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What about monitoring procalcitonin levels?
- David Bihari (23 April 2004)
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Obese Patients with Acute Pancreatitis
- Y. C. Chan (24 April 2004)
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Antibiotics should never be used to prevent infections in pancreatic necrosis.
- Richard G Fiddian-Green (24 April 2004)
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David Bihari, Associate Professor, University of New South Wales Lismore Base Hospital, Lismore, NSW 2480, Australia
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In their discussion of the important issue of antibiotic prophylaxis in acute pancreatitis, I was surprised that O'Reilly and Kingsnorth made no mention in their editorial of monitoring the plasma procalcitonin level. There is now a considerable literature establishing the value of procalcitonin monitoring in acute pancreatitis (1,2,3,4) and it is our practice to use the APACHE II score and the level of this inflammatory marker to guide the requirement for early antibiotic prophylaxis with a carbipenem AND fluconazole. Indeed, a recent study has suggested that the plasma concentration of procalcitonin may reflect the derangement in gut barrier function (rather than the extent of systemic inflammation) and may hence predict those patients in whom the translocation of bacteria and fungi into dead pancreas is more likely (5). I agree with the authors that we do not want to give all patients with acute pancreatitis antibiotic prophylaxis. But I have experience of fatal acute pancreatitis from untreated gram negative sepsis because of too "purist" an approach. The issue in my mind is how to identify the patients at risk early on and then include both bacterial and fungal prophylaxis. 1.Rau B, Steinbach G, Gansauge F, Mayer JM, Grunert A and Beger HG. The potential role of procalcitonin and interleukin 8 in the prediction of infected necrosis in acute pancreatitis. Gut 1997; 41: 832-840 2.Mandi Y, Farkas G, Takacs T, Boda K and Lonovics J. Diagnostic relevance of procalcitonin, IL-6, and sICAM-1 in the prediction of infected necrosis in acute pancreatitis. Int J Pancreatol 2000; 28: 41-49 3.Kylanpaa-Back M-L, Takala A, Kemppainen EA, Puolakkainen PA, Leppaniemi AK, Karonen S-L, Orpana A, Haapiainen RK and Repo H. Procalcitonin, soluble interleukin-2 receptor and soluble E-selectin in predicting the severity of acute pancreatitis. Crit Care Med 2001; 29: 63- 69 4.Ammori BJ, Becker KL, Kite P, Snider RH, Nylen ES, White JC, Larvin M and McMahon MJ. Calcitonin precursors in the prediction of severity of acute pancreatitis on the day of admission. British Journal of Surgery 2003; 90: 197-204 5.Ammori BJ, Becker KL, Kite P, Snider RH, Nylen ES, White JC, Barclay GR, Larvin M and McMahon MJ. Calcitonin precursors: eraly markers of gut barrier dysfunction in patients with acute pancreatitis. Pancreas 2003: 27: 239-243 Competing interests: None declared |
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Y. C. Chan, SpR in Vascular & General Surgery Department of Surgery, University Hospital Lewisham, Lewisham High Street, London SE13 6LH.
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Acute pancreatitis often presents as a benign condition with minimal abdominal pain and hyperamylasemia, and may progress rapidly to a fulminant course, resulting in life-threatening systemic multi-organ failure. In the UK, due to shortage of intensive care unit/high dependency facilities in most hospitals, patients with moderate and severe acute pancreatitis are often mismanaged, with inadequate monitoring and with definitively treatment commenced too late. Guidelines have long been published regarding the management of acute pancreatitis, first by the British Society of Gastroenterology, with emphasis on the importance of expertise in hepato-pancreatobiliary surgery, availability of intensive care unit/high dependency unit and dynamic CT scanning (1); and in 2002, the International Association of Pancreatology also provided the most comprehensive evidenced-based guidelines on the management of acute pancreatitis (2). Norton et al. have highlighted that although acceptable mortality can be achieved for acute pancreatitis despite failure to implement British Society of Gastroenterology guidelines, inadequate investigation and treatment of gallstone disease often leads to an unacceptable incidence of recurrent acute pancreatitis (3). Many clinicians fail to appreciate that obesity (defined as BMI in excess of 30 kg/m2) is an independent prognostic factor favouring the development of systemic and local complications of acute pancreatitis (4). Not only should it be used routinely as part of the initial assessment of the severity of a case of acute pancreatitis, but combination of the APACHE-II and obesity scores by simple addition has been shown to be invaluable in predicting outcome in patients with acute pancreatitis (5). Obese patients with acute pancreatitis should be monitored closely, thus preventing development of complications. References: 1. Tunnemann J, Easterbrook JR, Firth J, Wedgwood KR. Management of acute pancreatitis: a comparative audit of clinical practice against the recommendations of the british society of gastroenterology. Br J Surg. 2000 Mar; 87(3): 362-373. 2. Uhl W, Warshaw A, Imrie C, Bassi C, McKay CJ, Lankisch PG, Carter R, Di Magno E, Banks PA, Whitcomb DC, Dervenis C, Ulrich CD, Satake K, Ghaneh P, Hartwig W, Werner J, McEntee G, Neoptolemos JP, Buchler MW; International Association of Pancreatology. IAP Guidelines for the Surgical Management of Acute Pancreatitis. Pancreatology. 2002; 2(6):565-573. 3. Norton SA, Cheruvu CV, Collins J, Dix FP, Eyre-Brook IA. An assessment of clinical guidelines for the management of acute pancreatitis. Ann R Coll Surg Engl. 2001 Nov; 83(6):399-405. 4. Martinez J, Sanchez-Paya J, Palazon JM, Suazo-Barahona J, Robles- Diaz G, Perez-Mateo M. Is obesity a risk factor in acute pancreatitis? A meta-analysis. Pancreatology. 2004; 4(1): 42-48. 5. Johnson CD, Toh SK, Campbell MJ. Combination of APACHE-II score and an obesity score (APACHE-O) for the prediction of severe acute pancreatitis. Pancreatology. 2004; 4(1): 1-6 Competing interests: None declared |
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Richard G Fiddian-Green, None None
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Acute pancreatitis can be a very difficult disease to treat effectively. There is, however, much room for improvement. Giving antibiotics to prevent secondary infection in patients with pancreatic necrosis (1) violates an established surgical principle, necrotic tissue is best treated by early and complete excision. Empiric antibiotic therapy for pancreatic necrosis cannot be expected to have a major effect upon outome. Judging from the wide range in operative mortality reported for an elective pancraticoduodenectomy and the unacceptably high mortality in many centers in the NHS unfamiliarity with and fear of pancreatic surgery may be the most important reason for the evolution of this marginally effective medical treatment. Giving prophylactic antibiotics might be best reserved for preventing infections in patients having definitive invasive procedures and the duration of administration limited to the day of the invasive treatment or possibly a few days longer. Several factors contribute to the high morbidity and mortality in acute pancreatitis. All with the possible exception of the pseudocysts are "surgical conditons". They include haemorrhage (2), pancreatic duct rupture with or without pseudocyst formation (3,4) and the development of a pancreatic abscess from secondary infection, an obstructed biliary or pancreatic duct, and a pancreatic abscess. Of these a honeycomb abscess which developed in the distal pancreas in a patient with a midbody pancreatic stricture and dilatation of the distal duct proved to be the most difficult to detect preoperatively in my experience. This occult cause of septic shock, which was not accompanied by any CT evidence of parenchymal disease or necrosis, might be much more common but missed because of the ease with which it can be overlooked. In our patient the diagnosis was established unequivocally with an indium-labeled white cell scan. Resectional therapy was curative. The timing of definitive surgical intervention is critical (5). The sooner definitive treatment is done the better (6) provided that the antecedent presence of shock is first eliminated for its presence has an adverse effect upon outcome (7). This might be best accomplished by fluids, antibiotics and/or percutaneous or endoscopic drainage. Whilst conservative therapy of pseudocysts is the rule in the UK and is considered definitive therapy (8) these means are neither definitive nor certain to produce a favourable outcome. In many cases they may be unncessary and in other cases they may serve only to introduce infection or cause haemorrhage. When percutaneous intervenion traverses bowel, and especially colon, the ability to lavage the gut clean in preparation for surgery and definitive surgical intervention may be compromised. These procedutes are, therefore, to be strongly condemned unless performed in the course of preparing a patient for surgery. Definitive surgical intervention following definition of duct anatomy is clearly the preferred option for dealing with pseudocysts provided it is done as it should be, without morbidity or mortality. Sewing "moon beams to flatus" in constructing a cyst enterostomy is asking for trouble especially if constucted through the a vascular mesentery or if a distal obstruction has caused duct rupture and a pseudocyst. It is most tempting to treat pseudocysts in the head by conservative means. Upon reflection of my experience I believe these might be far better treated with a pancreaticoduodenectomy especially as they may give rise to recurrent and chronic problems with persistent pain. I imagine that total pancreatectomy would be universally condemned as a therapeutic option in the UK but this opinion would reflect a strong bias towards conservatism. Animals and patients who have a total pancreatectomy for haemorrhagic pancreatitis do well provided they survive their operations (9,10). In most cases distal pancreatectomy and splenectomy, which makes a complete necrosectomy possible and relatively simple especially if preceded by taking down the transverse colon by dissection in the oedematous embryonic planes and accompaning Kocherisation of the duodenum, will suffice. A panceaticoduodenectomy might be a better resectional option for preserving pancreatic function in those cases with stricture in the head and duct rupture just distal to it. One of the cases in the prospective observation study performed under Dr Palizas's direction in Argentina (11)was admitted to his ICU after a total pancreatectomy for haemorrhagic pancreatitits. The patient looked terrible, he told me, and in his opinion was certain to die but to his great surprise his gastric intramucosal pH was normal and remained normal. He had an uneventful post operative course. It is an important case for it illustrates the opportunity for using tonometry as an aid in making timely decisons in the course of the management of the critically ill. Had the pH remained low or fallen in the ICU an aggressive search could have been made for a remediable cause such as a colonic leak or infarction. In summary knowing that the pHi was normal after admission for suspected acute pancreatitis should aid in avoiding unneccessary invasive interventions, deciding if invasive options are desirable, optimising patients in preparation for definitive surgery and following them after sugery. Antibiotic therapy should be used within this management framework and never empirically to prevent infection in necrotic tissue as considered in this study. Conservatism in the management of pancreatitis in the UK is the rule for chronic pancreatitis. Chronic inflammation is, by definition, an acute inflammatory response occurring in conjunction with healing. Pain, a cardinal feature of acute inflammation, will persist so long as the cause of the acute inflammatory reaction persists. In many cases this may be micropseudocyts. Histological examination of resected specimens sugggests that, regardless of its cause or causes, that complete resolution of the acute inflammatory response is unlikely to occur until there is no pancreatic tissue left to become inflammed. Resection removes the inflammatory tissue and with it the pain it causes. If resectional therapy were practiced more often in the UK the standard of pancreatic surgery would rise and with it the opportunities for treating acute pancreatitis and pancreatic neoplasms more effectively. undergoing debridement. 1. Derek A O'Reilly and Andrew N Kingsnorth Management of acute pancreatitis BMJ 2004; 328: 968-969 2. Ammori BJ, Madan M, Alexander DJ. Haemorrhagic complications of pancreatitis: presentation, diagnosis and management. Ann R Coll Surg Engl. 1998 Sep;80(5):316-25. 3. Lau ST, Simchuk EJ, Kozarek RA, Traverso LW. A pancreatic ductal leak should be sought to direct treatment in patients with acute pancreatitis. Am J Surg. 2001 May;181(5):411-5. 4. Gueroult S, Parc Y, Duron F, Paye F, Parc R. Completion pancreatectomy for postoperative peritonitis after pancreaticoduodenectomy: early and late outcome. Arch Surg. 2004 Jan;139(1):16-9. 5. Hartwig W, Maksan SM, Foitzik T, Schmidt J, Herfarth C, Klar E. Reduction in mortality with delayed surgical therapy of severe pancreatitis. J Gastrointest Surg. 2002 May-Jun;6(3):481-7 6. Tzovaras G, Parks RW, Diamond T, Rowlands BJ. Early and long-term results of surgery for severe necrotising pancreatitis. Dig Surg. 2004;21(1):41-7. Epub 2003 Dec 29 7. Poeze M, Takala J, Greve JW, Ramsay G. Pre-operative tonometry is predictive for mortality and morbidity in high-risk surgical patients. Intensive Care Med. 2000 Sep;26(9):1272-81. 8. Cheruvu CV, Clarke MG, Prentice M, Eyre-Brook IA. Conservative treatment as an option in the management of pancreatic pseudocyst. Ann R Coll Surg Engl. 2003 Sep;85(5):313-6. 9. Rodriguez Rilo HL, Ahmad SA, D'Alessio D, Iwanaga Y, Kim J, Choe KA, Moulton JS, Martin J, Pennington LJ, Soldano DA, Biliter J, Martin SP, Ulrich CD, Somogyi L, Welge J, Matthews JB, Lowy AM. Total pancreatectomy and autologous islet cell transplantation as a means to treat severe chronic pancreatitis. J Gastrointest Surg. 2003 Dec;7(8):978-89. 10. Connor S, Ghaneh P, Raraty M, Sutton R, Rosso E, Garvey CJ, Hughes ML, Evans JC, Rowlands P, Neoptolemos JP. Minimally invasive retroperitoneal pancreatic necrosectomy. Dig Surg. 2003;20(4):270-7. Epub 2003 May 15. 11. Doglio GR, Pusajo JF, Egurrola MA, Bonfigli GC, Parra C, Vetere L, Hernandez MS, Fernandez S, Palizas F, Gutierrez G. Gastric mucosal pH as a prognostic index of mortality in critically ill patients. Crit Care Med. 1991 Aug;19(8):1037-40. Competing interests: Patents issued in my name |
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