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Approximately 75% of pancreatitis cases can be explained on the basis of biliary tract disease or alcohol abuse, although the exact mechanism for the production of pancreatitis remains theoretical.

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Gallstone pancreatitis is thought to be induced by the inflammation that results from continued passage of stones into the common bile duct. Most often, the gallstone has passed by the time the patient is studied.

The pancreatic duct and the bile duct empty into a common papilla, which is subject to trauma in a patient with biliary calculi.

The entire common channel can be obstructed if a large calculus becomes impacted in the papilla, and this situation can cause reflux of bile into the pancreatic duct. Experiments have shown that such reflux can induce pancreatitis. However, it is unclear whether this reflux actually occurs in humans.

Alcohol-induced pancreatitis may be the result of various mechanisms. Alcohol has been implicated in the direct damage of acinar cells and the increase of the concentration of enzymes in pancreatic secretion. High protein concentration with calcium carbonate precipitation in the protein-filled spaces encourages the development of stones. The resultant multifocal ductal obstruction and increased intraductal pressure along with increased permeability caused by alcohol destroys parenchyma and leads to inflammation and fibrosis.

Congenital abnormalities and hereditary pancreatitis. Duct strictures, pancreas divisum, cystic fibrosis, and various metabolic disorders (e.g., hypertriglyceridemia) are implicated as contributing factors in a small percentage of cases.

Iatrogenic. Pancreatitis can be caused by instrumentation (e.g., endoscopic retrograde cholangiopancreatography [ERCP]) or certain drugs.

C Acute pancreatitis

Clinical presentation of acute pancreatitis may vary from mild abdominal discomfort to profound shock with hypotension and hypoxemia. Usually the patient presents with epigastric pain that radiates to the back and is associated with nausea and vomiting. Findings vary with the severity of the inflammatory process.

Most patients have mild -to -moderate abdominal tenderness.

In severe cases, a rigid abdomen with epigastric guarding, rebound tenderness, and marked abdominal pain may be present.

Severe pancreatic inflammation and necrosis may cause retroperitoneal hemorrhage , which can lead to large third - space fluid losses, hypovolemia, hypotension, tachycardia, and shock with blood dissection (i.e., the blood extravasates and forces its way between tissue planes).

When blood dissection extends to the flank tissues, resulting in flank ecchymoses, it is known as Turner's sign.

When blood dissects up the falciform ligament and creates a periumbilical ecchymosis, it is known as Cullen's sign.

History. Often the patient mentions recent consumption of a heavy meal, many times with generous quantities of alcoholic beverages. The pain typically begins 1–4 hours after a meal and is often less severe when the patient is slumped forward.

Diagnosis of acute pancreatitis is aided by the following studies:

Serum amylase level. This level is increased in 95% of patients with acute pancreatitis.

Approximately 5% of all amylase determinations are falsely positive, and only 75% of patients with abdominal pain and an increased amylase level have pancreatitis.

The increase in amylase level is not proportional to the severity of the pancreatitis. Some inferences, however, can be made from the degree of increase.

An amylase level higher than 1,000 Somogyi units usually indicates gallstone pancreatitis.

An amylase level between 200 and 500 Somogyi units often indicates alcoholic pancreatitis. Approximately 17% of patients with amylase levels in this range have no other evidence of pancreatitis.

The pancreas must be intact and functional to synthesize amylase and release it into the circulation. Therefore, patients with acute pancreatitis superimposed on chronic pancreatitis may not show an increase in serum amylase.

A significant amount of circulating amylase is not of pancreatic origin. The major alternative source is the salivary glands.

An elevated lipase is also seen in pancreatitis.

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Amylase:creatinine clearance ratio. Amylase determinations are more sensitive identifiers when the amylase clearance rate is compared with the creatinine clearance rate and a ratio is established.

An amylase:creatinine clearance ratio higher than 5 is strongly suggestive of pancreatitis.

Using this ratio avoids the problem of rapid renal clearance of amylase, which tends to reduce serum levels below the point where a simple serum amylase determination would be positive.

Impaired renal function affects the creatinine clearance rate sooner than the amylase clearance rate. Even in this situation, however, the amylase:creatinine clearance ratio appears to be more sensitive than the serum amylase level if urine specimens are collected for at least 1 hour.

Radiographic imaging

Plain films of the upper abdomen are relatively insensitive with regard to diagnosing pancreatitis. Significant findings include the following:

Calcification in the area of the lesser sac and pancreas may indicate chronic pancreatitis, which is most often found in association with alcoholism.

A gas collection in the lesser sac suggests abscess formation in or around the pancreas.

Blurred psoas shadows from retroperitoneal pancreatic necrosis and fluid in the retroperitoneum may be found on plain films.

Soft tissue shadows and gas -containing viscera may be visibly displaced by collections and edema in the lesser sac and structures adjacent to the pancreas.

An area of colonic spasm adjacent to an inflamed pancreas causes the gas in the transverse colon to end abruptly (the “cutoff” sign).

Focal duodenal and jejunal ileus in the area of the pancreas can cause the reversed 3, or inverted 3 sign.

Barium studies may show upper gastrointestinal (GI) abnormalities.

The duodenal C-loop may be widened by pancreatic edema.

Hypotonic duodenography may show the “pad” sign, a smoothing out or obliteration of the duodenal mucosal folds by the edematous pancreas and the inflammatory response on the medial aspect of the C- loop.

Angiography is useful for delineating pancreatic and hepatic blood supply before radical surgery. Diagnostic aspects have been superseded by spiral computed tomography (CT) scan and magnetic resonance (MR) imaging.

Ultrasound (US) imaging of the pancreas is especially useful in the diagnosis of pancreatitis.

Changes in the normal anatomy of the pancreas and its vascular landmarks can be delineated.

Acute pancreatitis is suggested by swelling that is greater than the normal anteroposterior thickness and loss of tissue planes between the pancreas and the splenic vein.

Other anomalies of the pancreas may also be found (e.g., a change in duct size or calcification).

Chronic pancreatitis is often manifested by the presence of calcification or pseudocysts containing fluid or showing a complex cystic structure.

Ascites, which is easily diagnosed by US, may or may not be present in chronic pancreatitis.

Various pancreatic disorders can change the US echogenicity.

Most diseases decrease the echogenicity in the pancreas because they include edema and inflammation. Tumors are also often hypoechogenic.

Increased echogenicity is generally due to gas or calcification.

Fluid densities lying within the pancreas indicate cysts, abscesses, or possibly lymphoma.

Cholelithiasis may be identified, suggesting gallstone pancreatitis. US may also show the presence of cholecystitis or a dilated common bile duct.

US has a major limitation in that it cannot be performed when excessive bowel gas is present, as occurs with an ileus.

CT scan of the pancreas is extremely helpful. It provides higher resolution than US, and it is not limited by the masking effect of intestinal gas. The improvements in availability, speed,

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and resolution in CT have made it the most important imaging modality in initial diagnosis and treatment of pancreatitis. Dynamic CT can be used to diagnose pancreatic necrosis.

TABLE 15-1 Role of Endoscopic Retrograde Cholangiopancreatography

Reprinted with permission from Neoptolemos JP. In: Edward L. Bradley III, ed. Acute Pancreatitis: Diagnosis and Therapy. New York: Raven Press, Ltd.; 1994: 75.

MR pancreatograms and cholangiograms are now widely available and are very useful for delineating anatomy before surgery. They can provide excellent detail of the pancreatic duct and bile ducts. MR angiography is increasingly available and has replaced invasive angiography in most preoperative workups for planned pancreatic surgery.

The use of ERCP in the first 5 days of severe acute pancreatitis is dangerous and is associated with an increased mortality rate (Table 15 -1).

Prognosis in acute pancreatitis is aided by certain signs that are associated with a higher mortality rate and, therefore, are useful prognostic indicators (e.g., Ranson's signs; Table 15 -2).

Treatment. Certain measures are considered standard, but not all of them are indicated in each case. The patient's symptoms dictate much of the treatment.

Nasogastric suction is used to control nausea and vomiting, decrease pancreatic stimulation, and decrease GI distention from an ileus. This suction also makes the patient more comfortable, although it does not appear to shorten the hospital stay.

Intravenous fluids are used to replace the third -space fluid loss from edema and extravasation into the peripancreatic spaces. Crystalloid solutions are usually adequate.

Monitoring similar to that for burn patients should be initiated.

Patient monitoring should include the use of a Foley catheter to measure urine output.

In severe cases with unstable hemodynamics, the patient's fluid status should be closely monitored with a Swan -Ganz catheter.

TABLE 15-2 Ranson's Eleven Criteria for Determining the Severity of Pancreatitis

HCT, hematocrit; WBC, white blood cell count; BUN, blood urea nitrogen; Ca2+, calcium ion; LDH, lactate dehydrogenase; PaO2, partial pressure of oxygen in arterial blood; SGOT, serum

glutamine-oxaloacetic transaminase.

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Antibiotics may reduce the risk of abscess formation and of lesser sac collections, which often progress to abscess formation.

The early use of antibiotics is thought to promote the maturation of these collections into pseudocysts (see II F) rather than abscesses.

Antibiotics also act as prophylaxis against cholangitis, which can develop if a swollen pancreatic head obstructs the biliary tract.

If the pancreatitis is due to biliary calculi, the bile is almost certainly contaminated with bacteria, and antibiotics

are indicated.

PaO 2 monitoring and chest radiograph. For patients who have severe pancreatitis, respiratory distress is common,

as are pleural effusions. These effusions are more often on the left and contain high concentrations of amylase. Therefore, the PaO 2 should be monitored closely in patients who have severe pancreatitis, and serial chest

radiographs should be obtained to rule out the presence of effusions and parenchymal disease.

Withhold oral feedings until laboratory test results return to normal and pain is gone for 48 hours. Exacerbations of pancreatitis are common with premature feedings and removal of the nasogastric tube.

Somatostatin has been shown to prevent or reduce the symptoms of ERCP -induced pancreatitis.

Surgery

Indications

To confirm the diagnosis in severe cases that do not respond to medical management

The symptoms of acute pancreatitis can be mimicked by visceral perforation, mesenteric arterial occlusion, and other intra -abdominal catastrophes.

Surgery may be needed to establish the diagnosis before the situation is irreversible.

To relieve biliary or pancreatic duct obstruction

Early biliary tract surgery may increase the mortality rate in patients who have severe pancreatitis.

If possible, therefore, surgery should be delayed until the pancreatitis has subsided. The offending stone will have passed by the time of exploration in more than 90% of patients.

If the patient's status continues to deteriorate, surgical exploration may become necessary.

Cholecystostomy or common bile duct drainage should be considered, with definitive dissection deferred, when there are acute severe inflammatory changes in the duodenum and region of the ampulla.

Definitive biliary tract surgery to correct the cause of the pancreatitis (e.g., removal of common bile duct stones or gallstones; repair of the sphincter of Oddi) should be performed on the same hospital admission as the treatment of acute pancreatitis to prevent recurrence.

To drain the lesser sac

Pancreatic or lesser sac drainage increases morbidity and therefore should be performed only after septic complications have occurred. It is not effective as a prophylactic measure.

Drainage has been shown to improve the prognosis when sepsis has already occurred and lesser sac collections and pancreatic necrosis are present.

For established lesser sac abscesses, drains can be inserted after opening the lesser omentum widely. Irrigation catheters can also be used as part of the therapeutic plan. Dependent drainage through the transverse mesocolon is a useful approach when the upper abdomen is obliterated by inflammation and adhesions.

Operative procedures

Cholecystectomy may be required in patients who have gallstone pancreatitis and persistent acute pancreatitis that do not respond to supportive measures.

Resection for acute pancreatitis is a dangerous procedure and is not indicated. It has not been shown to decrease morbidity; in some studies, resection has even increased the mortality rate. Removing necrotic pancreas (nonanatomic dissection) may be required in patients with pancreatic abscess. These operations are