Management of acute pancreatitis is supportive at its core: no drug reverses the injury once it has begun, so care is directed at the hypovolaemia and inflammation of the early phase, at the complications that follow, and at the cause that would otherwise trigger another attack. Patients with organ failure or the systemic inflammatory response syndrome are admitted to a monitored or intensive-care bed, because the outcome is better when they are watched closely from the start.
Fluid resuscitation
Acute pancreatitis causes marked endothelial injury and increased vascular permeability, so fluid shifts into the interstitium and peritoneum and the patient becomes hypovolaemic on top of losses from vomiting and reduced intake. Early intravenous fluid is given to reverse that hypoperfusion and prevent pancreatic necrosis, and it is most effective in the first 24 hours. The recommended approach is moderately aggressive rather than maximal resuscitation: isotonic crystalloid at around 1.5 mL/kg per hour if there is no evidence of hypovolaemia, with a 10 mL/kg bolus added if there is. Lactated Ringer solution is preferred to normal saline, because it has been associated with less systemic inflammation and better outcomes in the randomised trials that compared it with saline. Fluid needs are reassessed within 6 hours of presentation and again over the next 24–48 hours, with the goal of lowering the blood urea nitrogen and preventing a rise in haematocrit; most patients need about 3–4 L over the first 24 hours, and once severe disease is established or after 24 hours, aggressive fluid beyond that is more likely to harm than help. Older patients and those with cardiac or renal disease need particular caution, since volume overload, pulmonary oedema and abdominal compartment syndrome are the risks of over-resuscitation.
Nutrition
The old practice of keeping patients nil by mouth until pain and enzymes settle has been abandoned. In mild acute pancreatitis, oral feeding is started early, within 24–48 hours as tolerated, and a low-fat solid diet is used rather than a stepwise progression from clear liquids to solids; waiting for the enzymes to normalise is not necessary. Feeding maintains the gut mucosal barrier and reduces bacterial translocation into inflamed or necrotic pancreatic tissue. In moderately severe and severe disease, enteral nutrition prevents infectious complications. A nasogastric tube is preferred over a nasojejunal one because it is easier to place and equally safe and effective. Parenteral nutrition is avoided unless the enteral route is impossible, not tolerated or not meeting caloric needs.
Antibiotics
Antibiotics are not given prophylactically, because trials have not shown a benefit in sterile necrosis and their use selects for resistance. They are reserved for proven or strongly suspected infection. When infection of pancreatic necrosis is suspected, antibiotics that penetrate necrotic tissue are used, and they can delay or even replace drainage: in stable patients, antibiotic treatment is continued for about 4 weeks to let the collection organise before any intervention. Fine-needle aspiration of necrosis is not required to make the decision in most patients.
ERCP and the biliary tree
Most gallstones pass into the duodenum on their own, so not every patient with biliary pancreatitis needs ERCP. Urgent ERCP within the first 24 hours is indicated for cholangitis, and for progressive cholestasis (a rising bilirubin) in severe or moderately severe disease; without cholangitis or jaundice, medical therapy is preferred to early ERCP. If a common bile duct stone is suspected without these features, MRCP or EUS is used to confirm it before any ERCP, and purely diagnostic ERCP is avoided. When ERCP is performed, rectal indomethacin and a pancreatic duct stent are used in patients at high risk of post-ERCP pancreatitis.
Cholecystectomy
In mild gallstone pancreatitis, the gallbladder is removed early, preferably before discharge, because waiting carries a substantial risk of a recurrent biliary event. Patients with necrotising disease are an exception: surgery is deferred and timed around the management of the necrosis.
Necrosis
Intervention for pancreatic necrosis is delayed, if the patient is stable, for about 4 weeks, to allow the collection to wall off and liquefy. When intervention is needed, minimally invasive methods — endoscopic, radiologic or laparoscopic — are preferred to open surgery, and a step-up approach, beginning with drainage and moving to necrosectomy only if needed, reduces complications. Many patients with sterile necrosis, and some with infected necrosis, improve without any intervention at all.
Preventing recurrence
A first attack is followed by another in roughly 20–29% of patients, so finding and treating the cause is part of management. Gallstone disease is treated by cholecystectomy. Alcohol-associated disease requires abstinence and support for stopping. Hypertriglyceridaemia is treated by diet, control of diabetes and lipid-lowering drugs. Idiopathic episodes, especially recurrent ones, are investigated further, and a cause such as occult sludge or microlithiasis is treated when found.