Acute pancreatitis

Suspected cases of acute pancreatitis require urgent admission to hospital, writes Dr Simon Gowda.

Pancreatitis (blue) is most often caused by gallstones or alcohol abuse (Photograph: SPL)

Simply put, pancreatitis is the inflammation of the pancreas gland. It varies from mild, characterised by interstitial oedema with inflammatory exudates, to severe (approximately 10-15% of cases), characterised by glandular necrosis.

1. Aetiology
In the UK, pancreatitis accounts for around 3% of all emergency admissions with abdominal pain. Incidence in the UK is rising, and varies between 150 to 420 cases per million.

Gallstones and alcohol account for 70-85% of cases of pancreatitis. Other causes are listed in the box below. However, in many cases (up to 20%), no obvious cause is found.

2. Clinical features
The classic history is that of sudden onset severe epigastric pain with nausea and vomiting, which is partially relieved by leaning forward. Pain may radiate to the back. Clinical suspicion may be raised in those with known gallstones or history of alcohol abuse.

Physical findings may include guarding and rigidity of the abdomen, tachycardia, dehydration, hypotension and pyrexia. Bowel sounds may be reduced as the gut may go into an ileus. The patient may be very unwell.

Cullen's sign (bruising around the umbilicus) and Grey Turner's sign (flank bruising) are due to haemorrhagic fluid tracking from the retroperitoneum and both are rare. If acute pancreatitis is suspected the patient should be admitted urgently.

3. Diagnosis
Serum amylase more than three times the upper limit of normal is considered characteristic of pancreatitis. Other abdominal conditions may result in a mild amylase rise, for example perforated duodenal ulcer, mesenteric infarction and a ruptured abdominal aorta.

The amylase rise is short-lived as levels do peak early in acute pancreatitis and decline over two to four days, so a normal amylase may not necessarily exclude the condition, depending on what time it was taken in relation to the onset of symptoms.

Serum pancreatic lipase is a more sensitive and specific marker than amylase for acute pancreatitis and where available is preferred. The pancreas is the only source for lipase. Again, a level more than three times normal is characteristic of pancreatitis.

Both amylase and lipase leak from the inflamed pancreas into the bloodstream. An erect chest X-ray is performed to exclude a perforated duodenal/gastric ulcer - one of the differential diagnoses. There is no other role for plain film radiology in acute pancreatitis.

There are validated scoring systems that can determine the severity of pancreatitis (for example, Ranson's criteria, Glasgow score, Atlanta criteria or the acute physiology and chronic health evaluation), but these are in part dependent on biochemical markers and are only used in secondary care.

Other biochemical abnormalities which may be found during testing in patients with acute pancreatitis include raised WCC, hypocalcaemia, raised blood glucose, raised urea, reduced serum albumin and a metabolic acidosis with low partial pressure of oxygen on arterial blood gas testing. Ranson's criteria are only used when alcohol is the causative agent.

Contrast enhanced CT can be used to assess the extent and evolution of the disease and is a better imaging modality than ultrasound scan, which is used to identify the presence or absence of gallstones.

Key points
  • Acute pancreatitis is a serious and potentially fatal condition.
  • If you suspect pancreatitis the patient should be admitted.
  • Sending blood for an amylase check in primary care is pointless.
  • Recurrence of similar but milder symptoms approximately six weeks after an acute attack may indicate pseudocyst formation.
  • If alcohol is implicated as a causative agent ideally the patient should never drink again.

4. Management
In hospital, management is mainly supportive, with the use of oxygen, aggressive fluid resuscitation, opiate analgesia and strict fluid and observation monitoring. The general aim is to halt disease progression and prevent organ failure.

There is no single proven therapy for the treatment of acute pancreatitis. Severe episodes are managed in high dependency or intensive therapy environments. Multidisciplinary care is the norm. Severe necrosis of the pancreas gland may be surgically debrided.

Severe acute pancreatitis results in nutritional deficiencies as pancreatitis is a catabolic state. If nutritional support is needed, the enteral route is preferred. This is in the form of nasogastric or nasojejunal feeds. If feeding cannot be performed enterally then total parenteral nutrition is given via a central line intravenously, but this has potential risks and complications.

Updated British Society of Gastroenterologists guidelines suggest that where gallstones are the causative agent, early endoscopic retrograde cholangiopancreatography (ERCP) is recommended within the first 72 hours of pain. Definitive treatment, such as cholecystectomy, should be done on admission or within two weeks of discharge. Preventing further attacks depends on identifying a cause and removing it.

Potential causes
  • Gallstones.
  • Alcohol.
  • Iatrogenic (post-ERCP).
  • Infection (Coxsackie, mumps, mycoplasma pneumonia).
  • Trauma.
  • Hyperlipidaemia.
  • Hypothermia.
  • Hyperparathyriodism (due to hypercalcaemia).
  • Medication (corticosteroids, azathioprine, furosemide).
  • Malignancy.
  • Structural abnormalities, for example, pancreas divisum.
  • Pregnancy.

5. Complications
Patients with mild pancreatitis should make a full recovery with no long-term sequelae. Mortality varies between 5-10% for a severe attack.

In hospital, complications of acute pancreatitis may result in adult respiratory distress syndrome, sepsis, renal failure, disseminated intravascular coagulation, metabolic and nutritional deficiencies, pancreatic abscess formation and pancreatic necrosis.

Late complications include pseudocyst formation (where pancreatic juices are enclosed by fibrous or granulation tissue). These can be surgically or radiologically drained.

Repeated attacks of acute pancreatitis can lead to development of chronic pancreatitis. Chronic pancreatitis mimics the pain of an acute episode, but does not give an amylase rise. Pain control is the mainstay of management.

Reflect on this article and add notes to your CPD Organiser on MIMS Learning

  • Dr Gowda is a salaried GP in Sandbach, Cheshire

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