Acute Cholecystitis Essay Example

Acute Cholecystitis Essay Example Acute Cholecystitis Essay Acute Cholecystitis Essay kulasekar Definition Cholecystitis is inflammation of the gallbladder, usually resulting from a gallstone blocking the cystic duct. Gallbladder inflammation usually results from a gallstone blocking the flow of bile. Typically, people have abdominal pain that lasts more than 6 hours, fever, and nausea. Ultrasonography can usually detect signs of gallbladder inflammation. The gallbladder is removed, often using a laparoscope. Cholecystitis is the most common problem resulting from gallbladder stones. It occurs when a stone blocks the cystic duct, which carries bile from the gallbladder Causes In 90% of cases, acute cholecystitis is caused by gallstones in the gallbladder. Severe illness, alcohol abuse and, rarely, tumors of the gallbladder may also cause cholecystitis. Acute cholecystitis causes bile to become trapped in the gallbladder. The build up of bile causes irritation and pressure in the gallbladder. This can lead to bacterial infection and perforation of the organ. Gallstones occur more frequently in women than men. Gallstones become more common with age in both sexes. Native Americans have a higher rate of gallstones. Symptoms The main symptom is abdominal pain particularly after a fatty meal that is located on the upper right side of the abdomen. Occasionally, nausea and vomiting or fever may occur. Exams and Tests A doctors examination of the abdomen by touch (palpation) may reveal tenderness. Tests that detect the presence of gallstones or inflammation include: Abdominal ultrasound Abdominal CT scan Abdominal x-ray Oral cholecystogram Gallbladder radionuclide scan A CBC shows infection by an elevated white blood cell count [pic] Outlook (Prognosis) Patients who have cholecystectomy usually do very well. Possible Complications Empyema (pus in the gallbladder) Peritonitis (inflammation of the lining of the abdomen) Gangrene (tissue death) of the gallbladder Injury to the bile ducts draining the liver (a rare complication of cholecystectomy) Cholecystitis is classified as acute or chronic. Acute Cholecystitis: Acute cholecystitis begins suddenly, resulting in severe, steady pain in the upper abdo men. At least 95% of people with acute cholecystitis have gallstones. The inflammation almost always begins without infection, although infection may follow later. Inflammation may cause the gallbladder to fill with fluid and its walls to thicken. Rarely, a form of acute cholecystitis without gallstones (acalculous cholecystitis) occurs. Acalculous cholecystitis is more serious than other types of cholecystitis. It tends to occur after the following: Major surgery Critical illnesses such as serious injuries, major burns, and bodywide infections (sepsis) Intravenous feedings for a long time Fasting for a prolonged time A deficiency in the immune system It can occur in young children, perhaps developing from a viral or another infection. Chronic Cholecystitis: Chronic cholecystitis is gallbladder inflammation that has lasted a long time. It almost always results from gallstones. It is characterized by repeated attacks of pain (biliary colic). In chronic cholecystitis, the gallbladder is damaged by repeated attacks of acute inflammation, usually due to gallstones, and may become thick-walled, scarred, and small. The gallbladder usually contains sludge (microscopic particles of materials similar to those in gallstones), or gallstones that either block its opening into the cystic duct or reside in the cystic duct itself. A gallbladder attack, whether in acute or chronic cholecystitis, begins as pain. The pain of cholecystitis is similar to that caused by gallstones (biliary colic) but is more severe and lasts longer- more than 6 hours and often more than 12 hours. The pain peaks after 15 to 60 minutes and remains constant. It usually occurs in the upper right part of the abdomen. The pain may become excruciating. Most people feel a sharp pain when a doctor presses on the upper right part of the abdomen. Breathing deeply may worsen the pain. The pain often extends to the lower part of the right shoulder blade or to the back. Nausea and vomiting are common. Within a few hours, the abdominal muscles on the right side may become rigid. Fever occurs in about one third of people with acute cholecystitis. The fever tends to rise gradually to above 100. 4 ° F (38 ° C) and may be accompanied by chills. Fever rarely occurs in people with chronic cholecystitis. In older people, the first or only symptoms of cholecystitis may be rather general. For example, older people may lose their appetite, feel tired or weak, or vomit. They may not develop a fever. Typically, an attack subsides in 2 to 3 days and completely resolves in a week. If the acute episode persists, it may signal a serious complication. A high fever, chills, a marked increase in the white blood cell count, and essation of the normal rhythmic contractions of the intestine (ileus- see Gastrointestinal Emergencies: Appendicitis) suggest pockets of pus (abscesses) in the abdomen near the gallbladder from gangrene (which develops when tissue dies) or a perforated gallbladder. If people develop jaundice (see Manifestations of Liver Disease: Jaundice) or pass dar k urine and light-colored stools, the common bile duct is probably blocked by a stone, causing a backup of bile in the liver (cholestasis). Inflammation of the pancreas (pancreatitis) can develop. It is caused by a stone blocking the ampulla of Vater, near the exit of the pancreatic duct. Acalculous cholecystitis typically causes sudden, excruciating pain in the upper abdomen in people with no previous symptoms or other evidence of a gallbladder disorder. The inflammation is often very severe and can lead to gangrene or rupture of the gallbladder. In people with other severe problems (including people in the intensive care unit for another reason), acalculous cholecystitis may be overlooked at first. The only symptoms may be a swollen (distended), tender abdomen or a fever with no known cause. If untreated, acalculous cholecystitis results in death for 65% of people. Diagnosis Doctors diagnose cholecystitis based mainly on symptoms and results of imaging tests. Ultrasonography is the best way to detect gallstones in the gallbladder. Ultrasonography can also detect fluid around the gallbladder or thickening of its wall, which are typical of acute cholecystitis. Often, when the ultrasound probe is moved across the upper abdomen above the gallbladder, people report tenderness. Cholescintigraphy, another imaging test, is useful when acute cholecystitis is difficult to diagnose. For this test, a radioactive substance (radionuclide) is injected intravenously. A gamma camera detects the radioactivity given off, and a computer is used to produce an image. Thus, movement of the radionuclide from the liver through the biliary tract can be followed. Images of the liver, bile ducts, gallbladder, and upper part of the small intestine are taken. If the radionuclide does not fill the gallbladder, the cystic duct is probably blocked by a gallstone. Liver blood tests are often normal unless the person has an obstructed bile duct. Other blood tests can detect some complications such as a high level of a pancreatic enzyme (lipase or amylase) in pancreatitis. A high white blood cell count suggests inflammation, an abscess, gangrene, or a perforated gallbladder. Treatment People with acute or chronic cholecystitis need to be hospitalized. They are not allowed to eat or drink and are given fluids and electrolytes intravenously. A doctor may pass a tube through the nose and into the stomach, so that suctioning can be used to keep the stomach empty and reduce fluid accumulating in the intestine if the intestine is not contracting normally. Usually, antibiotics are given intravenously, and pain relievers are given. If acute cholecystitis is confirmed and the risk of surgery is small, the gallbladder is usually removed within 24 to 48 hours after symptoms start. If necessary, surgery can be delayed for 6 weeks or more while the attack subsides. Delay is often necessary for people with a disorder that makes surgery too risky (such as a heart, lung, or kidney disorder). If a complication such as an abscess, gangrene, or perforated gallbladder is suspected, immediate surgery is necessary. In chronic cholecystitis, the gallbladder is usually removed after the acute episode subsides. In acalculous cholecystitis, immediate surgery is necessary to remove the diseased gallbladder. Surgical removal of the gallbladder (cholecystectomy) is usually done using a flexible viewing tube called a laparoscope. After small incisions are made in the abdomen, the laparoscope and other tubes are inserted, and surgical tools are passed through the incisions and used to remove the gallbladder. [pic] Pain After Surgery: A few people have new or recurring episodes of pain that feel like gallbladder attacks even though the gallbladder (and the stones) have been removed. The cause is not known, but it may be malfunction of the sphincter of Oddi, the muscles that control the release of bile and pancreatic secretions through the opening of the bile and pancreatic ducts into the small intestine. Pain may occur because pressure in the ducts is increased by sphincter spasms, which hinders the flow of bile and pancreatic secretions. Pain also may result from small gallstones that remain in the ducts after the gallbladder is removed. More commonly, the cause is another problem, such as irritable bowel syndrome or even peptic ulcer disease. Endoscopic retrograde cholangiopancreatography (ERCP) may be necessary to determine if the cause of pain is increased pressure. For this procedure, a flexible viewing tube (endoscope) is inserted through the mouth and into the intestine, and a device to measure pressure is inserted through the tube. If pressure is increased, surgical instruments are inserted into the tube and used to cut and thus widen the sphincter of Oddi. This procedure (called endoscopic sphincterotomy) can relieve symptoms in people who have an abnormality of the sphincter. Background Acute cholecystitis (AC) occurs as a result of inflammation of the gallbladder (GB) wall usually secondary to cystic duct obstruction. In 90% of patients, AC is initiated by impaction of a calculus in the neck of the GB or in the cystic duct. 22 Acute acalculous cholecystitis (AAC) represents inflammation of the GB in the absence of GB calculi. AAC occurs more commonly in children and adults who are critically ill or in those who have recently undergone stress in the form of severe trauma, burns, or major surgery. Acute emphysematous cholecystitis is characterized by the presence of gas within the wall and/or lumen of the GB. It occurs more commonly in diabetic men and less frequently in association with cholelithiasis. Emphysematous cholecystitis is considered either a complication of AC or a separate entity. For excellent patient education resources, see eMedicines Liver, Gallbladder, and Pancreas Center. Also, visit eMedicines patient education article Gallstones. Pathophysiology AC represents an acute inflammation of the GB caused in most instances by obstruction of the cystic duct, usually by a gallstone and resulting in acute inflammation of the GB wall. AC is one of the major complications of cholelithiasis. The inflammatory process begins with a calculous obstruction of the cystic duct or GB neck. The exact mechanism by which GB inflammation is initiated is unknown. Microorganisms can be identified in 80% of cases early in the disease onset; such organisms include primarily  Escherichia coli, other gram-negative aerobic rods, enterococci, and a number of anaerobes. The bacterial invasion is not considered  to be  a primary event, because in 20% of patients, no bacterial growth  occurs in  surgical specimens. 1 The general consensus is that bacterial infection is a secondary event,  not an initiating one. Spontaneous resolution of AC may occur within 5-7 days after onset of symptoms,  because of reestablishment of cystic duct patency. In the majority of such cases, fibrotic wall thickening of the GB occurs, which  is characteristic of chronic cholecystitis. In more than 90% of cholecystectomy specimens, the histologic pattern is  AC superimposed on chronic cholecystitis. If the cystic duct patency is not reestablished, inflammatory cell infiltration of the GB wall follows,  with the occurrence of  mural and mucosal hemorrhagic necrosis. Gangrenous cholecystitis may  be seen  in as many as 21% of AC patients. Acalculous cholecystitis occurs in a different clinical setting, occurring  more often in males, usually children and in those older than 65 years. The pathophysiology of acalculous cholecystitis is  not well  understood but is probably multifactorial. Systemic mediators of inflammation, localized or generalized tissue ischemia, and bile stasis probably work to gether. The population at risk for acalculous AC often has predisposing factors for bile stasis; such  populations include patients with  starvation, on parenteral nutrition, using narcotic analgesics, and  lacking mobility in postoperative states. Hypovolemia and shock also predispose such patients to tissue ischemia, although ischemia may be a primary event causing acalculous AC,  such as  small-vessel vasculitis,  or may be  a complication of hepatic chemoembolization. Often, functional cystic duct obstruction is present and is related to inflammation and viscous bile. Extrinsic compression may also play a role in the development of bile stasis. The majority of patients with acalculous AC disease have secondary infection with gram-negative enteric flora3; however, in patients with typhoid fever, infection as a primary event has been  identified with  Salmonella organisms. AIDS-related cholecystitis and cholangiopathy may be secondary to cytomegalovirus (CMV) infection  and infections with Cryptosporidium organisms. In patients who have  emphysematous cholecystitis,  ischemia of the GB wall is followed by infection with gas-forming organisms that produce gas in the GB lumen, in the GB  wall, or both. In 30-50% of patients, preexisting diabetes mellitus is present,  and the  male-to-female ratio  is 5:1. 22 Gas may be confined to the GB; however, in 20% of cases, gas is also seen in the rest of biliary tree. Gallstones are not present in 30-50% of cases, and the mortality rate is 15%. 2  There is a predisposition  for gangrene formation and perforation, but clinical symptoms are mild, which can be deceptive. Emphysematous cholecystitis  may occur after  chemoembolization  as palliation  for hepatocellular carcinoma,  following atheromatous embolism during aortography, and after GB hypoperfusion during cardiorespiratory resusc itation. The following factors have been  associated with acalculous cholecystitis4: Surgery, particularly abdominal Severe burns Gastroenteritis Severe trauma Total parenteral nutrition (TPN) Mechanical ventilation Blood transfusion reactions Dehydration Narcotic analgesia Diabetes mellitus Antibiotics, particularly broad spectrum Hepatic arterial embolization (islet cell tumors and hepatocellular carcinoma) Postpartum complications Vascular insufficiency and vasculitis such as systemic lupus erythematosus (SLE) and Sjogren syndrome Arteriostenosis/hypertension AIDS, CMV, Cryptosporidium infections Typhoid Empyema of the GB may develop as a complication of AC. In AC, the GB is usually distended  as a result of  inflammatory cells mixed with bile and calculi. The bile becomes infected as the disease progresses. In 85% of patients, the cystic duct disimpacts, and  the inflammation in the GB settles. If the cystic duct remains obstructed, the inflammatory process may progress to a GB empyema and  eventually  result in  perforation. Frequency United States Because of the close relationship between gallstones and AC, the distribution and the incidence of AC follow that of cholelithiasis. Gallstones may be present in more than 20 million  persons in the United States,  resulting in 500,000 cholecystectomies annually. In 10-20% of patients, AC complicates the course of symptomatic gallstones. 2   AAC accounts for 5-15% of cases of AC,22 with the  incidence  being higher in ICU patients, particularly  those with burns and trauma. Most cases of AC in the ICU are acalculous, but in this setting, the overall incidence of acalculous AC is only 0. 2%. In the majority of postoperative cases (90%), AC is acalculous. 5 Mortality/Morbidity The AC mortality of 5-10% is  mostly confined to patients older than 60 years. AC may be complicated by empyema, gangrenous cholecystitis, GB perforation, pericholecystic abscess, and bilioenteric fistula. Gangrenous cholecystitis is a frequent cause of GB perforation. Suppurative complications are more frequent in the elderly. Most localized perforations can be satisfactorily treated by means of surgery. Although free intraperitoneal perforation is  rare, it is associated with a mortality of 25%. Necrosis of the GB wall occurs in about 60% of cases of acalculous cholecystitis because gangrene and perforation are frequent. Mortality can be as high as 9-66%. 6 The higher mortality in AAC  has been  attributed to delayed diagnosis and comorbidities. The morbidity associated with emphysematous cholecystitis is also higher, because  GB wall gangrene and perforation. Recurrent symptoms are common in patients with AC who are treated expectantly, and most patients need elective cholecystectomy. Race Because of the close relationship between gallstones and AC, the incidence of  AC is expected to be higher in races with a higher incidence of gallstones. Such populations include Native Americans and persons of Chinese or Japanese descent. Sex The male-to-female ratio of AC is 1:3. AAC is more common in men than in women; the male-to-female ratio in AAC is 2-3:1. Acute emphysematous cholecystitis is also more common in men than in women. Age AC affects all age groups, but the peak incidence is in  persons aged 40-60 years. Approximately 50% of cases of AC in children are acalculous. Anatomy The GB stores and concentrates bile,  and the ducts function as a bile drainage system. The flow of bile through the bile ducts is affected by several factors, including hepatic secretory pressure, tone in the sphincter of Oddi, the rate of GB fluid absorption, and GB contraction. Anatomically, the GB is a pear-shaped musculomembranous reservoir lying in the GB fossa on the inferior aspect of the liver. The fundus of the GB lies close to the nterior abdominal wall and near the hepatic flexure of the colon. The surface marking of the GB fundus is in the region of the costal cartilage. At this point, it is covered by peritoneum, and its proximity to the hepatic flexure of the colon may obscure it. The body of the GB is adjacent to the duodenum, which indents and produces a frequent ultrasonographic artifact that mimics gallstones or a mass in the GB. An inflamed GB may perforate into the colon or duodenum because of the close proximity of the GB to these structures. The mucosa of the GB neck is thrown into folds, giving an echogenic appearance that may also mimic gallstones. A small pouch, known as the Hartmann pouch, projects from the right side of the GB neck. When visible, this finding is frequently associated with pathology, particularly dilatation. The GB fundus is often folded over, and the GB then assumes a double-barrel appearance. Pseudoseptation of the GB fundus  caused by  kinking or, occasionally, a true septum called the phrygian cap is seen in 2-6% of GBs. The phrygian cap is of no pathologic significance. A cystic artery supplies the GB, and it is usually a branch of the right hepatic artery. The artery lies in the triangle made by the liver, the cystic duct, and the common hepatic duct (CHD). Other, smaller tributaries supply the GB  through the right hepatic artery via the GB bed through the liver. Usually, the right hepatic artery passes behind the CHD and the cystic artery crosses behind the cystic duct. In 25% of cases, the common hepatic artery passes in front of the CHD and the cystic artery in front of the cystic duct. Recognition of GB blood supply is gaining increased importance because of vascular intervention in the liver, particularly chemoembolization. Catheters should be placed distal to the cystic artery to prevent embolic material from entering the cystic artery and causing GB ischemia. Ultrasonographic anatomy The GB is a pear-shaped anechoic structure indenting the inferomedial aspect of the right lobe of the liver. A linear echogenic line representing fat in the main interlobar fissure is interposed between the GB and the right main portal vein. The GB mucosa is hyperechoic, the submucosa and the muscle layer are hypoechoic, and the serosal surface fatty layer is hyperechoic. A linear fold is present on the posterior GB wall at the junction of the body and neck. Called the junctional fold, this structure is of no pathologic significance. Sound waves from the spiral valve of the neck may cast an acoustic shadow and mimic a gallstone. The normal thickness of the GB wall is usually less than 3 mm. Provided that the patient has been fasting for 8-12 hours, visualization of the normal GB should be nearly complete. In a truly fasting patient, nonvisualization of the GB is a pathologic finding in 96% of patients. GB dimensions The normal GB usually measures 7-10 X 2-3. 5 cm. In the fasting patient, the normal dimensions of the GB seldom exceed 4 X 10 cm. The size of the GB generally increases with age, but the GB wall thickness is unaffected by age. The normal wall thickness is 2-3 mm. Neonatal GB dimensions are 0. 5-1. 6 cm (mean, 0. 9 cm) X 2. 5 cm. The wall thickness is usually 1 mm. GB anomalies Many anatomic anomalies affect the GB. The recognition of these anomalies is important in the context of GB disease. Errors in GB surgery are frequently a result of the failure to appreciate variations in the anatomy of the biliary system. Anomalous positioning or orientation of the GB includes situs inversus when the GB is in the left upper quadrant. A GB  in the left lobe of the liver without situs inversus is rare. Heterotaxia, which represents an intermediate situs with GB in the midline, may be associated with asplenia, polysplenia, pulmonary isomerism, and congenital heart disease. An anomalous orientation may be present when the GB is vertical or horizontal. It may descend into the right iliac fossa, particularly in the presence of the Riedel lobe. Unusual locations include intrahepatic, suprahepatic, lateral, anterior abdominal wall, and retrorenal sites. The GB may also be present in the thorax, in the falciform ligament and/or interlobular fissure, and in the transverse mesocolon. A wandering GB results when the GB is suspended on its own mesentery. Recognition of this anomaly is important because  such a GB is  prone to torsion. Agenesis is a rare anomaly found in 0. 04-0. 07% of autopsies. Agenesis may be associated with biliary atresia, imperforate anus, CHD, and common bile duct (CBD) anomalies. Rarely, the GB opens separately into the duodenum. The most common anomalous shape is due to the phrygian cap, in which the fundus of the GB is folded back on itself, producing a kink in the fundus. The GB may rarely appear as a diverticulum with no cystic duct. Other anomalies include fishhook, a siphon, and an hourglass configuration. A diverticulum of the GB is extremely rare and usually located at the neck of the GB. This is rarely symptomatic unless it is complicated by calculus disease. Regarding GB duplication, true duplication is rare, but it has been reported in as many as 1 in 3000-4000 people, with a male-to-female ratio of 2:1. Triplication is even rarer, and it may be an incidental finding at autopsy. In duplication, each GB may have a separate cystic duct or there may be 1 shared cystic duct. A septate GB may have an isolated transverse septum. True duplication has a longitudinal septum. A multiseptate GB is extremely rare, with multiple loculi connected by small pores; patients with this condition are particularly prone to bile stasis and calculus formation. With an anomalous cystic duct insertion, the cystic duct may insert into the CBD or CHD high or low. The cystic duct is often intramural, running for some distance in the wall of the CBD within a common sheath. Congenital stenosis of the cystic duct is extremely rare, and it may be complicated by calculus disease. Heterotopic tissue may be present within the GB, where gastric or pancreatic tissue has been described within the GB wall. This tissue may mimic tumors. Clinical findings AC usually occurs with right upper quadrant pain and tenderness. The abdominal pain increases with time. The site of pain is usually the right subcostal region, although the pain may begin in the epigastrium or the left upper quadrant and then shift to the right subcostal region to the area of the GB inflammation. Referred pain to the right shoulder or the interscapular region may be experienced. Approximately 70% of patients have had previous attacks of similar pain that spontaneously resolved. Anorexia, nausea, and vomiting may occur, but vomiting is seldom severe. Most patients are afebrile and have no leukocytosis. When fever occurs, the patients temperature is seldom  higher than 38 °C. Chills are unusual, and their presence suggests a complicated cholecystitis (abscess or associated cholangitis). Palpation of the right subcostal area reveals muscle spasm. During deep inspiration, the tenderness becomes suddenly worse and produces an inspiratory arrest called the Murphy sign. The Murphy sign  cab be elicited with an ultrasound probe. In approximately 35% of patients, a distended, tender GB may be palpable as a distinct mass. This is an important clinical finding and may confirm the diagnosis. Approximately 20% patients with AC may have mild jaundice, which may be related to common hepatic and/or bile duct edema or to the presence of calculi within the CBD. 22 Most patients improve within 24 hours after hospitalization, and signs and symptoms gradually subside. However, persistent pain, fever and leukocytosis, chills, and more severe localized or generalized tenderness may indicate complicated disease such as abscess formation or GB perforation. The development of empyema of the GB can produce systemic toxicity, and it may be a predictor of GB perforation. Leukocytosis is pronounced with empyema and is usually in the range of 10,000-15,000/? L. The clinical differential diagnosis includes acute pancreatitis, perforated peptic ulcer, gonococcal perihepatitis (Fitz-Hugh-Curtis syndrome) in women, acute hepatitis, pneumonitis, pyelonephritis, cardiac disease, sickle cell crises, and leptospirosis. AAC is difficult to diagnose clinically. It occurs often in children (50%) and in patients who are critically ill or who have recently undergone stress from severe trauma, burns, or surgery. Predisposing factors include prolonged fasting, immobility, and hemodynamic instability. Often, these patients cannot express pain; however, fever, jaundice, vomiting, abdominal tenderness, leukocytosis, and hyperbilirubinemia should lead to a high index of clinical suspicion. Children with AAC more often present in the outpatient setting than in other settings, and they usually present with  right upper quadrant  pain in the absence of gallstones. These patients are usually treated by means of cholecystectomy. Some elderly patients have few signs during their initial presentation with AC. A minority of adult patients, mostly elderly patients with AAC, also present in the outpatient setting. These cases are diagnosed and treated early and are associated with a good prognosis. Causes Hemolytic o Hemolytic anemias such as congenital spherocytosis (43-85%), sickle cell disease (7-37%), and thalassemia o Cardiac causes such as mitral valve stenosis and prosthetic heart valves o Pernicious anemia o Aortic aneurysm o Hypersplenism Metabolic o Overweight, female sex, fair complexion, fertile, and age of 40 years or older o Diabetes mellitus o Obesity o Hemosiderosis o Pregnancy o Prolonged use of estrogen/progesterone o Hyperparathyroidism o Cystic fibrosis o Pancreatitis o Hypothyroidism Muscular dystrophy o Crohn disease o Ileal resection and intestinal malabsorption o Type IV hyperlipidemia o Surgical bypass for obesity o Cholestasis Miscellaneous o Chronic hepatitis o Cirrhosis o Congenital biliary malformation (eg, Caroli disease) o Parasites (eg, ascariasis, liver flukes), which form a nidus for development of calculi o Drugs such as methadone o Biliary strictures ( eg, oriental cholangiohepatitis [bile stasis]) Genetic o Genetic predisposition in populations such as Native Americans o Higher incidence of intrahepatic gallstones in Chinese and Japanese populations Preferred Examination Clinically, few signs differentiate uncomplicated AC from complicated AC. Complications of AC may have serious clinical implications. These complications include perforation, pericholecystic abscess, and development of empyema and bilioenteric fistula. Therefore, radiologic imaging makes a substantial contribution to the differential diagnosis. Ultrasonography significantly aids  in the diagnosis of AC, although most ultrasonographic signs are not typical but suggestive of AC. Inflammatory pericholecystic reaction in the GB fossa is better depicted with CT than with other techniques. Also, CT is useful in making the differential diagnosis when obesity or gaseous distention limits the use of ultrasonography. MRI can demonstrate the same morphologic changes as CT, displaying inflammatory changes in the GB wall, pericholecystic fat, and intrahepatic periportal tissues. Plain radiography greatly contributes to the diagnosis of emphysematous pyelonephritis, and ultrasonographic and CT scan results can further confirm the diagnosis (although  CT scanning is  not strictly needed  to make  the diagnosis). Cholescintigraphy is an extremely sensitive diagnostic modality in diagnosing AC, although the findings are nonspecific. Oral cholecystography is of historical interest and has no role in the diagnosis of AC. Arteriography is seldom required for AC. Limitations of Techniques Plain radiographic findings may be entirely normal. Radiolucent calculi are visible. Opaque calculi in the  right upper quadrant  on plain abdominal radiographs may be an incidental finding and is not necessarily related to AC. Oral cholecystography is of historical interest and has a low sensitivity and specificity in the diagnosis of AC. The main features of AC on ultrasonography are all nonspecific findings. Examples include GB thickening, calculi in the GB, a positive ultrasonographic Murphy sign, and pericholecystic fluid. The sonographic Murphy sign is negative in as many as 70% of patients with AC. In a perforated GB, the wall of the GB is not well delineated, and a localized interruption of the wall may not be noted at the site of perforation. Ultrasonography has problems in making the diagnosis in obese patients and in patients with gaseous distention. The technique remains operator dependent. CT exposes the patient to a radiation burden, which may not be necessary. Arteriography is invasive and is seldom indicated. MRI has a limited availability; it is expensive; and it has problems in making the diagnosis in patients with certain prosthetics, surgical clips, cardiac pacemakers, or claustrophobia. Although cholescintigraphy is  sensitive, it has a low specificity and involves the use of ionizing radiation.