Core Topics in General & Emergency Surgery: Companion to Specialist Surgical Practice (39 page)
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Authors: Simon Paterson-Brown MBBS MPhil MS FRCS
Acute pancreatitis is defined as an acute inflammatory process of the pancreas, with variable involvement of other regional or remote organ systems.
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It is a common acute illness, with epidemiological data from the Health Service Statistics Division in Scotland reporting an annual incidence of 318 cases per million (365 cases per million in men, 275 cases per million for women).
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Analysis of patterns of incidence in this particular population (which has remained relatively constant over the past decade) suggests an increase in the incidence of acute pancreatitis, particularly in those over 40 years of age. Similar increases in the incidence of acute pancreatitis have also been observed in Germany, Finland and Denmark. The factors giving rise to the observed increased incidences are not clear; however, at least in Finland, the increase in the incidence of acute pancreatitis is strongly correlated with an increase in alcohol consumption.
In practical terms the management of acute pancreatitis can be divided into two broad phases. The first phase includes the establishment of diagnosis, severity stratification, initial resuscitation and the choice of appropriate disease-specific initial therapy. The second phase relates to those with severe disease who will usually require further intervention for intra-abdominal complications or support for ongoing multiple organ failure. Guidelines
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–
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suggest that patients with complications arising from severe acute pancreatitis are most appropriately managed in a unit with specialist expertise and therefore this chapter only focuses on the initial phase of management.
Within this chapter the terminology used to describe patients with acute pancreatitis is in keeping with definitions agreed by the 1992 Atlanta consensus conference (
Box 8.1
).
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The Atlanta classification attempted to introduce uniformity in the description of clinical severity and the various complications of the disease; however, with increasing understanding of the pathophysiology of pancreatitis, improved imaging techniques and newer therapeutic strategies, steps are being taken to revise the classification of acute pancreatitis. Alternative classfication techniques have already been proposed
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but still suffer from significant limitations as prognostic or predictive tools. A revision of the Atlanta criteria and management guidelines is anticipated.
Box 8.1
Terminology relating to acute pancreatitis as defined by the Atlanta consensus conference
Mild acute pancreatitis
Minimal organ dysfunction and an uneventful recovery
Severe acute pancreatitis
Associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst
Acute fluid collections
Occur early in the course of acute pancreatitis, are situated in or near the pancreas, and always lack a wall of granulation or fibrous tissue
Pancreatic necrosis
Diffuse or focal areas of non-viable pancreatic parenchyma, typically associated with peripancreatic fat necrosis
Acute pseudocysts
Collection of pancreatic juice surrounded by a wall of fibrous or granulation tissue
Pancreatic abscess
Circumscribed intra-abdominal collection of pus arising in close proximity to the pancreas, but containing little or no pancreatic necrosis, which arises as a consequence of acute pancreatitis
Acute pancreatitis may be caused by a wide variety of aetiological agents (
Box 8.2
), although the majority of cases are due to either gallstones or alcohol excess. Recent epidemiological studies have demonstrated that alcohol excess is an increasingly frequent cause of acute pancreatitis. The prevalence of idiopathic acute pancreatitis varies between reported series and is probably a function of the degree of investigation undertaken to identify a cause. Recent UK guidelines state that no more than 20% of patients should be labelled as having idiopathic acute pancreatitis.
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Box 8.2
Aetiological agents in acute pancreatitis
Common
Gallstones
Alcohol
Uncommon
Trauma
Endoscopic retrograde cholangiopancreatography
Sphincterotomy
Biliary manometry
Pancreatic duct obstruction
Ampulla of Vater neoplasia
Drugs
Azathioprine
Metabolic
Hypercalcaemia
Hyperlipidaemia
Infection
Mumps
Coxsackie B
HIV
Vascular
Vasculitis
Cardiopulmonary bypass
Hereditary pancreatitis
The mechanisms through which each aetiological agent causes pancreatic acinar cell injury are not clear. However, after the initial pancreatic insult, it is believed that regardless of the aetiological agent the pathogenetic mechanisms of disease progression in acute pancreatitis are similar. Following pancreatic acinar cell injury, local pancreatic inflammation occurs. Although the inflammatory process may remain confined to the pancreas and peripancreatic tissues, a systemic inflammatory response may be triggered. This systemic inflammatory response is characterised by the systemic activation of leucocytes and endothelial cells and the secretion of proinflammatory cytokines, and is responsible for the development of the organ dysfunction that characterises severe acute pancreatitis. It is not clear why some patients develop severe acute pancreatitis whilst others with similar aetiological agents develop mild acute pancreatitis; however, there is evidence to implicate both excessive proinflammatory mediators and decreased anti-inflammatory mechanisms.
Presenting symptoms may range from mild discomfort to overwhelming abdominal pain. Typically, patients present with increasing epigastric/central abdominal pain radiating through to the back. This pain may be eased by sitting forward. Nausea is a predominant early symptom, with associated vomiting or retching. Before presenting with gallstone-induced acute pancreatitis, patients may have had symptoms consistent with biliary colic. Likewise, in alcohol-induced acute pancreatitis, patients will often have a long history of alcohol ingestion and/or recent binge drinking.
Signs of cardiovascular and respiratory dysfunction may be present. Examination may reveal abdominal signs ranging from localised epigastric tenderness to generalised peritonitis. More specific signs of severe acute pancreatitis include periumbilical bruising (Cullen's sign) and flank bruising (Grey Turner's sign;
Fig. 8.9
).
Figure 8.9
Grey Turner's sign in severe acute pancreatitis.
Reproduced from Powell JJ, Parks RW. Diagnosis and early management of acute pancreatitis. Hosp Med 2003; 64:150–5. With permission from the BJHM.
Chapter 5
)
Traditionally, the diagnosis of acute pancreatitis has depended on the detection of a serum amylase concentration more than three times the upper limit of normal. However, hyperamylasaemia may occur in several other conditions (
Box 8.3
), and a serum amylase concentration above the ‘diagnostic’ threshold does not definitely indicate acute pancreatitis. Conversely, acute pancreatitis may exist with serum amylase concentrations below this threshold. In those patients with a prolonged history prior to admission to hospital, serum amylase concentrations may have normalised. Amylase measurement therefore needs to be timely. Serum amylase levels do not provide prognostic information, nor can they be followed in order to monitor the early disease process. However, very high levels of serum amylase on admission are often suggestive of a gallstone aetiology.
Box 8.3
Main differential diagnoses of hyperamylasaemia
Acute pancreatitis
Pancreatic pseudocyst
Mesenteric infarction
Perforated viscus
Acute cholecystitis
Diabetic ketoacidosis
Because of the limitations of the serum amylase test, other markers have been used to diagnose acute pancreatitis. Serum lipase is perhaps the most common and is more sensitive and specific than serum amylase. Moreover, because of its longer half-life, serum lipase is more accurate if there has been a delay in obtaining the initial sample.
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However, as with serum amylase, serum lipase concentrations do not correlate with disease severity. In contrast, newer markers such as urinary trypsinogen activation peptide and serum carboxypeptide B activation peptide provide both diagnostic and prognostic information, although these are not assayed routinely in most units.
Although the vast majority of cases of acute pancreatitis can be diagnosed either clinically or biochemically, contrast-enhanced CT may be required in equivocal cases (
Fig. 8.10
).
Figure 8.10
(a)
Contrast-enhanced CT image of severe acute pancreatitis demonstrating extensive necrosis with gas.
(b)
A radiologically guided drain has been placed.
(c)
Minimally invasive necrosectomy was performed to remove solid debris.
Finally, in a few patients, laparotomy may be required to confirm the diagnosis of acute pancreatitis while refuting other potential diagnoses such as acute mesenteric ischaemia or a perforated peptic ulcer. The decision to undertake diagnostic laparotomy should not be made lightly as there is evidence that early operation has an adverse effect on outcome in acute pancreatitis.
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In contrast, patients with acute intestinal ischaemia may present with abdominal pain and hyperamylasaemia and diagnostic delay may be critical. If the pancreas appears normal on CT, and in the absence of a firm diagnosis, laparoscopy or laparotomy should be considered if there are ongoing signs of peritonitis. Clearly, access to CT on a 24-hour basis is a prerequisite for this strategy.
