Clinical Review - Acute pancreatitis

By Miss Sophie-Anne Welchman, specialist registrar and Professor Andrew Kingsnorth, consultant surgeon, Derriford Hospital, and honorary professor at Peninsula Medical School, Devon.

CT showing acute pancreatitis and peri-pancreatic fluid collection
CT showing acute pancreatitis and peri-pancreatic fluid collection

Section 1: Aetiology and epidemiology
Acute pancreatitis (AP) is an inflammation of the pancreas gland. In the majority of patients it is a mild condition that resolves without complication. However, 10-15 per cent develop severe AP.

This is defined as an episode associated with a local or systemic complication and it follows a much more destructive course. It may result in extreme morbidity and mortality.

The incidence of this condition is rising in the UK, particularly in Scotland and the south of England.

Incidence is estimated to be between 150 and 420 cases per million population1,2 but it varies between populations due to aetiological association with other pathological conditions and social habits.

There is a wide range of causative factors, with gallstones and alcohol representing 70-80 per cent of all cases in the UK.

It is important to be aware that there is a variety of causes, and, furthermore, that in 20 per cent of patients diagnosed with AP the cause is never identified.

It is useful to categorise causes of AP into obstruction of the pancreatic duct (gallstones, tumour), toxic insult (alcohol and other drugs), pancreatic trauma (both accidental and iatrogenic in the form of endoscopic retrograde cholangio-pancreatography (ERCP) or surgery to the upper abdomen), metabolic (hyperlipidaemia and hypercalcaemia) and infection (the classic example being mumps).

Congenital abnormalities are rare causes of pancreatitis but patients often suffer repeated episodes of inflammation.

Autoimmune pancreatitis is a relatively newly described entity that is thought to be very rare.

Strict histological and radiological criteria must be met in order to make this diagnosis. It is thought to be a disease of young people with a strong association with other autoimmune conditions.

The pathogenesis of AP has been the subject of research for centuries, yet it remains a matter of controversy. A number of theories exist to explain how each known cause of AP initiates the disease process.

The predominant theories hold raised pancreatic duct pressure and inappropriate premature intrapancreatic activation of enzymes as key to the process of initiation.

Following the onset of the inflammatory process, a common pathway, co-ordinated by cytokine signals and other inflammatory products, results in the pathological changes of fluid extravasation and necrosis that typify AP.

Section 2: Diagnosis
The diagnosis of AP should be raised on clinical suspicion based on history and examination findings.

The classic history is of sudden onset of epigastric pain which is constant in nature and radiates to the back. Nausea and vomiting are common associated features.

This history may be difficult to differentiate from peptic ulcer disease, particularly perforation, and rupture of an abdominal aortic aneurysm.

Both of these diagnoses are life threatening so it is critical they are considered in the assessment of any patient with upper abdominal pain.

Careful abdominal examination will assist in narrowing down this diagnosis. Epigastric tenderness and signs of upper abdominal peritonism are common findings in AP.

It is also common for clinical examination to reveal signs of dehydration and hypovolaemia. Patients may be pyrexial due to the systemic inflammatory response that accompanies the local inflammation.

Amylase and lipase
Referral to secondary care for an erect chest X-ray may exclude perforated peptic ulcer, reducing suspicion of peptic ulcer disease.

The diagnosis of AP is confirmed by correlating the clinical picture with biochemical tests. The two tests currently in use quantify serum levels of amylase and lipase. These are pancreatic enzymes that leak from the acutely inflamed pancreas to enter the systemic circulation where they can be measured.

Amylase is the traditional test of choice for diagnosing AP, however it is neither completely sensitive nor specific (other causes of hyperamylasaemia include severe cholecystitis, generalised peritonitis, intestinal obstruction mesenteric infarction and, confusingly, ruptured aortic aneurysm and perforated peptic ulcer).

With both of these tests the diagnosis of AP is made if the level is raised more than three times above the upper limit of the laboratory normal value.

However, it is important that the duration of symptoms is monitored if using an arbitrary cut-off level of serum enzymes to rule out of AP in cases considered high probability.

Both lipase and amylase peak early in the disease process and decline over a few days (3-4 days for amylase, longer for lipase). Added to this, raised serum amylase or lipase depends on there being enough exocrine pancreatic function to produce detectable levels of these enzymes.

For patients who have had multiple episodes of AP or have chronic pancreatitis, an acute flare may present with normal serum levels of pancreatic enzymes.

Section 3: Management
All patients with clinical suspicion of AP require referral to hospital for immediate assessment. Although the majority of patients with AP have a mild clinical course, in order to detect those that may develop severe disease close observation of all patients and early intervention is required.

Many of the patients that develop severe disease seem well on admission yet deteriorate some days later.

The focus of management is on the assessment of cardiovascular stability, early and aggressive fluid resuscitation and oxygen therapy. All patients should have LFTs and an ultrasound scan to exclude ongoing biliary obstruction and cholangitis.

Severity scoring (CRP, Atlanta or APACHE scores are commonly used) is also important at this stage to recognise the high-risk patients.

Around 10-15 per cent of all patients with AP go on to develop severe disease. This carries a 20-40 per cent mortality and as such identifying this group helps target medical resources.

AP in all its forms is an extremely painful condition and adequate analgesia is vital. Mild symptoms often resolve within a few days and efforts should then concentrate on preventing further episodes.

In more severe cases, the early phase of AP is much more turbulent. As the systemic inflammatory response progresses, third space fluid losses result in early renal impairment and respiratory distress.

Prompt referral to critical care for organ support is pivotal. Patients with predicted or actual severe AP who also have ultrasound-proven gallstones or patients with cholangitis, jaundice or dilated common bile duct should undergo urgent ERCP with sphincterotomy to relieve biliary obstruction.

Mortality rates and complications peak in two waves during AP. The early phase is considered as up to two weeks. The second phase is seen two to eight weeks after the onset of symptoms. Problems at this time are usually secondary to sepsis.

Infection of the necrotic pancreas carries a poor prognosis. A more common and often less severe complication is the development of a pancreatic pseudocyst. This may be symptomatic through its mass effect or more seriously, it may become infected. These complications may present to primary care after an episode of 'missed' pancreatitis or following hospital discharge.

Upper abdominal pain, bloating, early satiety, nausea, vomiting and signs of infection including pyrexia, sweats and tachycardia are common presentations of these complications. Radiological or operative interventions at this stage aim to drain symptomatic intra-abdominal collections or remove infected necrotic pancreatic tissue.

Complications of pancreatic surgery include pancreatic fistula and peripancreatic fluid collections. Up to a quarter suffer post-operative exocrine insufficiency and a third develop diabetes within 12 months.3

Severe AP is a catabolic state that is aggravated by inherent difficulties in delivering and utilising nutrition.

After discharge many patients will require input from rehabilitation teams.

Late complications are often permanent and classically relate to pancreatic destruction.

Exocrine insufficiency is a common consequence of severe disease that will result in severe nutritional deficiencies if not addressed by an experienced multidisciplinary team.

The endocrine pancreas is more resistant to insult, but post-pancreatitis diabetes is seen in those patients that survive severe episodes of AP.

The loss of the moderating effect of glucagon on hypoglycaemia makes glucose control very difficult to achieve in these patients. Pancreatic duct stenosis and strictures in the common bile duct present as obstructive jaundice following AP.

Preventing recurrent attacks
The importance of defining the cause of each episode of AP lies in reducing the chance of recurrent disease.

Counselling concerning abstaining from alcohol is given during admission to hospital, but reiterating this advice and guiding patients toward local support services is important.

Reviewing medications and stopping those associated with AP should be done during the hospital stay but it is important that GPs bear this in mind before restarting old medications.

Assessing for hyperlipidaemia and hypercalcaemia and treating abnormalities as appropriate is also critical.

Gallstone pancreatitis
Guidelines suggest that patients with AP and ultrasound-proven gallstones should be offered elective cholecystectomy within two weeks of presentation.4

Cholecystectomy should be delayed in patients with severe AP until signs of systemic upset have resolved. For patients who are deemed unfit for cholecystectomy, ERCP with sphincterotomy may be considered.

Section 4: Prognosis and follow up
The prognosis for patients with AP is varied. For the majority, the illness is a painful but short one, with no long-term consequences.

For some the degree of inflammation will result in prolonged admission, severe morbidity, surgery and life-long incapacity. For 2-5 per cent of all patients the outcome is death.

Follow-up arrangements should be tailored to individual patients as the variation in complications and outcome is wide.

All patients with local complications must be seen by pancreatic surgeons in clinic to assess for resolution. If there are any outstanding investigations to identify the cause of AP at discharge these must be followed up in the outpatient setting.

Good communication between primary and secondary care should help both teams provide the extensive support that patients require.


1. McKay CJ, Evans S, Sinclair M, Carter CR, Imrie CW. High early mortality rate from acute pancreatitis in Scotland, 1984-95. Br J Surg 1999; 86(10): 1302-5.

2. Toh SK, Phillips S, Johnson CD. A prospective audit against national standards of the presentation and management of acute pancreatitis in the South of England. Gut 2000; 46(2): 239-43.

3. Sabater L, Pareja E, Aparisi L et al. Pancreatic function after severe acute biliary pancreatitis: the role of necrosectomy. Pancreas 2004; 28(1): 65-8.

4. Working Party of the British Society of Gastroenterology; Association of Surgeons of Great Britain and Ireland; Pancreatic Society of Great Britain and Ireland. Association of Upper GI Surgeons of Great Britain and Ireland. UK guidelines for the management of acute pancreatitis. Gut. 2005; 54 Suppl 3: iii1-9.


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