Chapter 10a
ACUTE PANCREATITIS
1. DEFINITION
Acute pancreatitis is a disease characterized clinically by abdominal pain and elevated serum pancreatic enzyme levels and pathologically by acute inflammatory changes in the pancreas and varying amounts of damage to adjacent organs. The ICD 10AM Code is K85.
2. CLASSIFICATION
There are several classification systems and none are clearly satisfactory.
These include:
• severity - mild - severe
• pathology - interstitial - necrotizing
• aetiology - obstructive - gall stones - microlithiasis
- Sphincter of Oddi etc
• toxic - alcohol - drugs
- scorpion envenomation
• metabolic - hyperlipidaemia - hypercalcemia
• infection - AIDS
- mumps
150 0 Chapter 10a - bacterial infections
• iatrogenic - ERCP - post operative - coronary bypass surgery
• autoimmune - ill understood and steroid responsive
• genetic
• trauma to the abdomen
• idiopathic – left over from when no alternative explanation available
• pancreas divisum
3. INCIDENCE
This is reported to vary from 10 to 50/10
5in the US but is varies widely throughout the world, principally because of variation in the prevalence of the major precipitating factors, alcohol abuse and gall stone disease. The best data come from the Oxford Record Study with hospital and death certificate data from 1963 – 1998 covering an area comprising 0.63 million in 1963 rising to 2.5 million in 1987 (1). Age standardised incidence rates doubled from 4.9/10
5in 1963-74 to 9.8/10
5in 1987-98 when standardised case mortality rates within 30 days of admission fell from 14.2% in 1963-74 to 7.6% in 1975-86 and remained fairly constant thereafter, being 6.7% in 1987-98. While around 7% died within one month of admission another 5%
died between then and 12 months later, a 30 fold increase over the population rate. The rise in admission rates was mainly seen in younger males and females. Unfortunately, the study provides no data on the aetiology of the pancreatitis. It is also increasingly recognized that there are mild self limited cases which may not be recognized in statistics. The further complicating factor is that the major diagnostic tests all have significant problems in sensitivity and specificity. Additionally, save for laparotomy or autopsy, no histological diagnosis is available.
4. COURSE AND PROGNOSIS
Mild cases are self limited and almost all settle within a few days. In severe cases presenting as an abdominal catastrophe death may occur within several days or follow after a series of local and/or general complications.
Mortality rates of 20-30% are the norm in the severe cases in which the galaxy of potential complications is awesome.
The evolution of acute pancreatitis into chronic pancreatitis is an
important aspect. Characteristically the acute pancreatitis of alcohol abuse
ACUTE PANCREATITIS 151 has repeated episodes of decreasing severity with progressive destruction of the gland which may evolve into a syndrome of persistent unremitting pain, resistant to analgesics associated with calcified hypofunctioning gland. On the other hand the evidence is that gall stone pancreatitis does not lead to chronic pancreatitis.
5. MANAGEMENT
Apart from early stone removal from impaction at the Ampulla of Vater in appropriate cases, management is based upon alimentary rest, IV fluids and pain relief.
6. EPIDEMIOLOGY
By and large, in an affluent society such as the US the causes numerically are:
• Biliary – on third or more
• Alcohol – one third or more
• The remainder – half idiopathic, half other causes.
Biliary causes are predominantly related to gall stones. There is good
evidence that obstruction by gall stones at the Ampulla of Oddi is a
precipitating cause, an obstruction which can be transient; studies have
shown that gall stones can be retrieved from the faeces in 30% of patients
presenting with acute pancreatitis and jaundice (2). If the stone remains
impacted, the pancreatitis is more severe. The link with gall stones is
strengthened by the finding that cholecystectomy for stone diminished the
risk of acute pancreatitis in subsequent years (3). Those with gall stones
have an increased risk of acute pancreatitis which is probably 20-30% above
the background but the risk remains low. In a Mayo Clinic study the risk
was on 0.17% pa; hence the risk of acute pancreatitis does not justify
cholecystectomy (3). It is also evident that the risk is greater the smaller the
stone and there is evidence that biliary sludge may cause acute pancreatitis
or even recurrent pancreatitis (4). This would explain the likelihood of acute
pancreatitis in association with total parenteral nutrition, extreme weight
loss, gastric surgery and some drugs such as somostatin analogues. With
increasing use of endoscopic retrograde pancreatic cholangiography (ERCP),
acute pancreatitis which complicates around 4% of procedures is becoming
important (5).
152 Chapter 2 10a 7. SPHINCTER OF ODDI DYSFUNCTION
The role of this in acute pancreatitis is yet to be defined. A wide variety of changes – anomalous response to gut hormones, stenosis after gall stone passage, spasm of the sphincter have all been described but the difficulty and indeed the danger of cannulation of the sphincter in investigating it and the problem inherent in determining normality make for a degree of obscurity.
8. PANCREAS DIVISUM
This is a congenital anomaly leading to an abnormal drainage pattern of the ducts of the pancreas. It has been blamed for a proportion of otherwise unexplained episodes of acute pancreatitis. However, its diagnosis is difficult at Endoscopy with wide variation in the endoscopic prevalence although at autopsy its prevalence is 7% so that proof of an aetiological link with acute pancreatitis is difficult and the issue is yet to be settled. It still could be that the link depends upon the coincidence of acute pancreatitis in a patient with an already anomalous drainage system.
References
1. Goldacre MJ, Roberts SE. Hospital admission for acute pancreatitis in a English population 1963-98 : database study of incidence and mortality. BMJ 328:1466-9 (2004).
2. Acosta JL, Ledesma CL. Gallstone migration as a cause for acute pancreatitis. N.Engl. J.
Med. 290-484 (1974)
3. Moreau JA, Zinmeister AR, Melton JP, Di Magno EP. Gallstone pancreatitis and the effect of cholecystectomy : a population-based cohort study. Mayo Clinic Proc. 63:466 (1988).
4. Diehl AK, Holleman DR, Chapman JB, Shwesinger WH, Kurtin WE. Gallstone size and the risk of pancreatitis. Arch. Int. Med. 157:1674 (1977).
5. Christensen M, Matzen P, Schulze S, Rosenberg J. Complications of ERCP : a prospective study. Gastrointest. Endosc. 60:721-31 (2004).
