Chapter 58
Acute Pancreatitis 
Acute pancreatitis (i.e., acute inflammation of the pancreas) has multiple causes and may manifest as mild disease or a life-threatening disorder that can result in multiple organ system failure, sepsis, and death. Acute pancreatitis typically presents as abdominal pain, in association with elevated blood levels of pancreatic enzymes. It may occur as an initial or recurrent attack. The pathogenesis is considered to be pancreatic autodigestion caused by intraparenchymal activation and release of proteolytic enzymes from zymogen granules. The resultant destruction and inflammation can produce a variety of local complications for which a clinically based system of classification and terminology has been developed (Table 58.1).
TABLE 58.1
Classification System for Acute Pancreatitis
| Term | Definition | Comments |
| Severe acute pancreatitis | Acute pancreatitis associated with organ failure, certain local complications (necrosis, abscess, or pseudocyst), or both. Most often it represents the development of pancreatic necrosis. | Early prognostic signs for severe disease: three or more Ranson criteria (see Table 58.4) or eight or more points in the APACHE II system.∗ |
| Acute fluid collections | These collections, localized in or near the pancreas, occur early in the course of acute pancreatitis and always lack a defined wall. | They are common, occurring in 30%–50% of patients with severe pancreatitis, and most regress spontaneously. Those persisting represent an early stage in the development of acute pseudocysts and pancreatic abscesses. |
| Pancreatic necrosis | Diffuse or focal area(s) of nonviable pancreatic parenchyma, typically associated with peripancreatic fat necrosis. Pancreatic necrosis may be sterile or become infected (the latter triples the risk of death). | Dynamic contrast-enhanced computed tomography shows a well-marginated zone of nonenhancement. |
| Acute pseudocysts | Collections of pancreatic fluid, enclosed by a defined wall of fibrous or granulation tissue, arising from acute pancreatitis. They are usually rich in pancreatic enzymes and most often sterile. | Sometimes palpable but most often discovered by imaging studies, which show a well-defined wall. They form 4 or more weeks from the onset of acute pancreatitis. |
| Pancreatic abscesses | Circumscribed intra-abdominal collections of pus, in or near the pancreas, but containing little or no pancreatic necrosis. Do not use this term to describe infected pancreatic necrosis (the latter has twice the mortality risk of a pancreatic abscess). | These occur 4 or more weeks after the onset of acute pancreatitis and likely arise as a result of limited necrosis with subsequent liquefaction and infection. |
| Pancreatic ascites | The presence of free fluid with pancreatic enzymes inside the peritoneal cavity. | Pancreatic ascites may be sterile or infected. |
| Infected pseudocyst | Variably used to describe infected pancreatic necrosis or pancreatic abscesses. | Avoid use of this ambiguous term. |
| Hemorrhagic pancreatitis | Defined by direct visualization of hemorrhage in the gland. | Incorrectly used as a synonym for pancreatic necrosis, which may not be hemorrhagic. |
| Pancreatic phlegmon | Originally referred to a palpable mass of sterile edematous tissues, but later used to describe pancreatic necrosis with infection. | Avoid use of this ambiguous term. |
∗Knaus WA, Draper EA, Wagner DP, et al: APACHE II: severity of disease classification system. Crit Care Med 12:818-829, 1985.
Modified from Bradley EL III: A clinically based classification system for acute pancreatitis. Arch Surg 128:586-590, 1993.
Etiology
More than 90% of cases of acute pancreatitis are due to ethanol abuse or cholelithiasis or are idiopathic. A variety of other agents, including medications and toxins, account for the remaining 10% (Box 58.1 and Table 58.2). Biliary microlithiasis (which is bile containing small crystals of cholesterol monohydrate, calcium bilirubinate, or calcium carbonate) is also recognized as a cause of acute and recurrent pancreatitis, accounting for up to 30% of pancreatitis previously considered idiopathic.
TABLE 58.2
Medications and Toxins Associated with Acute Pancreatitis
| Category | Definite Association | Probable Association |
| Antihypertensive agents | ACE inhibitors | |
| Methyldopa | ||
| Anti-inflammatory and analgesic agents | Acetaminophen Corticosteroids | |
| Mesalamine | ||
| NSAIDs | ||
| Salicylates | ||
| Anti-infective agents | Didanosine (ddI) Pentamidine Sulfonamides Tetracyclines | Erythromycin Metronidazole Nitrofurantoin |
| Chemotherapeutic agents | 6-MP, azathioprine | |
| l-Asparaginase | ||
| Diuretics | Furosemide Hydrochlorothiazide | Chlorthalidone Ethacrynic acid |
| Toxins | Ethanol Methanol | |
| Others | Estrogens (via hyperlipidemia) Intravenous lipid infusions Valproic acid |
Clinical Presentation
The hallmark of acute pancreatitis is abdominal pain associated with elevated blood levels of pancreatic enzymes. The pain generally comes on suddenly and rises to a peak within a few hours. It is steady, typically midepigastric, and bores through to the back. The patient prefers to remain still in bed and may assume a hunched-over or semifetal position in an attempt to release tension on the retroperitoneum; exaggerating the lumbar lordosis exacerbates the pain. Nausea and vomiting are present in more than 80% of patients. The presence of bluish discolorations of the flanks (Grey Turner sign) or periumbilical area (Cullen sign) is rare and does not occur at presentation but rather may develop several days into the illness because of dissection of peripancreatic bleeding into the subcutaneous tissues. Bowel sounds are diminished, or absent if a paralytic ileus is present. An abdominal radiograph may reveal a sentinel loop, which is a paralyzed air-filled segment of proximal small bowel in close proximity to the inflamed pancreas. The abdomen is typically soft but with exquisite tenderness to deep palpation. Peritoneal signs may be present in complicated cases. Subcutaneous fat necrosis may be present and resembles erythema nodosum or panniculitis. Altered mental status may be due to shock or complications of chronic alcoholism (e.g., alcohol withdrawal syndrome [AWS; Chapter 31], delirium tremens, and Wernicke-Korsakoff syndrome).
The serum amylase level rises in acute pancreatitis within 2 to 12 hours of the onset of symptoms and remains elevated for 3 to 5 days. Persistently raised levels suggest local complications. The lipase level may remain elevated longer than the amylase level. Elevation of both enzymes to levels greater than 10 times the upper limit of normal is highly specific but only 80% to 90% sensitive for acute pancreatitis. Levels less than 3 times the upper limit of normal should be considered non-specific.
Differential Diagnosis
There are multiple causes for an elevated pancreas enzyme level other than acute pancreatitis (Box 58.2). Several deserve special comment. Perforated peptic ulcer may present with pain and elevated pancreatic enzymes resulting from spillage into the peritoneal cavity. Abrupt onset of pain, peritoneal signs, and free air on radiography differentiates this entity from pancreatitis. Acute cholecystitis may sometimes be associated with mild hyperamylasemia. The pain of cholecystitis is typically right-sided, and ultrasonography or computed tomography can suggest the diagnosis. A stone in the bile duct (choledocholithiasis) may cause cholangitis with biliary colic, elevated liver-associated enzymes, and jaundice with or without concomitant pancreatitis. Bowel ischemia and infarction resulting from mesenteric vascular occlusion, volvulus, and hernia are important considerations because of the need for prompt surgical treatment. Salpingitis and ruptured ectopic pregnancy may cause abdominal pain and elevated amylase levels and may occasionally be confused with acute pancreatitis.
