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Acute pancreatitis

Created: 2/9/2005

 

Aetiology and pathogenesis

Acute pancreatitis is an acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.

Gallstones and high alcohol intake are associated with about 80% of cases. 10% of cases are idiopathic.

Other causes include:

  • hypertriglyceridaemia
  • hypercalcaemia
  • trauma
  • endoscopic retrograde cholangiopancreatography (ERCP)
  • drugs (e.g. sodium valproate, tetracycline, thiazides, furosemide [frusemide]).

The incidence of acute pancreatitis appears to be rising. Figures as high as 200/1,000,000 population have been quoted - a 10-fold increase since 1970. High alcohol intake accounts for much of this rise. The disease is most common in women aged 50–60 years.

The cellular mechanisms involved in the development of acute pancreatitis are unclear, although a key step appears to be intra-acinar activation of trypsinogen. This causes activation of other enzyme systems, including lipase, phospholipase A2, elastase, chymotrypsin and the kallikrein-kinin system, resulting in fat and tissue necrosis, coagulation, vascular damage, haemorrhage, oedema formation and inflammation.

Diagnosis and assessment of severity

The clinical presentation is of rapid onset of upper abdominal or back pain, vomiting, fever and tachycardia. Occasionally Grey Turner (bruising in the loin) and Cullen (bluish discoloration near the umbilicus) signs may be present. In about 80% of cases, the course is mild and resolves spontaneously.

Diagnosis is most commonly made using serum amylase estimation, although there are limitations to its specificity and sensitivity. The serum lipase level is more accurate and a better marker for alcoholic pancreatitis. However, the laboratory measurement of lipase was, until recently, more complicated and it is not available in many centres.

Assessment of severity – the most common scoring systems are those of Ranson and Glasgow (or Imrie). The criteria for the Glasgow system are:

  • patient aged over 55 years
  • white blood cell count over 15 x 109/L
  • serum glucose over 10 mmol/L
  • serum urea over 16 mmol/L
  • partial pressure of oxygen in arterial blood (PaO2) less than 60 mmHg (8.6 kPa)
  • serum calcium less than 2 mmol/L
  • serum albumin less than 32 g/L
  • serum lactate dehydrogenase over 600 units/L
  • serum aspartate transaminase over 100 units/L.

Three positive criteria within 48 hours indicate severe disease. The disadvantage of the above systems is that data collection is not complete until 48 hours after patient admission. Evidence suggests that APACHE II (Acute Physiology and Chronic Health Evaluation) scoring at 24 hours is at least as accurate.

Biochemically, C-reactive protein (CRP) is a useful test to assess severity, but only 72 hours after disease onset. An earlier marker is urinary trypsinogen activation peptide (TAP) which is valuable at 24 hours. It has an 86% sensitivity for identifying patients who will develop severe disease.

Imaging may be necessary to diagnose the disease or its cause. Ultrasound is useful in suspected pancreatitis only for diagnosing gallstones. Contrast CT scanning is the imaging procedure of choice to diagnose and monitor acute pancreatitis.

Management

General care: the basis of management is:

  • bed rest
  • analgesia
  • intravenous fluids
  • withholding of oral intake
  • support of failing organ systems
  • identification of severe cases
  • identification of complications.

In episodes with complications, or those predicted to be severe, the patient should be managed in a critical care area. Physiological supportive care is required because systemic inflammatory response syndrome (SIRS) or multiple organ failure may result.

Specific therapies include:

  • aprotinin
  • glucagons
  • somatostatin
  • octreotide
  • gabexate mesilate (an antiprotease agent)
  • fresh frozen plasma
  • lexipafant (an inhibitor of platelet activating factor)
  • peritoneal lavage.

None of these have any impact on the mortality rate, although there is weak evidence that lexipafant, commenced within 48 hours of disease onset, can reduce complications and organ failure.

Nutrition: in severe or prolonged cases, total parenteral nutrition is commonplace. Total parenteral nutrition seldom causes release of pancreatic enzymes, except when there is a high lipid load. Enteral nutrition promotes pancreatic enzyme production unless feed is delivered into the jejunum or below. Elemental feeds seem to stimulate the pancreas even if delivered directly to the jejunum, whereas standard feeds do not.

Endoscopic retrograde cholangiopancreatography and sphincterotomy may be necessary in the case of gallstone pancreatitis, even in the acute phase of the illness. It is recommended if there is evidence of obstructive jaundice, or for severe pancreatitis with gallstones that does not settle within 72 hours.

Complications: the main complications of pancreatitis are:

  • infection and/or abscess formation
  • pancreatic necrosis
  • multiple organ failure
  • hypocalcaemia
  • pseudocyst formation
  • chronic pancreatitis.

The mortality from infected severe pancreatitis is over 50%. There is evidence to support the use of prophylactic antibiotics in severe pancreatitis. Where there is proven infection, but a specific organism is unknown, treatment with imipenem, 500 mg 8 hourly, is suitable, because of its spectrum and penetration into pancreatic tissue.

CT scanning is used to recognise abscess or pseudocyst formation or necrosis (Figure 1). Even if a CT scan is not required for diagnostic purposes, it should be performed 3–10 days after the start of a severe attack. If signs of necrosis are seen, a fine needle aspirate of the pancreatic fluid is indicated to identify whether the tissue is infected or not. Sterile necrosis should be managed conservatively but, if there is infection, open necrosectomy is indicated. Repeat CT scanning is recommended every 1–2 weeks.

Figure 1: CT scans of the pancreas

Acute respiratory distress syndrome and multiple organ failure are common sequelae of severe pancreatitis and require supportive care. Specifically, hypocalcaemia may result, owing to hypoalbuminaemia, abnormal parathyroid activity or formation of intraperitoneal soaps with released free fatty acids.

Other metabolic complications include hyperlipidaemia and hyperglycaemia.

Prognosis and further management

80% of cases are mild attacks that settle in a few days with conservative management. Mortality in such cases is less than 2%. In severe cases, mortality is about 10% overall; 20% where there is necrosis and over 50% with infected necrosis. Data from the Intensive Care National Audit and Research Council case-mix programme indicate a hospital mortality of 44% for patients with pancreatitis admitted to the ICU.

Although the spectrum of severity is similar with different aetiology, there may be a difference in outcome. If pancreatitis is associated with alcohol, there is often evidence of chronic fibrosis and inflammation, but with acute biliary pancreatitis the gland usually returns to histological normality. Gallstone pancreatitis is likely to recur if the stones are not treated, and it is recommended that cholecystectomy and clearance of the common bile duct is performed within 4 weeks of the attack.

FURTHER READING

[i] Baron TH, Morgan DE.
Current concepts: acute necrotizing pancreatitis. N Engl J Med 1999; 340(18): 1412–17
[ii] Dervenis C, Johnson CD, Bassi C et al.
Diagnosis, objective assessment of severity and management of acute pancreatitis. (Santorini Consensus Conference).
Int J Pancreatol 1999; 25(3): 195–210
[iii] United Kingdom Guidelines for the Management of Acute Pancreatitis.
Gut 1997; 42 (suppl): 1–13.a

Tony Pickworth is Consultant in Anaesthesia and Intensive Care Medicine at the Great Western Hospital, Swindon, UK. He qualified from Emmanuel College, Cambridge, and Merton College, Oxford, and trained in anaesthesia in Stoke-on-Trent and East Anglia. He is an examiner in physiology for the MRCS (London). His particular interests are ventilation strategies and sedation for intensive care.

© 2003 The Medicine Publishing Company Ltd


ArticleDate:20050902
SiteSection: Article
 
   
    
                                            
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