Acute pancreatitis is the term used to describe the sudden onset of inflammation of the pancreas. The pancreas is a gland located behind the stomach which functions in the digestion of carbohydrates, proteins and fats by secreting digestive enzymes into the small intestine. The pancreas is also involved in the body’s regulation of glucose metabolism, through the secretion of the hormones insulin and glucagon into the bloodstream.
The two most common causes of acute pancreatitis are gallstone disease and alcohol use. Other causes include lipid (triglyceride) disorders, infections, medications, surgery/endoscopy, or trauma to the abdomen. In approximately 10% to 15% of patients with pancreatitis, the cause is unknown.
Though the exact mechanism of pancreatic inflammation is unknown, it is thought that pancreatic damage occurs when the digestive enzymes secreted by the pancreas are activated before they reach the intestine. Once activated these enzymes then attack the pancreas itself, the process of which has been referred to as autodigestion.
Clinically, acute pancreatitis may range from mild abdominal discomfort to a severe, life-threatening illness. Most patients with acute pancreatitis recover completely after a few days of medical treatment with intravenous fluids and pain medications in the hospital. In up to 20% of patients, however, the pancreatitis can be severe enough that it requires the patient be monitored in an intensive care unit (ICU). The disease may cause a rapid deterioration in the patient’s condition leading to dysfunction of other important organs such as the heart, lungs, or kidneys.
In the most severe cases of acute pancreatitis, the extent of injury to the pancreas caused by the release of its digestive enzymes can lead to the death of pancreatic tissue. This dead pancreatic tissue is termed pancreatic necrosis. Necrotic pancreatic tissue is susceptible to infection, or bleeding into the gland. Infection and bleeding into dead pancreatic tissue significantly increases the risk of mortality, and their presence requires prompt surgical intervention. Without aggressive surgical treatment to clear the infection, many patients do not survive the infection. When the dead pancreas is not infected, it is called sterile necrosis. The recommended treatment for patients with sterile pancreatic necrosis is close observation and monitoring for signs of infection.
There are certain situations in which surgical intervention can be considered in patients with sterile pancreatic necrosis. Recent studies have shown some benefit to surgery in patients with sterile necrosis whose condition has failed to improve after four weeks since the onset of pancreatitis with continued organ dysfunction or clinical deterioration. The timing of surgery has been controversial though the consensus in most studies is a minimum of four weeks after the onset of pancreatitis before surgery is undertaken for sterile pancreatic necrosis. This is because after four weeks dead pancreatic tissue can be well differentiated from living tissue and easily removed. The surgical removal of all dead or necrotic tissue is called debridement. Surgery earlier than four weeks has shown to lead to inadequate debridement of the necrosis, since the delineation between dead and living tissue has not occurred sufficiently.
Management of severe acute pancreatitis has changed significantly over the years. Early management is non-surgical and solely supportive. Today, more patients survive the early phase of severe pancreatitis due to improvements in critical care medicine. The role of surgery in severe acute pancreatitis applies only in selected cases, with pancreatic infection being a well accepted indication for surgical treatment. However, many patients often require multiple surgeries to remove all the dead and infected tissue, and patients often remain critically ill for a long period after their surgery until the infection subsides.