

The gall bladder is perforated in 10% of cases of acute cholecystitis—usually in patients who sought medical attention after a delay or in those who do not respond to conservative management. Perforation most commonly occurs at the fundus. After the gall bladder has perforated, patients may experience transient relief of their symptoms because the gall bladder decompresses, but peritonitis then develops.

Free perforation presents with generalised biliary peritonitis and is associated with a mortality of 30%. Localised perforation, with the formation of pericholecystic abscesses, is more common,

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because the adherent viscera adjacent to the perforation tend to localise spillage of the contents of the gall bladder. A mass may be palpable in patients with localised perforation, and computed tomography is the most useful investigation.

(3) Cholecystoenteric fistulas

An acutely inflamed gall bladder may create a cholecystoenteric fistula by adhering to and causing a perforation in other parts of the gastrointestinal tract. The most common sites for fistulas are the duodenum and the hepatic flexure of the colon. Decompression of the gall bladder because of a fistula may cause resolution of the acute cholecystitis. Air in the biliary tree (pneumobilia) can be seen on abdominal radiographs, and imaging enhanced with contrast agents may show fistulas.

(4) Gallstone ileus

Gallstone ileus—obstruction of the small intestine caused by a gall stone passing from the biliary tract into the intestinal tract through a fistula—should be considered in elderly patients with no obvious cause for the intestinal obstruction. Patients may not have a history of cholecystitis. Mortality (15-20%) is attributed to delays before surgery is performed or to coexisting medical illnesses. Classic findings on abdominal radiographs include pneumobilia, intestinal obstructions, and gall stones in unusual sites.

Prognosis

For uncomplicated cholecystitis, the prognosis is excellent, with a very low mortality rate. In patients who are critically ill with cholecystitis, the mortality rate approaches 50-60%,

especially in the setting of gangrene or empyema. Once complications such as perforation/gangrene develop, the prognosis becomes less

favorable. In patients who are critically ill with acalculous cholecystitis and perforation or gangrene, the mortality rate can be as high as 50-60%.

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CHRONIC CHOLECYSTITIS

Chronic cholecystitis is usually caused by repeated attacks of acute cholecystitis. This leads to thickening of the gallbladder walls. The gallbladder begins to shrink and eventually loses the ability to perform its function, which is concentrating, storing, and releasing bile.

There are several common causes of this disorder, but the most common by far is the blocking of the cystic duct leading from the gall bladder to the intestines by gall stones. This leads to build up of bile in the gall bladder, or bile stasis as it is called in the medical world. Bile stasis in turn leads to an infection by mostly E.coli and Bacteroides species. The infection leads to an even further inflammation of the gall bladder. The pain that results is sometimes accompanied by a fever that results from the body fighting off the infection. If the condition remains untreated, shock and jaundice may set in.

The disease occurs more often in women than in men. The incidence increases after age 40. The main risk factors include the presence of gallstones (in which case, the symptoms are due to gallstones).

Gallbladder with chronic cholecystitis and cholelithiasis

Possible complications of chronic cholecystitis :

Cancer of the gallbladder (rarely) Jaundice Pancreatitis Worsening of the condition

PreventionBecause most cases of cholecystitis are caused by gallstones, you can reduce your risk of

cholecystitis by taking the following steps to prevent gallstones:

Don't skip meals. Try to stick to your usual mealtimes each day. Skipping meals or fasting can increase the risk of gallstones.

Exercise most days of the week. Being inactive may increase the risk of gallstones, so incorporate physical activity into your day. If you haven't been active lately, start slowly and work your way up to 30 minutes or more of activity on most days of the week.

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Lose weight slowly. If you need to lose weight, go slow. Rapid weight loss can increase the risk of gallstones. Aim to lose 1 or 2 pounds (0.5 to about 1 kilogram) a week.

Maintain a healthy weight. Obesity and being overweight increase the risk of gallstones. Work to achieve a healthy weight by reducing the number of calories you eat and increasing the amount of physical activity you get. Once you achieve a healthy weight, work to maintain that weight by continuing your healthy diet and continuing to exercise.