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Acute pancreatitis
is sudden inflammation of the pancreas that may be mild or life
threatening but that usually subsides.
Gallstones (biliary tract disease—see Gallbladder and Bile Duct Disorders: Gallstones) and alcohol abuse account for almost 80% of hospital admissions for acute pancreatitis. About 1½ times as many women as men have acute pancreatitis caused by gallstones. Normally, the pancreas secretes pancreatic fluid through the pancreatic duct to the duodenum. This pancreatic fluid contains digestive enzymes in an inactive form and inhibitors that inactivate any enzymes that become activated on the way to the duodenum. Blockage of the pancreatic duct by a gallstone stuck in the sphincter of Oddi stops the flow of pancreatic fluid. Usually, the blockage is temporary and causes limited damage, which is soon repaired. But if the blockage remains, activated enzymes accumulate in the pancreas, overwhelm the inhibitors, and begin to digest the cells of the pancreas, causing severe inflammation.
Drinking as little as 2 ounces of alcohol a day (half a bottle of wine, 4 bottles of beer, or 5 ounces of liquor) for several years may cause the small ductules in the pancreas that drain into the pancreatic duct to clog, eventually causing acute pancreatitis. An attack of pancreatitis may be precipitated by an alcoholic binge or by an excessively large meal. Many other conditions can also cause acute pancreatitis.
Many drugs can irritate the pancreas. Usually, the inflammation resolves when the drugs are stopped. Viruses can cause pancreatitis, which is usually short-lived.
Symptoms
Almost everyone with acute pancreatitis suffers severe abdominal pain in the upper abdomen, below the breastbone (sternum). The pain often penetrates to the back in about 50% of people. Rarely, the pain is first felt in the lower abdomen. When acute pancreatitis is caused by gallstones, the pain usually starts suddenly and reaches its maximum intensity in minutes. When pancreatitis is caused by alcoholism, pain develops over a few days. The pain then remains steady and severe, has a penetrating quality, and persists for days.
Coughing, vigorous movement, and deep breathing may worsen the pain. Sitting upright and leaning forward may provide some relief. Most people feel nauseated and have to vomit, sometimes to the point of dry heaves—retching without producing any vomit. Often, even large doses of an injected opioid analgesic (see Pain: Opioid Analgesics) do not relieve pain completely.
Some people, especially those who develop acute pancreatitis because of alcohol abuse, may never develop any symptoms other than moderate pain. Others feel terrible. They look sick and sweaty and have a fast pulse (100 to 140 beats a minute) and shallow, rapid breathing. Rapid breathing may occur if people have inflammation of the lungs, areas of collapsed lung tissue (atelectasis—see Atelectasis), or accumulation of fluid in the chest cavity (pleural effusion—see Pleural Disorders: Pleural Effusion). These conditions decrease the amount of lung tissue available to transfer oxygen from the air to the blood.
At first, body temperature may be normal, but it increases in a few hours to between 100° F and 101° F (37.7° C and 38.3° C). Blood pressure may be high or low, but it tends to fall when the person stands, causing faintness. As acute pancreatitis progresses, people tend to be less and less aware of their surroundings—some are nearly unconscious. Occasionally, the whites of the eyes (sclera) become yellowish.
Complications:
Damage to the pancreas may permit activated enzymes and toxins such as cytokines (see Biology of the Immune System: Cytokines) to enter the bloodstream and cause low blood pressure and damage to organs outside of the abdominal cavity, such as the lungs and kidneys. The part of the pancreas that produces hormones, especially insulin, tends not to be damaged or affected. One of five people with acute pancreatitis develops some swelling in the upper abdomen. This swelling may occur because the movement of stomach and intestinal contents stops (a condition called ileus—see Gastrointestinal Emergencies: Appendicitis).
In severe acute pancreatitis, parts of the pancreas die (necrotizing pancreatitis), and blood and pancreatic fluid may escape into the abdominal cavity, which decreases blood volume and results in a large drop in blood pressure, possibly causing shock (see Shock). Severe acute pancreatitis can be life threatening.
Infection of an inflamed pancreas is a risk, particularly after the first week of illness. Sometimes, a doctor suspects an infection because the person's condition worsens and because a fever and high white blood cell count develop after other symptoms had initially started to subside. The diagnosis is made by culturing blood samples (growing large numbers of bacteria) to identify bacteria that are causing the infection and performing a computed tomography (CT) scan. A doctor may be able to withdraw a sample of infected material from the pancreas by inserting a needle through the skin and into the pancreas. An infection is treated with antibiotics, and surgical removal of infected and dead tissue usually is necessary.
Sometimes, a collection of pancreatic enzymes, fluid, and tissue debris resembling a cyst (a pseudocyst) forms in the pancreas and expands like a balloon. If a pseudocyst grows larger and causes pain or other symptoms, a doctor drains it quickly because death can result if the pseudocyst expands further, becomes infected, bleeds, or ruptures. Depending on its location, the pseudocyst is drained either by performing a surgical procedure or by inserting a catheter through the skin or through an endoscope (a flexible viewing tube) that is passed through the mouth and into the stomach or intestine and allowing the pseudocyst to drain for several weeks.
Diagnosis
Characteristic abdominal pain leads a doctor to suspect acute pancreatitis, especially in a person who has gallbladder disease or who is an alcoholic. On examination, a doctor often notes that the abdominal wall muscles are rigid. When listening to the abdomen with a stethoscope, a doctor may hear few or no bowel (intestinal) sounds.
No single blood test proves the diagnosis of acute pancreatitis, but certain tests corroborate it. Blood levels of two enzymes produced by the pancreas, amylase and lipase, usually increase on the first day of the illness but return to normal in 3 to 7 days. If the person has had other flare-ups (bouts or attacks) of pancreatitis, however, the levels of these enzymes may not increase, because so much of the pancreas may have been destroyed that few cells are left to release the enzymes. The white blood cell count is usually increased.
X-rays of the abdomen may show dilated loops of intestine or, rarely, one or more gallstones. Chest x-rays may reveal areas of collapsed lung tissue or an accumulation of fluid in the chest cavity. Ultrasound may show gallstones in the gallbladder or sometimes in the common bile duct and also may detect swelling of the pancreas.
A CT scan is particularly useful in detecting inflammation of the pancreas and is used in people with severe acute pancreatitis and in people with complications, such as extremely low blood pressure. Because the images are so clear, a CT scan helps a doctor make a precise diagnosis.
Prognosis
In severe acute pancreatitis, a CT scan helps determine the prognosis. If the scan indicates that the pancreas is only mildly swollen, the prognosis is excellent. If the scan shows large areas of destroyed pancreas, the prognosis is poor.
When acute pancreatitis is mild, the death rate is about < 5%. However, in pancreatitis with severe damage and bleeding, or when the inflammation is not confined to the pancreas, the death rate can be as high as 10 to 50%. Death during the first several days of acute pancreatitis is usually caused by failure of the heart, lungs, or kidneys. Death after the first week is usually caused by pancreatic infection or by a pseudocyst that bleeds or ruptures.
Treatment
Treatment of mild pancreatitis usually involves short-term hospitalization where analgesics are given for pain relief and the person fasts to try to “rest” the pancreas. Usually, normal eating can resume after 2 to 3 days without further treatment.
People with moderate to severe pancreatitis need to be hospitalized. They must initially avoid food and liquids, because eating and drinking stimulate the pancreas. Symptoms such as pain and nausea are controlled with intravenous drugs. Intravenous fluids are given as well. People with severe acute pancreatitis are admitted to an intensive care unit, where vital signs (pulse, blood pressure, and rate of breathing) and urine production can be monitored continuously. Blood samples are repeatedly drawn to monitor various components of the blood, including hematocrit, sugar (glucose) levels, electrolyte levels, white blood cell count, and amylase and lipase levels. A tube may be inserted through the nose and into the stomach (nasogastric tube) to remove fluid and air, particularly if nausea and vomiting persist and gastrointestinal ileus is present. Nutrition is given intravenously, via a nasogastric tube, or by both means.
For people with a drop in blood pressure or who are in shock, blood volume is carefully maintained with intravenous fluids, and heart function is closely monitored. Some people need supplemental oxygen and the most seriously ill require a ventilator.
When acute pancreatitis results from gallstones, treatment depends on the severity. If the pancreatitis is mild, removal of the gallbladder can usually be delayed until symptoms subside. Severe pancreatitis caused by gallstones can be treated with endoscopic retrograde cholangiopancreatography (ERCP—see Diagnostic Tests for Liver, Gallbladder, and Biliary Disorders: Imaging Tests and Understanding Endoscopic Retrograde Cholangiopancreatography ). Although more than 80% of people with gallstone pancreatitis pass the stone spontaneously, ERCP with stone removal is usually needed for people who do not improve over the initial 24 hours of hospitalization and who have an infection of the bile duct system (cholangitis).
Last full review/revision August 2007 by Steven D. Freedman, MD, PhD
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