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Pathophysiology
Because the pancreas is located in the retroperitoneal space with no capsule, inflammation can spread easily. In acute pancreatitis, parenchymal edema and peripancreatic fat necrosis occur first. This process is known as acute edematous pancreatitis.
When necrosis involves the parenchyma, accompanied by hemorrhage and dysfunction of the gland, the inflammation evolves into hemorrhagic or necrotizing pancreatitis.
Pseudocysts and pancreatic abscesses can result from necrotizing pancreatitis because of enzymes being walled off by granulation tissue (ie, pseudocyst formation) or bacterial seeding of pancreatic or peripancreatic tissue (ie, pancreatic abscess formation). Ultrasonography or, preferably, CT can be used to detect both.
The inflammatory process can cause systemic effects because of the presence of cytokines, such as bradykinins and phospholipase A. These cytokines may cause vasodilation, increase in vascular permeability, pain, and leukocyte accumulation in the vessel walls. Fat necrosis may cause hypocalcemia. Pancreatic B-cell injury may lead to hyperglycemia.
Causes
The major causes are long-standing alcohol consumption and biliary stone disease.
- In developed countries, the most common cause of acute pancreatitis is alcohol abuse.
- On the cellular level, ethanol leads to intracellular accumulation of digestive enzymes and their premature activation and release.
- On the ductal level, ethanol increases the permeability of ductules, which allow enzymes to reach the parenchyma, resulting in pancreatic damage.
- Ethanol increases the protein content of the pancreatic juice and decreases bicarbonate levels and trypsin inhibitor concentrations. This leads to the formation of protein plugs that block the pancreatic outflow and obstruction.
- Another major cause of acute pancreatitis is biliary stone disease (eg, cholelithiasis, choledocholithiasis). A biliary stone may lodge in the pancreatic duct or ampulla of Vater and obstruct the pancreatic duct, leading to extravasation of enzymes into the parenchyma.
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Minor causes of acute pancreatitis
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Medications, including azathioprine, corticosteroids, sulfonamides, thiazides, furosemides, nonsteroidal anti-inflammatory drugs (NSAIDs), mercaptopurine, methyldopa, and tetracyclines
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Endoscopic retrograde cholangiopancreatography (ERCP)
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Hypertriglyceridemia (When the triglyceride [TG] level exceeds 1000 mg/U, an episode of pancreatitis is more likely.)
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Abdominal or cardiopulmonary bypass surgery, which may insult the gland by ischemia
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Trauma to the abdomen or back, resulting in sudden compression of the gland against the spine posteriorly
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Carcinoma of the pancreas, which may lead to pancreatic outflow obstruction
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Viral infections, including mumps, coxsackievirus, cytomegalovirus (CMV), hepatitis virus, Epstein-Barr virus (EBV), and rubella
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Bacterial infections, such as mycoplasma
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Intestinal parasites, such as Ascaris, which can block the pancreatic outflow
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Vascular factors, such as ischemia or vasculitis
CT Severity Index
It is critical to identify patients who are at high risk for severe disease, since they require close monitoring and possible intervention.
Early staging is based on the presence and degree of systemic organ failure (cardiovascular, pulmonary, renal) and on the presence and extend of pancreatic necrosis.
Balthazar et al constructed a CT severity index (CTSI) for acute pancreatitis that combines the grade of pancreatitis (A-E) with the extent of pancreatic necrosis.
The CTSI assigns points to patients according to their grade of acute pancreatitis - which can be determined on a non-contrast CT as well as a contrast-enhanced CT - as well as the degree of pancreatic necrosis - which requires the use of intravenous contrast material.
More points are given for a higher grade of pancreatitis and for more extensive necrosis.
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A Transaxial Portal Venous phase scan was acquired of the abdomen from the lower thoracic cavity to below the pubic symphisis. There is an obvious stranding around the head and mid portion and tail of the pancreas which is highly consistant with acute pancreatitis. There is extensive stranding of inflammation between the tail of the pancreas and the inner fossa of the spleen. There is also an incidental finding of liver cirrohsis which could be possibly linked to excessive acohol consumption.
Complications
Clinical outcome
The 1992 Atlanta Symposium on Acute Pancreatitis has classified this entity into a mild acute pancreatitis and a severe acute pancreatitis.
80-85% of cases of acute pancreatitis run a mild course without the development of multiple organ failure.
This group has a mortality of < 1%.
15-20% of cases of acute pancreatitis run a serious clinical course with pancreatic necrosis and the development of multiple organ failure.
Of these, pancreatic necrosis remains sterile in 60% of patients, whereas in 40% of these patients the necrosis becomes infected.
This last category of patients has the highest mortality rate of 25-70%.
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