Acute Pancreatitis

In the western world gallstones and alcohol account for the vast majority of cases. Other causes include hyperlipidaemia, hypercalcaemia, medications, trauma, viral infection and ERCP. The severity of the pancreatitis may range from mild and self-limiting to extremely severe with extensive pancreatic and peripancreatic necrosis as well as haemorrhage. In its most severe form the mortality rises to between 40-50%. Pathogenesis Mechanisms by which pancreatic necrosis occurs remain speculative. Any theory must take into account how a very diverse group of aetiological factors can produce the same end point. There is some suggestion that the final common pathway is a marked elevation of intracellular calcium which in turn leads to activation of intracellular proteases. It is these activated enzymes which are responsible for cellular necrosis. In the case of gallstone-related pancreatitis it is believed stones occlude the pancreatic drainage at the level of the ampulla leading to pancreatic ductular hypertension. Such ductular hypertension has been shown in animal models to increase cytosolic free ionized calcium. There is also evidence that alcohol interferes with calcium homeostasis in pancreatic acinar cells.

Clinical features Acute pancreatitis is a differential diagnosis in any patient with upper abdominal pain. The pain usually begins in the epigastrium accompanied by nausea and vomiting. As inflammation spreads throughout the peritoneal cavity the pain becomes more intense. Involvement of the retroperitoneum frequently leads to back pain. The patient may give a history of previous similar episodes or be known to have gallstones. An attack may follow an alcoholic binge. However, in many cases there are no obvious aetiological factors. severity Initial assessment: clinical + amylase/ lipase + organ failure + APACH II 24-48 hours: Glasgow score and CRP 72 hours: CT or MRI. Complete extent of pancreatic and peripancreatic necrosis may only be clear after 72 hr after the onset.

Treatment The initial management of acute pancreatitis is similar, whatever the cause. A multiple factor scoring system (ideally APACHE II with a modification for obesity) should be carried out at the end of the first 24 hours after presentation to allow identification of the 25% of patients with a predicted severe attack. This should be repeated at 48 hours to identify a further subgroup who appear to be moving into the severe category. These patients should then be managed on a high-dependency or intensive care unit. Even patients outside of the severe category may require considerable supportive care. Early fluid losses in acute pancreatitis may be large, requiring well-maintained intravenous access as well as a central line and urinary catheter to monitor circulating volume and renal function. Nasogastric suction prevents abdominal distension and vomitus and hence the risk of aspiration pneumonia. Baseline arterial blood gases determine the need for continuous oxygen administration. Prophylactic antibiotics. Broad-spectrum antibiotics, e.g. cefuroxime or aztreonam, reduce the risk of infective complications and are given from the outset. 20 % develop extra-pancreatic infection. Use of routine prophylactic antibiotic is not recommended. Analgesia requirements. Pethidine and tramadol are the drugs of choice, usually administered by a patient control system. The morphine derivatives should be avoided because they can cause sphincter of Oddi contraction. Feeding. In patients with a severe episode there is little likelihood of oral nutrition for a number of weeks. Total parenteral nutrition has been associated with a high risk of infection and has been replaced by enteral nutrition. This is administered via a nasojejunal tube, which is well tolerated and can maintain adequate nutritional input. The nasojejunal position of the feeding tube placed endoscopically overcomes the frequent problem of gastric paresis and there is less likelihood of pancreatic stimulation. In a small proportion of patients, multiorgan failure will develop in the first few days after presentation reflecting the extent of pancreatic necrosis. Such patients will require positive-pressure ventilation and often renal support. The mortality in this group is extremely high (in excess of 80%). Gallstone-related pancreatitis In patients with gallstone-related pancreatitis and associated cholangitis, endoscopic intervention with sphincterotomy and stone extraction is of proven benefit and is the treatment of choice. In the absence of cholangitis, sphincterotomy and stone extraction is only of proven benefit when the episode of pancreatitis is predicted as severe. In less severe cases of gallstone-related pancreatitis intervention can be deferred until full recovery is obtained (an approximate 6-week period).