Mrs T is a 44 year old lady who is usually fit and well. She came in one morning with a two-hour history of epigastric pain which came on very suddenly when she was ironing.
She described it as a very severe, sharp pain which radiated through to her back. The pain eased slightly when she sat forward. She felt nauseated with the pain and had vomited twice.
She had a history of migraine and was not on any regular medication. She was a non-smoker and did not drink any alcohol. Her BMI was 22kg/m2.
On examination she did not look well and was in considerable pain. Her pulse was 88/min, BP 120/72 and she was very tender in her epigastrium with mild rebound tenderness but no guarding.
I arranged for her to be admitted to the local surgical team where she was found to have acute pancreatitis. Her amylase level was 5000u/l. An ultrasound, MRCP and endoscopic ultrasound (EUS) failed to demonstrate any gallstones. Viral titres were also normal.
Further investigation and treatment
She was followed up in the regional pancreatitis clinic and continued to have some epigastric discomfort and some upper abdominal distension.
A CT abdomen with undertaken which showed some delayed gastric emptying and she was started on domperidone which improved her symptoms. A (99m)technetium (Tc)-labelled hepatic iminodiacetic acid analogue (HIDA) scan was also performed which showed a reduced ejection fraction of her gall bladder of 25%, so she was referred for a cholecystectomy.
She had a laparoscopic cholecystectomy and has since been symptom-free and is no longer taking any domperidone.
Acute pancreatitis is acute inflammation of the pancreas. It is sometimes associated with a systemic inflammatory response that can impair the function of other organs or systems. The incidence of acute pancreatitis is rising in the UK and varies between 150 to 420 cases per million population.1
Gallstones are the underlying cause of acute pancreatitis, in around half of cases, and around a quarter of cases are related to alcohol abuse. Around 10% of patients have idiopathic pancreatitis.
Less than 5% of cases are caused by:
- Drugs such as valproate, steroids, azathioprine
- Endoscopic retrograde cholangiopancreatography (ERCP)
- Lipoprotein lipase deficiency
- Some viral infections
Patients classically present with severe onset abdominal pain, which is usually associated with vomiting. The pain may radiate to the back. The Atlanta classification is a useful framework for assessing the severity of acute pancreatitis.2
Clinical features of abdominal pain and vomiting, together with elevation of plasma concentrations of pancreatic enzymes (at least more than three times normal levels), are the cornerstones of diagnosis.
The levels of pancreatic enzymes peak early, and decline over 3–4 days. Amylase has traditionally been the enzyme tested for, however, more recently lipase levels are being undertaken in some hospitals. Lipase has a longer half-life than amylase and it is also more specific.
Other blood tests include liver function tests, fasting blood lipids and calcium concentrations. Viral antibody titres (for example, for mumps and Coxsackie B4) are often taken.
Recommendations are for there to be at least two good quality ultrasound scans undertaken before a diagnosis of gallstones can be excluded.
It is increasingly common for an endoscopic ultrasound and/or magnetic resonance cholangiopancreatography (MRCP) to be undertaken if the first ultrasound examination is normal. Endoscopic ultrasonography (EUS) is as accurate and safer than ERCP for the detection of common bile duct stones.
A HIDA scan was undertaken in this case as a biliary cause for this patient’s pancreatitis was thought to be most likely. Cholecystectomy is indicated in symptomatic patients without gallstones who have a low-ejection fraction HIDA scan.3
Patients need to be admitted to hospital and have intravenous fluids, oxygen and analgesia. There is some evidence that early oxygen supplementation and fluid resuscitation is associated with resolution of organ failure. There is no specific drug treatment for the management of acute pancreatitis.
Urgent therapeutic ERCP should be performed in patients with acute pancreatitis of suspected or proven gallstone aetiology who satisfy the criteria for predicted or actual severe pancreatitis, or when there is cholangitis, jaundice, or a dilated common bile duct. The procedure is best carried out within the first 72 hours after the onset of pain.
The risk of recurrent pancreatitis is directly related to the interval between first attack and cholecystectomy.4 Current recommendations are that all patients with biliary pancreatitis should undergo definitive management of gallstones during the same hospital admission, unless a clear plan has been made for definitive treatment within the next two weeks. However, in practice this is not always possible.
Patients should be advised to abstain from alcohol for at least 6-12 months, regardless of the underlying cause of pancreatitis.5
Complications and prognosis
The inflammation may settle spontaneously or may progress to necrosis of the pancreas or surrounding fatty tissue. The distant organ or system dysfunction may resolve or may progress to organ failure. Around 80% of patients have a mild attack and recover within a few days, whereas around 20% of patients have a severe episode with prolonged hospital stay, the need for critical care support, and a 15-20% risk of death.6
Infection of necrosis is the most serious local complication of acute pancreatitis and is associated with a mortality rate of around 40%. Some centres give prophylactic antibiotics to reduce this potential complication; however, there is still no robust evidence to support this use.7
Paralytic ileus is very common in the first few days of developing acute pancreatitis. Many patients gradually increase their oral intake as their symptoms improve. If nutritional support is needed, then enteral nutrition should be used if it can be tolerated. However, if an ileus lasts for more than five days then parenteral nutrition is often given as an alternative.
Pancreatic exocrine insufficiency can occur in the recovery phase after severe acute pancreatitis. Endocrine insufficiency (diabetes) is less common but can occur in some cases.
- Dr Newson is a GP in the West Midlands
- UK Working Party on Acute Pancreatitis. UK guidelines for the management of acute pancreatitis. Gut. 2005 May;54 Suppl 3:iii1-9
- Banks PA, Bollen TL, Dervenis C et al. Classification of acute pancreatitis--2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-11
- Mahid SS, Jafri NS, Brangers BC et al. Meta-analysis of chloecystectomy in symptomatic patients with positive hepatobiliary iminodiacetic acid scan results without gallstones. Arch Surg. 2009 Feb;144(2):180-7
- van Baal MC, Besselink MG, Bakker OJ, et al. Timing of Cholecystectomy after Mild Biliary Pancreatitis: A Systematic Review. Ann Surg 2012;255:860-6
- Nikkola J et al. Abstinence after first acute alcohol-associated pancreatitis protects against recurrent pancreatitis and minimizes the risk of pancreatic dysfunction Alcohol Alcohol 2013;48:483-6
- Johnson CD, Besselink MG, Carter R. Acute pancreatitis. BMJ 2014;349:g4859
- Villatoro E, Mulla M, Larvin M. Antibiotic therapy for prophylaxis against infection of pancreatic necrosis in acute pancreatitis. Cochrane Database Syst Rev 2010 12;5:CD002941