Acute Pancreatitis



Acute pancreatitis is a potentially life threatening acute inflammatory process that affects the pancreas and may extend into the adjacent retroperitoneal tissue. The incidence is approximately 5 per 100,000 per year and the male to female ratio is equal. Most cases occur over the age of 40 years.

There are a variety of causes of acute pancreatitis.


The exocrine pancreas produces several potent digestive enzymes that are equally capable of digesting cells and tissues as food. The normal physiology of the pancreas ensures that these enzymes are only activated within the lumen of the small bowel. This system is disrupted in acute pancreatitis. Pancreatic enzymes become activated within the pancreas and begin the autodigestion of the pancreas and later adjacent tissues. The enzymes can destroy cell membranes and kill cells.

Processes that obstruct the flow of the secretions of the exocrine pancreas along the pancreatic ducts and into the duodenum can cause acute pancreatitis: the enzymes have nowhere to go and can spill into the pancreas. Gallstones and tumours operate in this fashion.

Alcohol can dehydrate pancreatic fluid, making it more viscous and liable to obstruct the pancreatic duct. Other causes also induce pancreatitis in this fashion.

Surgery and trauma to the pancreas can damage the ducts and force the enzymes into the parenchyma of the pancreas.

The pathological changes in the pancreas are those of acute inflammation and necrosis. Involvement of adjacent organs follows a similar pattern and peritonitis can result. There may be considerable loss of fluid into the abdominal cavity as a consequence of increased capillary permeability and tissue damage and this can produce circulatory hypovolaemia.

Clinical Features

Acute pancreatitis is one of the causes of an acute abdomen and presents with a sudden onset of severe abdominal pain that is located in the epigastrium and can radiate to the back, flanks, chest and lower abdomen. The pain is relieved by sitting forwards. The pain is accompanied by nausea and vomiting.

Bruising can occur in the flanks (Turner's sign) and there may be periumbilical bruising (Cullen's sign).

The features of shock and peritonitis are usually present.


The chaos that rages in the autodigesting pancreas can cause assorted complications, especially if the process extends beyond the pancreas.

Hypotension can develop and may be accompanied by acute renal failure. Adult respiratory distress syndrome can occur. Ascites may develop and can be haemorrhagic in nature.

The acute inflammatory swelling of the pancreas can obstruct the distal common bile duct and induce obstructive jaundice.

With all hell breaking lose in the pancreas the nearby bowel can enter a state of ileus.

The acute inflammation can also activate the clotting cascade and cause thrombosis of the portal vein. Systemic clotting problems can occur in the form of disseminated intravascular coagulation.

Calcium can become deposited in the necrotic tissue that results from the acute pancreatitis and this may be sufficient to induce hypocalcaemia. Damage to the islets of Langerhans can impair the release of insulin and hyperglycaemia may develop.

Rarely, Putscher's retinopathy can occur.

In the aftermath of an attack of acute pancreatitis a pancreatic abscess can form. A pancreatic phlegmon is a solid mass of partially necrotic tissue in the pancreas that persists for a couple of weeks and is associated with pain and fever.

A pancreatic pseudocyst is a collection of inflammatory and necrotic gunge which accumulates in the lesser sac and causes a failure of complete resolution of the features of the acute pancreatitis.


The key diagnostic investigation in acute pancreatitis is the serum amylase. Although the serum amylase can be raised in a variety of diseases, only acute pancreatitis cranks it up to over 1000IU/L. Imaging can supplement the amylase, especially in instances of equivocal levels.

The amylase is only the beginning of the blood tests. The diverse range of complications that can be caused by acute pancreatitis requires various other blood tests to be performed, including the full blood count, urea and electrolytes, calcium, clotting, liver function tests and arterial blood gases. Prognostic systems exist that use the results of these test to determine the severity of the attack of acute pancreatitis.


The initial treatment aims to stabilise the patient's hypotension, hypovolaemia and other complications. The patient is kept nil by mouth and has nasogastric suction via a nasogastric tube; the aim of this strategy is to rest the GI tract and therefore to minimise pancreatic exocrine activity and thus halt the delivery of new pancreatic enzymes to the fomenting chaos.

Surgery is reserved for situations where the above management fails and usually involves resection of necrotic tissue. Surgery is also required to deal with a pseudocyst.

Despite the havoc that acute pancreatitis can wreak it is self-limiting in 80-90% and subsides in around 3 to 7 days.