Infectious Diseases I

are associated with local and systemic complications (e.g., multiple organ failure). An Acute Physiology

and Chronic Health Evaluation II (APACHE II) score of 8 or higher and a Ranson’s criteria score

of 3 or greater, together with clinical presentation, have been used historically to categorize patients

as having severe acute pancreatitis. The more recent revised Atlanta classification categorizes severe

acute pancreatitis as the presence of single or multiple organ failure for 48 hours or more, whereas

the Determinant-Based Criteria (DBC) classification system defines it as persistent organ failure or

infected pancreatic or peripancreatic necrosis. The DBC adds a category of critical acute pancreatitis

for patients with persistent organ failure and infected necrosis.

Between 30% and 78% of patients with necrotizing pancreatitis will have concomitant organ failure,

with the highest incidence in patients having infected necrosis. Pancreatitis-associated systemic

sequelae and organ failure includes:

Systemic inflammatory response syndrome (SIRS)

Hypovolemic shock

Hypoxemia secondary to ARDS

Gastrointestinal (GI) bleeding

Disseminated intravascular coagulation and severe metabolic disturbances can also occur.

Although most pancreatic necrosis is sterile and does not require treatment with antimicrobials, about

one-third of patients with necrotizing pancreatitis will have infected necrosis.

Overall, crude mortality for acute pancreatitis is 2%–9%; however, mortality rates for necrotizing and

infected necrotic pancreatitis with organ failure are as high as 44% and 62%, respectively.

Pancreatitis is a result of glandular autodigestion from excessive ductal and tissue exposure to amylase,

lipase, and protease caused by trypsin-related hyperstimulation, macro-ductal blockade, or micro-

ductal blockade.

Excessive activation or decreased inactivation of trypsin leading to activation of pancreatic

exocrine enzymes

Local inflammatory and immune response to pancreatic injury

Systemic inflammatory and immune response, including SIRS, hypovolemia, and ARDS

Common causes of acute pancreatitis include biliary obstruction (e.g., gallstones), direct toxicity (e.g.,

alcohol), trauma, surgery/biliary procedures, hypertriglyceridemia, and drugs.

Severe pancreatitis is defined as pancreatitis associated with organ failure that persists for more than

48 hours. Hypovolemia may increase the risk of pancreatic necrosis and intestinal ischemia because of

tissue hypoperfusion.

often associated with peripancreatic fat necrosis. In general, greater than 30% of the pancreas should

be affected. Infected necrosis is defined as the presence of pathogenic microorganisms in the necrotic

tissue. The presence of retroperitoneal gas on CT scan may indicate infected pancreatitis in patients

with severe acute pancreatitis. The timing of infected necrosis varies, but infected necrosis usually

peaks 2–4 weeks from the onset of acute pancreatitis.

Pancreatic pseudocyst is a non-epithelialized wall containing pancreatic excretions caused by acute or

chronic pancreatitis or pancreatic trauma. Pseudocysts are usually sterile.

Pancreatic abscess is an infected pseudocyst or liquefaction of pancreatic necrosis that becomes infected.