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Acute pancreatitis is a dynamic, often progressive disease; 14-20% require intensive care in its severe form due to multiorgan dysfunction and/or failure. This review was created using systematic literature review of articles published on this subject in the last 5 years. The outcome of severe acute pancreatitis is determined by the inflammatory response and multiorgan dysfunction - the prognostic scores (Acute Physiology and Chronic Health Evaluation, Glasgow Prognostic Index, Sepsis-related Organ Failure Assessment, Multi Organ Dysfunction Syndrome Scale, Ranson Scale) can be used to determine outcome. Clinical signs (age, coexisting diseases, confusion, obesity) and biochemistry values (serum amylase, lipase, C-reactive protein, procalcitonin, creatinine, urea, calcium) have important prognostic roles as well. Early organ failure increases the risk of late abdominal complications and mortality. Intensive care can provide appropriate multi-function patient monitoring which helps in early recognition of complications and appropriate target-controlled treatment. Treatment of severe acute pancreatitis aims at reducing systemic inflammatory response and multiorgan dysfunction and, on the other side, at increasing the anti-inflammatory response. Oral starvation for 24-48 hours is effective in reducing the exocrine activity of the pancreas; the efficacy of protease inhibitors is questionable. Early intravascular volume resuscitation and stable haemodynamics improve microcirculation. Early oxygen therapy and mechanical ventilation provide adequate oxygenation. Electrolyte and acid-base control can be as important as tight glucose control. Adequate pain relief can be achieved by thoracic epidural catheterization. Early enteral nutrition with immunonutrition should be used. There is evidence that affecting the coagulation cascade by activated protein C can play a role in reducing the inflammatory response. The complex therapy of acute pancreatitis includes appropriate antibiotics, thrombo-embolic prophylaxis and in certain cases plasmapheresis and/or haemofiltration. Reducing intraabdominal pressure may be necessary in the acute phase. Intensive care multidisciplinary teamwork can reduce the mortality of severe acute pancreatitis from 30% to 10%.

Has early jejunal glutamine-rich diet any advantage in the treatment of patients suffering from acute pancreatitis and after oesophagectomy? Eleven patients suffering from necrotizing pancreatitis and 23 patients operated on radically for esophageal cancer were fed intra jejunally with glutamine-rich Stresson Multi Fibre diet. Eight patients with necrotising pancreatitis and 13 oesophagectomy patients were fed with glutamine-poor Nutrition Multi Fibre. Nutritional status, serum proteins, acute phase proteins, immune-globulins, complement components (C3, C4), the ratio of subsets of peripheral lymphocytes were analysed on the 1st, 2nd, 4th and 10th days. Serum protein parameters were measured by laser nephelometry. CD cell surface antigen expression was measured with flow cytofluorometry, activity of phagocytes with whole blood chemiluminescences. Laboratory parameters showed an improvement during the 10-day-treatment in both diet types, but significant improvement could be measured only in patients with necrotizing pancreatitis and fed with Stresson Multi Fibre: IgG (p < 0.05), serum protein (p < 0.02), prealbumin (p < 0.05), retinol binding protein (p < 0.03). The different diets did not cause difference in the laboratory results of the oesophagectomy patients. Early immune-enhancing diet improved serum proteins, acute phase proteins and immunoglobulins significantly in necrotizing pancreatitis. The length of hospital stay also decreased.

Procalcitonin test (PCT) has been proposed to check severity of generalized infections or sepsis. The authors measured the PCT values with PCT-Q quick test (BRAHMS DIAGNOSTICA GmbH, Berlin) at 14 surgical patients treated in their intensive care unit (7 sepsis, 4 peritonitis, 2 localized pancreatic abscess, 1 postoperative fever). At 3 septic patients (2 pancreatitis, 1 intestinal necrosis) they measured the PCT levels repeatedly during treatment. In 2 patients with localized pancreatic abscess and in 1 patient with postoperative fever without evidence of infection the PCT levels were low (< 0.5 ng/ml). At 4 patients with peritonitis following gastric or colon perforation the PCT levels were highly elevated (> 10 ng/ml). At 7 patients with severe sepsis the PCT values were high (> 2 ng/ml), except for 1 patient with intestinal necrosis. At this patient the PCT levels were repeatedly low. In 2 septic patients with pancreatitis elevated PCT levels indicated the need for surgery. In most patients PCT was a good indicator of generalized infections. PCT levels measured repeatedly in sepsis were lower than in patients with peritonitis.