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See article in J. Gastroenterol. Hepatol. 2005; 20: 1385–1389.

‘Resting the pancreas’ has been a central dogma in the early management of acute pancreatitis. Every patient admitted with acute pancreatitis was made strictly ‘nil by mouth’ and had a naso-gastric tube to empty the stomach. When the patient was deemed to have severe pancreatitis, nutritional support was provided by total parenteral nutrition. Even a decade ago John Ranson reviewed the role of nutritional support in acute pancreatitis and underlined the primacy of parenteral feeding.1 He stated that jejunal feeding was ‘not a therapeutic option early in the course of pancreatitis because of the associated paralytic ileus’. The avoidance of enteral feeding was also supported by the belief that stimulation of pancreatic exocrine secretion would exacerbate the severity of acute pancreatitis.

How things have changed. In the absence of direct clinical evidence to support the concept of pancreatic rest, many patients are now allowed to drink limited clear fluids by mouth as soon as there is resolution of abdominal pain. There is no evidence to show that the naso-gastric tube alters the course of pancreatitis. Randomized trials have now defined best practice as the commencement of enteral nutrition (EN) in all patients with predicted moderate to severe acute pancreatitis and as soon as they are hemodynamically stable.2 A naso-jejunal tube, often placed by the radiologist using fluoroscopic guidance, best delivers EN. Compared with total parental nutrition (TPN), the advantages of EN are safety, ease of administration, cost, and it is associated with lower markers of inflammation and pancreatitis severity. Parenteral nutrition is still sometimes required, but in a secondary role when the full calorie and protein requirements cannot be tolerated by the enteral route. It was no surprise to find that 2 weeks of total parenteral nutrition in patients with acute pancreatitis only managed to preserve body composition, and could only improve total body protein in the absence of sepsis or recent surgery.3

Further changes are on the way. It now appears safe to commence EN immediately on admission, and before the patient has been hemodynamically stabilized.4 And it may not be necessary to deliver EN to the jejunum, in order to avoid gastro-duodenal stimulation of the pancreas. The Glasgow group have shown that providing fine bore naso-gastric feeding within 48 h of admission is safe, well tolerated and practical.5 Are we moving full circle? The next development might be patient controlled intake with ‘ad libitum’ intake from the time of admission, but that is speculation.

What about patients with mild pancreatitis? The focus has been, quite rightly, on the nutritional support of patients with moderate to severe acute pancreatitis. But there remain a number of unanswered questions about the nutritional support in patients with predicted mild disease.

The first question is whether we can determine, with confidence and on admission, which patients do not require EN? A recent study showed that 75% of patients with acute pancreatitis settle with 48 h of bowel rest and intravenous fluids, and could be discharged within 48 h.6 One of the difficulties is that we cannot, with absolute certainty, using current predictors of pancreatitis severity identify at the time of admission the individual patients with this benign and self-remitting course.7 The best prognostic markers increase the likelihood of severe pancreatitis from 20 to 55%, which still leaves many patients in a gray zone. For these patients it is probably best to provide nutritional support early rather than incur significant delays. ‘When in doubt, feed’ appears to be good advice.

This leads on to the second question that is when should patients be encouraged to start eating and drinking if EN is not indicated? The traditional approach, supported by common sense and experience, is to wait until the abdominal pain has subsided and the serum amylase has returned to near normal. This constitutes a ‘trial by re-feeding’ as some of these patients will have a relapse of pancreatitis after the commencement of oral intake.

The next question is whether it is possible to predict which patients will have recurrence of abdominal pain after the introduction of oral feeding? Three studies have sought to answer this question. The first was published in 1997 and was based on 116 patients with mild and severe acute pancreatitis.8 Levy et al. found that a fifth of patients had a relapse of abdominal pain following oral re-feeding and this occurred in half of these patients within 48 h. They showed that the total duration of pain in those without pain relapse was 6 days, and this was significantly different from those that did relapse (11 days, P < 0.002). In this multicenter study the indications for re-feeding were subjective, leaving the individual clinician to decide when to start. This decision was not based on the level of serum amylase or lipase. It was interesting to note in this study that the abdominal pain had settled for a mean of 6 days before oral re-feeding was commenced. And then the low calorie and fat diet was gradually introduced over 5 days. Multidimensional analysis showed that the score from the computed tomography (CT), the duration of pain and the concentration of serum lipase were the factors that were independently associated with an increased risk of pain relapse. Pain relapse increased total hospital stay and hospital stay after the first attempt at oral re-feeding.

The next study to address this question is a small randomized study from India.9 Pandey et al. confirmed that the duration of initial pain and a higher CT severity index were associated with pain relapse.

The Brazilian study by Chebli et al.,10 published in this issue of the Journal, seeks to identify risk factors for pain relapse in only patients with predicted mild pancreatitis. They found that a quarter of the patients did not tolerate the resumption of oral intake even though they had fulfilled the criteria that were the loss of pain, return of bowel sounds, and hunger. Multivariate analysis identified risk factors for the relapse of abdominal pain as a persistent elevation of serum lipase (on the day prior to re-feeding, adjusted odds ratio [OR] 8.2), elevated serum C reactive protein (on day 4 of admission, adjusted OR 7.4) and more extensive peripancreatic fluid collections on CT scanning (on day 3 of admission, adjusted OR 6.2). The patients who developed a relapse were then managed with naso-jejunal EN.

These three studies are consistent. The relapse of pain after oral re-feeding occurs in 20–25% of patients with predicted mild acute pancreatitis. These patients tend to have a longer duration of initial abdominal pain, persistent elevation of serum enzymes and a higher CT severity score. In other words, the patients who fail re-feeding are those with more severe pancreatitis. Current methods used to predict severity cannot reliably identify this subgroup of patients at the severe end of the spectrum of mild pancreatitis. The prediction and prevention of pain relapse is an important goal because of both economic (doubling hospital stay) and clinical (delay to optimal nutritional support) implications. These three studies have pointed the way forward. It should be possible to predict failure of oral re-feeding with close attention to these three identified factors. This concept needs to be tested prospectively.

Other unanswered questions remain. When should re-feeding occur in patients with predicted mild pancreatitis? What should be given with oral re-feeding? Can oral re-feeding contribute to the more rapid resolution of pancreatitis by supplementing with antioxidants or probiotics? Should clear fluids precede food? Should there be a graduated approach? Is a low fat diet best? Are there oral supplements that might decrease pancreatic stimulation? Might long acting somatostatin enable earlier re-feeding in patients with mild pancreatitis? It appears to reduce the risk of pain relapse (from 35% to 4.3%) following oral re-feeding in patients with necrotizing pancreatitis.11 Such questions must guide further research, both clinical and basic.

In the meantime, what practical advise can be given in relation to eating after mild pancreatitis? It would seem prudent to suggest that patients with predicted mild pancreatitis and who have abdominal pain and/or elevation of serum enzymes (> 2 × normal) for more than 4 days should have naso-jejunal feeding instituted rather than a trial of oral re-feeding. The interval of 4 days is taken from the Chebli study.10 A CT severity score is not routinely available in patients with predicted mild pancreatitis2 and cannot be used to select oral feeding or EN. To err on the side of caution and commence early naso-jejunal EN in the subgroups of patients with predicted mild acute pancreatitis who have persistent pain and enzyme elevation should avoid unnecessary delays in commencing nutritional support, and will likely reduce hospital stay.

REFERENCES

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  2. REFERENCES
  • 1
    Pisters PW, Ranson JH. Nutritional support for acute pancreatitis. Surg. Gynecol. Obstet. 1992; 175: 27584.
  • 2
    British Society of Gastroenterology. United Kingdom guidelines for the management of acute pancreatitis. British Society of Gastroenterology. Gut 1998; 42: S113.
  • 3
    Chandrasegaram MD, Plank LD, Windsor JA. The impact of total parenteral nutrition on the body composition of patients with acute pancreatitis. JPEN J. Parenter. Enteral Nutr. 2005; 29: 6573.
  • 4
    Gupta R, Patel K, Calder PC, Yaqoob P, Primrose JN, Johnson CD. A randomized clinical trial to assess the effect of total enteral and total parenteral nutritional support on metabolic, inflammatory and oxidative markers in patients with predicted severe acute pancreatitis. Pancreatology 2003; 3: 40613.
  • 5
    Eatock FC, Brombacher GD, Steven A, Imrie CW, McKay CJ, Carter R. Nasogastric feeding in severe acute pancreatitis may be practical and safe. Int. J. Pancreatol. 2000; 28: 239.
  • 6
    Abous-Assi S, Craig K, O'Keefe SJ. Hypocaloric feeding is better than total parenteral nutrition in acute pancreatitis: results of a randomized comparative study. Am. J. Gastroenterol. 2002; 97: 225562.
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  • 7
    Windsor JA. Search for prognostic markers for acute pancreatitis. Lancet 2000; 355: 19245.
  • 8
    Levy P, Heresbach D, Pariente EA et al. Frequency and risk factors of recurrent pain during refeeding in patients with acute pancreatitis: a multivariate multicentre prospective study of 116 patients. Gut 1997; 40: 2626.
  • 9
    Pandey SK, Ahuja V, Joshi YK, Sharma MP. A randomized trial of oral refeeding compared with jejunal tube refeeding in acute pancreatitis. Ind. J. Gastroenterol. 2004; 23: 535.
  • 10
    Chelbi JMF, Gaburri PD, De Souza AFM et al. Oral refeeding in patients with mild acute pancreatitis: Prevalence and risk factors of relapsing abdominal pain. J. Gastroenterol. Hepatol. 2005; 20: 13851389.
  • 11
    Levy P, Arotcavena R, Bartolie E et al. Efficacy of lanreotide 30 mg on prevention of pain relapse after oral refeeding in patients with necrotizing acute pancreatitis: a Phase II prospective multicentre study. Pancreatology 2004; 4: 22932.