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Any severe acute pain in the abdomen or back should suggest the possibility of acute pancreatitis. The diagnosis is established by two of the following three criteria: (1) typical abdominal pain in the epigastrium that may radiate to the back, (2) threefold or greater elevation in serum lipase and/or amylase, and (3) confirmatory findings of acute pancreatitis on cross-sectional abdominal imaging. Pathologically, acute pancreatitis varies from interstitial pancreatitis, which is usually a mild and self-limited disorder, to necrotizing pancreatitis, in which the degree of necrosis may correlate with the severity of the attack and its systemic manifestations.

Etiology !!navigator!!

Most common causes in the United States are cholelithiasis and alcohol. Others are listed in Table 154-1 Causes of Acute Pancreatitis.

Clinical Features !!navigator!!

Can vary from mild abdominal pain to shock. Common symptoms: (1) steady, boring pain in the epigastric and periumbilical region may radiate to the back, chest, flanks, and lower abdomen; (2) nausea, vomiting, abdominal distention.

Physical examination: (1) low-grade fever, tachycardia, hypotension; (2) erythematous skin nodules due to subcutaneous fat necrosis; (3) basilar rales, pleural effusion (often on the left); (4) abdominal tenderness and rigidity, diminished bowel sounds, palpable upper abdominal mass; (5) Cullen's sign: blue discoloration in the periumbilical area due to hemoperitoneum; (6) Turner's sign: blue-red-purple or green-brown discoloration of the flanks due to tissue catabolism of hemoglobin.

Laboratory !!navigator!!

  1. Serum amylase and lipase values threefold or more above normal almost always secure the diagnosis if gut perforation, ischemia, and infarction are excluded. Serum lipase is the preferred test. There is no correlation between the severity of pancreatitis and the degree of serum lipase and amylase elevations. After 3-7 days, amylase values tend to return toward normal; however, pancreatic lipase levels may remain elevated for 7-14 days.
  2. Other tests: Hypocalcemia occurs in 25% of pts. Leukocytosis (15,000-20,000/µL) occurs frequently. Hemoconcentration may be the harbinger of more severe disease (i.e., pancreatic necrosis), azotemia is a significant risk factor for mortality. Hypertriglyceridemia occurs in 5-10% of cases and can cause a spuriously normal serum amylase level. Hyperglycemia is common. Serum bilirubin, alkaline phosphatase, and aspartate aminotransferase can be transiently elevated. Hypoalbuminemia and marked elevations of serum lactic dehydrogenase (LDH) are associated with an increased mortality rate. Hypoxemia is present in 5-10% of pts and may herald the onset of ARDS.

Imaging !!navigator!!

  1. Ultrasound often fails to visualize the pancreas because of overlying intestinal gas but may detect gallstones, pseudocysts, mass lesions, or edema or enlargement of the pancreas.
  2. CT can confirm the clinical impression of acute pancreatitis. It can also be helpful in evaluating the complications of acute pancreatitis.

Differential Diagnosis !!navigator!!

Intestinal perforation (especially peptic ulcer), cholecystitis, acute intestinal obstruction, mesenteric vascular occlusion, renal colic, inferior myocardial infarction, aortic dissection, connective tissue disorders, pneumonia, and diabetic ketoacidosis.

Severity and Complications !!navigator!!

Risk factors and markers of severity are listed in Table 154-2 Severe Acute Pancreatitis.

In the modified Marshall scoring system 3 organ systems are assessed to define organ failure: respiratory, cardiovascular, and renal. The median prevalence of organ failure is 54% in necrotizing pancreatitis. With single-organ system failure, the mortality is 3-10% but increases to 47% with multisystem organ failure.

Three severity classifications have been defined:

  • Mild acute pancreatitis-without local complications or organ failure.
  • Moderately severe acute pancreatitis-transient organ failure (resolves in <48 h) or local or systemic complications in the absence of persistent organ failure.
  • Severe acute pancreatitis-persistent organ failure (>48 h). CT or MRI should be obtained to assess for necrosis or other local complications.

Systemic Complications

Shock, GI bleeding, common duct obstruction, ileus, splenic infarction or rupture, disseminated intravascular coagulation, subcutaneous fat necrosis, acute respiratory distress syndrome, pleural effusion, acute renal failure, sudden blindness.

Local Complications

  1. Sterile or infected pancreatic necrosis. Percutaneous aspiration of necrosis with Gram stain and culture should be considered if there are ongoing signs of possible pancreatic infection such as sustained leukocytosis, fever, or organ failure. Repeated fine-needle aspiration and Gram stain with culture of pancreatic necrosis may be done every 5-7 days in the presence of persistent fever. Repeated CT or MRI imaging should also be considered with any change in clinical course to monitor for complications. Sterile necrosis is most often managed conservatively unless complications arise. Once a diagnosis of infected necrosis is established and an organism identified, targeted antibiotics should be instituted. Pancreatic debridement (necrosectomy) should be considered for definitive management of infected necrosis, but clinical decisions are generally influenced by response to antibiotic treatment and overall clinical condition. A step-up approach (percutaneous or endoscopic transgastric drainage followed, if necessary, by open necrosectomy) has been successfully reported by some pancreatic centers.
  2. Pancreatic pseudocysts. The incidence of pseudocyst is low, most acute collections of fluid resolve over time, <10% of pts have persistent fluid collections after 6 weeks that would meet the definition of a pseudocyst. Only symptomatic collections should be drained with surgery or endoscopy or by percutaneous route.
  3. Other complications: Pancreatic ascites, pancreatic duct disruption, walled-off necrosis, pancreatic fluid collections, involvement of contiguous organs by necrotizing pancreatitis, thrombosis of blood vessels, pancreatic enteric fistula, bowel infarction, obstructive jaundice.
TREATMENT

Acute Pancreatitis

Most (85-90%) cases are self-limited and subside over a period of 3-7 days. Following diagnosis, the most important treatment is safe, aggressive IV fluid resuscitation. Severity should be assessed to determine if ICU care is required. Other conventional measures: no oral alimentation and analgesics for abdominal pain. A low-fat solid diet can be given with mild acute pancreatitis after the abdominal pain has resolved. Precipitating factors (alcohol, medications) must be eliminated.

Outline

Section 11. Gastroenterology