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Vincenzo Fodale, Researcher Professor of Anesthesia and Intensive Care Policlinico Universitario. Via C. Valeria, 98125 Messina, Italy,, Caterina Pratico' and Letterio B. Santamaria
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Marik and Zaloga (1) reported that in patients with acute pancreatitis total parenteral nutrition, as compared to enteral nutrition, significantly increases the risk of infective complications, the likelihood of a surgical intervention and the length of hospital stay (1). Moreover, the detrimental effects of total parenteral nutrition were also associated with a trend towards increased complications, as well as adult respiratory distress syndrome, multi-organ failure, acute pseudocysts, and pancreatic fistula (1). Nevertheless, an important complication of total parenteral nutrition appears to be omitted. Parenteral nutrition, per se, has been related to the occurrence of critical illness polyneuropathy (2). Moreover, several cases of a polyneuropathy associated with pancreatitis are reported (3), and some patients with necrotizing pancreatitis may develop persistent polyneuropathy restricting daily life in survivors (4). In addition, infection and sepsis, complications related by Marik and Zaloga (1) to pancreatitis, may trigger peripheral neuropathy (5). These data, taken together, widely suggested that patients with acute pancreatitis who underwent total parenteral nutrition are at increased risk of critical illness polyneuropathy. As a consequence, enteral nutrition should be the preferred route of nutritional support in patients with acute pancreatitis not only since infection is the most severe complication of parenteral nutrition in acute pancreatitis, as suggested by Marik and colleagues (1), but because the critical illness polyneuropathy could be the true spectrum for these patients. This aspect should be emphasized. References: 1. Marik PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 2004;328: 1407. 2. Bolton CF, Young GB. Critical illness polyneuropathy due to parenteral nutrition. Intensive Care Med 1997;23: 924-5. 3. Gross ML, Fowler CJ, Ho R, Russell RC, Harrison MJ. Peripheral neuropathy complicating pancreatitis and major pancreatic surgery. J Neurol Neurosurg Psychiatry 1988;51: 1341-4. 4. Bosscha K, Reijnders K, Jacobs MH, Post MW, Algra A, van der Werken C. Quality of life after severe bacterial peritonitis and infected necrotizing pancreatitis treated with open management of the abdomen and planned re-operations. Crit Care Med 2001;29: 1539-43. 5. Wijdicks EF, Litchy WJ, Harrison BA, Gracey DR. The clinical spectrum of critical illness polyneuropathy. Mayo Clin Proc 1994;69: 955- 9. Competing interests: None declared |
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David JW Knight, SpR Anaesthetics and Critical Care Queens Medical Centre, Nottingham, NG7 2UH
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Editor, Marik et al [1] are to be congratulated on their meta- analysis of feeding in acute pancreatitis. Their results may not hold true for the subgroup of patients with the most severe forms of pancreatitis in whom gastrointestinal function is the most severely limited. Many of these patients have sub-clinical small bowel ischaemia and feeding directly into the small bowel can lead to non-occlusive bowel necrosis, which cannot be detected early [2]. The addition of glutamine to parenteral feeds may also redress some of the negative impact of using this route. Parenteral glutamine may restore impared immune function, particularly T cell-mediated acquired immunity and this has been shown to reduce late infection rates and subsequent multiorgan failure in ICU [3]. Finally it is interesting to note that one of the papers used in the meta-analysis comes from a group that have previously demonstrated a significant reduction in rates of pancreatitis related sepsis with the addition of the probiotic Lactobacillus plantarum 299 [4]. It may be that routine admission of probiotics to enteral feed will have significant impact on infection rates and mortality in pancreatitis. 1.Marik PE, Zaloga GP.Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 2004;328:1407- 1409. 2.Marvin RG, McKinley Ba, et al. Nonocclusive bowel necrosis occuring in critically ill trauma patients receiving enteral nutrition manifests not rliable clinical signs for early detection. Am J Surg 2000; 179:7-12. 3.Griffiths RD, Allenn KD, et al. Infection, multi organ failure and survival in the intensive care unit: influence of glutamine-supplemented parenteral nutrition on acquired infection. Nutrition 2002; 18:546-552. 4. Olah A. Effect of lactobacillus on pancreatitis related sepsis. Nutrition 2002; 18: 259-62 Competing interests: None declared |
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Richard G Fiddian-Green, None None
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I am very concerned that studies of this nature serve only to detract from the real issues and might be used to support an evidence base for clinical pathways of dubious value whose adoption might even be enforced by legal means in this political climate. The real issue in the management of this difficult disease is very much earlier detection of potentially fatal disease and the adoption of much more aggressive means for dealing with it a timely and definitive manner without killing the patient. If this were done the need for enteral or parenteral feeding should be eliminated, enteral feeding being a highly dubious and potentially fatal practice in my book. The problem is that management is invariably delegated too late in the course of the disease to those unable to perform pancreatic and salvage surgery for acute intra- abdominal catastrophes without an unacceptably high complication and fatality rate. This is another meta-analysis that needs to be thrown into the trash can. I feel much the same way about enteral feeding in all other conditions there being very few occasions in my bbok in which it is not simply a marker of inferior practices. Competing interests: None declared |
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Alvaro Sanabria, General Surgeon Professor Department of Surgery Pontificia Universidad Javeriana-Hospital San Ignacio Bogota, Colombia
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Bogota, julio 13 de 2004 Sir Editor British Medical Journal Sir: Some comments are pertinent to the article by Marik and Zaloga (1). The authors define severe pancreatitis as that corresponding to an APACHE II score higher than 10. However, international consensus state that severe pancreatitis is defined as that with an APACHE II score higher than 8. So, the definition used in the study could introduce bias in the analysis of results. Studies included in this meta-analysis are different from those reported by Al-Omram (2) in a previous Cochrane Review, but there is not obvious reason to explain this difference. Although Jadad scale is accepted as a good method to evaluate methodological quality of primary RCT, its performance in surgical studies is far from ideal. As stated by the authors, blind evaluation of the results in this kind of studies is almost impossible, although this do not compromise the validity of conclusions, as the scale score can suggest. Furthermore, except Kalfarentzos (3) , the other selected studies include patients of low severity, in whom the timing to return to oral feeding and the number of infections and other complications are negligible, so enteral nutrition is not a therapeutic option. However, as severity is an important prognostic factor, it is very likely that the effects of enteral nutrition in patients with severe disease could be even considerably greater than those reported in this study, a clear example of a bias that acts in favour of the outcome. Sincerely Alvaro Sanabria 1.Marik P, Zaloga G. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 2004; 328:1407 -0 2.Al-Omran M, Groof A, Wilke D. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev. 2003;(1):CD002837 3. Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos CA. Enteral nutrition is superior to parenteral nutrition in severe acute pancreatitis: results of a randomized prospective trial. Br J Surg. 1997 Dec;84(12):1665-9. Competing interests: None declared |
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