A 51-year-old male with postprandial epigastric pain

Many conditions can cause abdominal pain. In addition to pain from intra-abdominal pathology, referred pain must also be considered.

Epigastric pain can be a result of dyspepsia, ulcer disease, gastritis, ruptured or dissecting aortic aneurysm, kidney infection, cholangitis, pancreatitis, acute gastric distention (as might occur with diabetic sympathetic neuropathy), acute hepatitis, pneumonia, acute myocardial infarction, intestinal obstruction or volvulus, gastroenteritis, splenic pathology (bleeding, enlargement, or rupture), intestinal ischaemia, renal calculus, ovarian cyst, and peritonitis or intra-abdominal abscess.

In a patient with an abrupt onset of pain and nausea, it is important to first rule out life-threatening causes, such as myocardial infarction, ruptured or dissecting aortic aneurysm, perforated or ischaemic viscera, ascending cholangitis, and peritonitis. Results of this patient's initial evaluation suggested a localized pathology in the right upper quadrant, and the initial differential diagnosis (on the basis of the presence of right upper quadrant tenderness, no fever, normal bowel sounds, and no palpable mass) included acute cholecystitis, peptic ulcer disease, and dyspepsia/gastritis.

Symptoms that are consistent with acute cholecystitis resulting from gallstones include epigastric or right upper quadrant pain, nausea and possibly vomiting, right upper quadrant tenderness, a palpable gallbladder (in only about 20% of cases), and, in some persons, fever and chills. A person with ascending cholangitis can present with similar symptoms, but those patients have a high fever and other signs of sepsis and they usually have jaundice.

Patients with acalculous cholecystitis have a similar presentation. However, the onset of symptoms is insidious and often includes a fever and leukocytosis because of associated gallbladder infection. Acalculous cholecystitis is more likely to develop in patients who are debilitated or are being treated in the critical care unit than in younger, healthy patients.

Biliary dyskinesia is an abnormality in gallbladder function that can cause symptoms that are identical to those of cholecystitis, but biliary dyskinesia is difficult to diagnose. Functional studies may be useful, but results of imaging studies are often normal in these patients.

The imaging study of choice for patients with suspected cholecystitis is ultrasonography (US) of the gallbladder, which can demonstrate the presence of stones or biliary sludge, as well as signs of gallbladder inflammation (i.e. distention, wall thickening, gas). In patients with no apparent stones, a hepatobiliary iminodiacetic acid (HIDA) scan may be useful (the biliary tree is visible, and the gallbladder is not). In patients who may have a common bile duct obstruction and the diagnosis cannot be made with US or HIDA scan, an endoscopic retrograde cholangiogram (cholangiopancreatography) may be useful as long as pancreatitis is not also present.

The sonographic Murphy's sign is a very accurate diagnostic tool that is readily available. Essentially, the ultrasound technician notes the point of maximal tenderness evoked by the use of the transducer during the ultrasonography. If the image indicates the point of maximal tenderness is over the gallbladder, the diagnosis is confirmed.

Abnormalities, such as an elevated white blood cell count, and elevated liver enzymes and bilirubin levels may be present. Serum amylase and lipase levels may be elevated if an obstruction of the common bile duct exists and leads to pancreatic inflammation.

The gallbladder epithelium provides active sodium chloride transport that leads to concentration of the bile into a form that is up to 10 times more concentrated than the originally excreted form. As the bile is concentrated, the solubility of cholesterol and calcium in the bile is altered, and this can lead to precipitation into stones.

Any condition that increases bile stasis or provides a nidus for precipitation can increase the risk for stone formation. About 70% of bile stones are formed around a nidus of calcium, and about 10% of stones are pure cholesterol stones. Bacteria can also provide a nidus [1].

Haemolysis can lead to the formation of pigmented stones as a result of excess haemoglobin by-products. About 20% of stones are this type. Pigmented-stone formation also is associated with cirrhosis. Black and brown stones appear to have a similar chemical composition and usually contain bacteria [2].

Biliary sludge also can cause obstruction of the gallbladder and biliary tree. Sludge is a precipitate formed from the same materials as stones and may provide a nidus for stone formation. Sludge can develop in patients treated with ceftriaxone as a result of the formation of ceftriaxone-calcium precipitates. Sludge formation is also common in patients treated with total parenteral nutrition.

Risk factors for gallstone formation include haemolytic disease, pregnancy, rapid weight loss, treatment with oestro- gen replacement, obesity, total parenteral nutrition, and disease of the terminal ileum (which prevents reabsorption of bile acids, leading to excess cholesterol concentration in the bile). Gallstone formation is more common in women than in men, and the risk of developing gallstones increases with age.

Persons with gallstones are asymptomatic unless the gallstones obstruct the biliary tree or damage the gallbladder. It is estimated that about 10% of asymptomatic patients with biliary stones will experience symptoms within 5 years of the diagnosis [3].

Untreated cholelithiasis can lead to recurrent cholecystitis; patients with symptomatic cholelithiasis have a 20% recurrence rate and a 4% complication rate [3]. Complications of both include obstruction of the biliary tree, pancreatitis as a result of gallstone obstruction, gallstone ileus, and, after many years, gallbladder cancer. Because of the potential complications, treatment is indicated for symptomatic patients or those who are very likely to become symptomatic (e.g. those with multiple small stones, those who have undergone bariatric surgery).

The treatment of choice for cholecystitis is surgical removal of the gallbladder. In most cases, endoscopic cholecystectomy is safe and is associated with a more rapid recovery compared with open cholecystectomy. If infection or other complications are present, open cholecystectomy may be necessary. Asymptomatic gallstone disease (cholelithiasis) does not require treatment, but with the development of any associated symptoms, the likelihood of complications increases and surgery is indicated. Most (nearly 92%) patients have improvement or cure with surgery for cholecystitis or biliary dyskinesia [3].

Cholecystitis also can develop in children, and the recommended treatment and management are generally the same as for adults. Children with cholelithiasis with atypical abdominal pain may respond to a low-fat, high-fibre diet [4].

Rarely, patients may be unable or unwilling to undergo surgical treatment. For these patients, treatment with bile salts may be useful. However, the stone recurrence rate is 25% for patients treated with ursodeoxycholic acid [3]. In patients undergoing bariatric surgery, ursodeoxycholic acid treatment often has been used prophylactically to reduce the risk of stone formation during the expected period of rapid weight loss. However, these patients have a high risk for the development of symptomatic disease, and they would be more likely to benefit from prophylactic surgical treatment [5].