|Year : 2022 | Volume
| Issue : 1 | Page : 12
Timing and Route of Nutritional Therapy for Severe Acute Pancreatitis: From Bench to Bedside
Siying Chen, Xin Chu, Chenyi Di, Zhigang Chang
Department of Critical Care Medicine, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, China
|Date of Submission||13-Nov-2021|
|Date of Acceptance||19-Apr-2022|
|Date of Web Publication||29-Jun-2022|
Dr. Zhigang Chang
Department of Critical Care Medicine, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, 1st Dahua Road, Dong Dan, Beijing 100730
Source of Support: None, Conflict of Interest: None
Nutritional support is one of the core issues in the treatment of severe acute pancreatitis (SAP). With the continuous progression of research on nutritional therapy, a large volume of evidence has emerged on the strategies and approaches of nutritional support for SAP patients. At the same time, the pathogenesis of SAP and the metabolic characteristics have been intensified in the acute phase of critically ill patients, which helps better understand the nutritional treatment strategy of SAP in terms of pathophysiology and pathogenesis. In this article, by searching electronic databases (PubMed, EMBASE, and Web of Science) from the earliest achievable date of each database to November 13, 2021, we discuss and analyze recent hot spots of SAP nutritional support to help individualize the implementation of nutritional strategies.
Keywords: Enteral nutrition, nutritional support, severe acute pancreatitis
|How to cite this article:|
Chen S, Chu X, Di C, Chang Z. Timing and Route of Nutritional Therapy for Severe Acute Pancreatitis: From Bench to Bedside. J Transl Crit Care Med 2022;4:12
|How to cite this URL:|
Chen S, Chu X, Di C, Chang Z. Timing and Route of Nutritional Therapy for Severe Acute Pancreatitis: From Bench to Bedside. J Transl Crit Care Med [serial online] 2022 [cited 2022 Dec 7];4:12. Available from: http://www.tccmjournal.com/text.asp?2022/4/1/12/348886
| Introduction|| |
The incidence of acute pancreatitis (AP) is increasing annually,, with severe acute pancreatitis (SAP) accounting for approximately 20% of the incidence of AP. According to the revised Atlanta classification (2012), SAP was defined as patients with AP who develop persistent organ failure (>48 h). SAP is often accompanied by pancreatic and peripancreatic necrosis and organ failure, with a mortality rate of 20%–40%., Animal experiments and in vitro studies have described pathophysiological processes at the onset of AP,,, with severe damage to glandular alveolar cells and an enhanced inflammatory response, leading to systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction syndrome (MODS), resulting in increased AP mortality. The treatment of SAP includes early resuscitation, pain management, local treatment of infected necrosis (endoscopic or surgical interventions), and nutritional support. SAP is often accompanied by significant catabolism, and nutritional support is therefore an important part of the treatment strategy., This article combines the latest advances and reviews the controversies that remain in the nutritional treatment of SAP, focusing on the approaches and timing of initiation.
| Data Sources and Searches|| |
We searched the electronic databases of PubMed, EMBASE and Web of Science. The search terms and MeSH heading were as follows: “acute pancreatitis,” or “severe acute pancreatitis,” or “acute necrotizing pancreatitis” and “nutrition” or “nutritional therapy” or “nutritional support” or “nutritional intervention” or “enteral nutrition” or “parenteral nutrition” or “nasogastric feeding” or “nasojejunal feeding” or “total parenteral nutrition” or “supplementary parenteral nutrition.” The search included literature published from the earliest achievable date of each database to November 13, 2021. The selected articles were discussed.
| Etiology and Pathophysiology of Severe Acute Pancreatitis|| |
AP is more common in patients with gallstones and alcoholism, and other causative factors include drugs, endoscopic retrograde cholangiopancreatography, hypercalcemia, hypertriglyceridemia, surgery, and trauma., The pathogenesis of SAP includes the classic theory of pancreas autodigestion and the leukocyte overactivation–inflammatory cytokines cascade, calcium overload in pancreatic acinar, and apoptosis. Among them, premature trypsinogen activation plays a leading role in the pathogenesis of pancreatitis. Alcohol and other pancreatic toxins impair the function of microtubules and thus impair exocytosis at the top of zymogen granules in acinar cells, resulting in the accumulation of zymogen granules in the cells, and the synthesis of lysosomes and digestive enzymes. After the fusion of lysosomes and zymogen particles, cathepsin B in lysosomes activates trypsinogen into trypsin, the latter activates a series of digestive enzymes, which are released into the cytoplasm, resulting in membrane damage and cell necrosis.,
Recent studies on the mechanism of SAP have shown that in the early stage of pancreatitis, in addition to the activation pathway of trypsinogen in the acinar cells, the Nuclear Factor Kappa-B (NF-kB) pathway might also play an important role. The NF-kB activation and zymogen activation pathways parallel each other; approximately 50% of acinar cells are damaged by early trypsinogen activation, while NF-kB activation leads to a severe local inflammatory response, accounting for the other half., The progression of early AP is caused by inflammatory factors produced by acinar cells and their proinflammatory response, leading to the spread of systemic inflammation. In fact, the early activation of NF-kB in AP does not depend on trypsin. NF-kB activates inflammatory factors/immune cells, leading to late acinar cell necrosis and SIRS, which is another important pathway of AP.,
Furthermore, recent studies have shown that pancreatic duct secretions can reduce pancreatic injury. Pancreatitis still occurs and progresses in animal models lacking trypsinogen activation, while cytokines play an increasingly important role in predicting the occurrence of AP. The activation of inflammatory signal transduction in the acinar cells may lead to autophagy and dysfunction of lysosomes and mitochondria. Reactive oxygen species, calcium signaling pathways, and changes in cystic fibrosis transmembrane regulatory factor are also important mechanisms in the pathogenesis of AP., Alcohol, nicotine, and bile acids can also damage acini and activate the above mechanisms.
| Controversies in the Nutrition Support of Severe Acute Pancreatitis|| |
In SAP, inflammation caused by necrosis or secondary infection will lead to increased calorie demand, loss of a large amount of protein, as well as abdominal pain, abdominal distension, and nausea and vomiting, which will lead to reduced food intake and decreased pancreatic exocrine function. Coupled with some complications, these events will lead to nutritional deterioration and negative nitrogen balance, and finally damage to the function and structure of vital organs.
In the early years, many nutritional treatment concepts for severe pancreatitis were put forward based on the classical theory of pancreatic self-digestion, the main purpose of which was to reduce/inhibit self-digestion, including intestinal rest[25-28] (nothing by mouth, gastrointestinal decompression, and early total parenteral nutrition [TPN]), to reduce pancreatic exocrine secretion, and to reduce the activation of trypsin by gastric fluid stimulation (gastrin) and small intestinal fluid stimulation (cholecystokinin)., Somatostatin and its analogs were also used to inhibit the secretion of pancreatic exocrine enzymes, which was thought to decrease the severity of pancreatitis. Early studies implied that the decrease in pancreatic exocrine secretion and trypsin during TPN treatment can reduce the inflammatory response induced by trypsin, which is theoretically beneficial to the recovery of pancreatic function., In addition, TPN can partially meet the energy needs of the body and reduce metabolic-related complications. However, a recent meta-analysis suggested that enteral nutrition (EN) is recommended as the initial treatment option for patients with SAP compared with TPN., At present, there is increasing evidence that intestinal rest is related to the increase in infectious complications caused by intestinal mucosal atrophy and bacterial translocation. Therefore, to maintain intestinal barrier function, EN has received increasing attention in the nutritional treatment of SAP.[37-39]
| Route of Nutrition|| |
Route of nutrition: Enteral or parenteral?
A recent meta-analysis showed that, early EN can greatly reduce the incidence of infectious complications, while there was no significant difference in mortality compared with early parenteral nutrition (PN) in critically ill patients. Similarly, studies on severe pancreatitis have shown that compared with PN, EN can significantly reduce the incidence of infective peripancreatic necrosis and single organ failure/multiple organ failure.,,
In fact, the intestinal epithelium is damaged in patients with severe pancreatitis who lack EN. In the absence of food stimulation, the contractility of the small intestine decreases, which promotes the excessive growth of bacteria in the intestinal cavity and attaches to the intestinal epithelial cells, resulting in programmed apoptosis and intestinal barrier dysfunction., Second, the decrease in visceral blood flow leads to ischemia–reperfusion injury, which increases intestinal vascular permeability and enables bacteria to activate macrophages in the blood vessels.[49-51] Once macrophages are activated, circulating neutrophils are activated and spread far away (such as to the lungs, liver, and kidneys), further promoting oxidative stress. These pathological processes may enhance the systemic inflammatory response.
Therefore, EN and PN are different not only in nutritional approaches. EN therapy has many theoretical and laboratory advantages, including protection of gastrointestinal barrier function (such as tight junctions),, preservation of intestinal B cells/lymphoid tissue, regulation of intestinal microecology to maintain the normal growth of intestinal flora, stimulation of intestinal blood flow to promote the release of endogenous factors, and protection of intestinal immune function.[56-58] At the same time, it may help prevent stress ulcers and protect distal organs through the enteropulmonary axis.
At present, most studies have found that EN can reduce infectious complications, even reduce the length of hospitalization and mechanical ventilation, and improve the prognosis, and is more economic., However, critically ill patients often develop gastrointestinal dysfunction that leads to underfeeding, which increases nutritional risk, infection, and intensive care unit (ICU) hospitalization. PN can easily reach the feeding target and avoid the risk of malnutrition. There is also a theoretical possibility for avoiding stimulated gastrointestinal pancreatic exocrine secretion; however, PN was found to increase the risk of infection (controversial), to be prone to overfeeding and metabolic complications, and to increase costs. In summary, many current guidelines and consensuses believe that critically ill patients, including SAP, prefer EN treatment to PN.,, Summary of articles regarding comparison of EN and PN in SAP is presented in [Table 1].
|Table 1: Summary of articles regarding comparison of enteral and parenteral nutrition in severe acute pancreatitis|
Click here to view
Route of enteral nutrition: Nasojejunal or nasogastric?
Nasojejunal feeding has been believed to decrease pancreatic secretion, which helps restore gut mucosal integrity, whereas gastric or duodenal feeding has been believed to stimulate pancreatic secretion, causing an exacerbation of the inflammatory process in the pancreas., However, recent randomized controlled trials (RCTs) on pancreatitis have not found a significant advantage of nasojejunal feeding over gastrointestinal feeding in terms of mortality, infectious complications, gastrointestinal complications, energy balance, or length of hospital stay.,,, Feeding intolerance, risk of aspiration, and risk of pneumonia were the main factors that need to be considered for critically ill patients when choosing the nasojejunal or nasogastric route. The incidence of pneumonia by jejunal feeding was relatively low while preserving a high nutritional efficiency compared with gastric feeding, but there was no difference in mortality or ICU admission.,, If the nasojejunal feeding approach cannot be conducted in a short time, it is recommended not to wait and to choose nasogastric feeding. Based on the current research, patients with gastric feeding intolerance and ineffective prokinetic drugs, as well as patients with a high risk of aspiration, should be given nasojejunal feeding.
Current studies on AP have also shown that early nasogastric tube EN is not superior to oral feeding., For mild AP, both American and European guidelines recommend early oral feeding as long as patients can tolerate it.,,, However, AP is often complicated with abdominal pain, nausea, vomiting, and even paralytic intestinal obstruction, resulting in difficulties when implementing early oral feeding. Summary of articles regarding comparison of nasojejunal or nasogastric feeding in SAP is presented in [Table 2].
|Table 2: Summary of articles regarding comparison of nasogastric versus nasojejunal tube in enteral nutrition in severe acute pancreatitis|
Click here to view
| Timing of Nutrition Support|| |
Early enteral nutrition versus delayed enteral nutrition?
Studies of early EN versus delayed EN in critically ill patients have shown that early EN reduces mortality and infection rates in critically ill patients,,, and studies of AP have also shown that delayed feeding significantly increased the risk of pancreatic necrosis compared with early feeding., However, the PYTHON study showed no significant benefit in terms of infection and mortality in patients with early nasal feeding compared with oral feeding after 3 days. In fact, studies of early initiation of EN in critically ill patients and in patients with SAP have not been confirmed by large high-quality RCTs; nevertheless, current guidelines consistently recommend early implementation of EN; as the timing of EN initiation varies from study to study, no consensus recommendation has been reached on a specific time for initiation, which can be within 24–72 h if available.,,,
The early stage of SAP is often combined with hypovolemia and distributive shock. For SAP patients with unstable hemodynamics, the primary focus is resuscitation and respiratory support, and EN should be started within 24–48 h after resuscitation or after hemodynamic stabilization, which is defined as adequate perfusion pressure, stable doses of vasoactive drugs, stabilized or decreasing levels of lactate and metabolic acidosis, and mean arterial pressure ≥60 mmHg associated with improved outcomes. In the NUTRIREA-2 study, early EN and PN were performed in patients admitted to the ICU with mechanical ventilation and vasoactive drugs within 24 h of admission, and it was found that diarrhea, vomiting, gastrointestinal ischemia, and pseudointestinal obstruction presented less in the early PN group than in the early EN group, but mortality and infection rates were not significantly different between the two groups. Subsequent hematological analysis also showed that although the level of citrulline, which reflects the quality of intestinal epithelial cells, was significantly increased in the early EN group, it was also accompanied by an increase in the level of entero-fatty acid-binding protein, which reflects intestinal ischemia, suggesting that early EN requires attention to intestinal blood flow and intestinal function.
The early stage of SAP is often characterized by circulatory instability and reduced peritoneal perfusion, as well as microvascular leakage and massive fluid loss due to pancreatic inflammation, causing visceral vasoconstriction, intra-abdominal hypertension (IAH), and even abdominal compartment syndrome (ACS), which can affect intestinal blood flow and intestinal function. Animal studies have shown that increased intra-abdominal pressure (IAP) leads to decreased abdominal perfusion pressure, decreased superior mesenteric artery and portal venous blood flow, decreased perfusion of visceral organs, and decreased microcirculatory blood flow, resulting in intestinal mucosal and systemic circulatory acidosis. A study by Smit et al. included 59 cases of SAP, of which 29 were continuously monitored for IAP; 13 cases (44.8%) were found to progress to ACS, of which 10 cases underwent open decompressions and revealed varying degrees of intestinal ischemia and necrosis (small bowel/terminal ileum/sigmoid colon/colon, local or total ischemic necrosis). Thus, special attention should be given to gastrointestinal function and blood flow when providing early EN in SAP. Usually, IAH requires gastrointestinal decompression, which also causes difficulties in implementing early EN. Summary of articles regarding comparison of early and delayed EN in SAP is listed in [Table 3].
|Table 3: Summary of articles regarding comparison of early and delayed enteral nutrition in severe acute pancreatitis|
Click here to view
In addition, whether EN increases IAP and whether it is tolerated by patients with IAH are also issues that need to be considered. In a study of 60 patients with SAP, early EN (within 48 h) did not cause IAH compared with delayed EN (initiated after 8 days) but increased feeding intolerance. Further analysis found that feeding intolerance was significantly increased when IAP was ≥15 mmHg, regardless of early or delayed EN. Nevertheless, early EN still reduced ICU length of stay, ameliorated MODS, and reduced infections. For patients with IAH, when IAP ≤20 mmHg, EN should be given earlier, while feeding intolerance and changes in IAP should be monitored carefully; if feeding intolerance fails to improve or IAP still increases after active measures are taken, enteral feeding should be reduced or suspended; for patients with grade III or higher IAP and ACS, EN should be delayed.,
Combining the recent recommendations of the European Society for Critical Care Medicine and the European Society for Parenteral Enteral Nutrition, early EN should be performed within 24–48 h if hemodynamically stable, and when there are no contraindications to EN; in cases of circulatory instability, hypoxia/acidosis, intestinal ischemia, ACS, and gastric residual volume >500 ml/6 h, EN needs to be delayed. SAP per se as well as weak bowel sounds and diarrhea are not reasons to delay EN.,
Timing of parenteral nutrition initiation
There is a consensus that early and adequate EN reduces infection and ICU length of stay and improves prognosis. However, patients with SAP usually present with gastrointestinal dysfunction or feeding intolerance, resulting in insufficient feeding. At the same time, SAP is often complicated by intestinal obstruction, ACS, and mesenteric ischemia, which are also contraindications of EN. Currently, it is generally accepted that PN can be supplemented when EN is insufficient; however, controversies still exist regarding the time to add PN when enteral feeding is insufficient. Timing of SPN in SAP patients may refer to studies in critically ill patients, as there is a paucity of evidence exclusively in SAP. Studies have shown that early addition of PN may increase infectious complications and length of hospital stay, while conversely, delayed PN may lead to low feeding and poor clinical outcomes if PN is delayed.,
According to the characteristics of energy metabolism, critical illness is comprised of two different phases, namely, the acute phase and chronic rehabilitation phase. The acute phase includes two periods: an early period (1–2 days) with unstable metabolism and increased catabolism and a late period (3–7 days) with muscle wasting and stabilization of metabolic disturbances. Worse still, pancreatic inflammation triggers an SIRS, increases metabolic rates, and generates a catabolic state. The early acute phase of critically ill patients is characterized by increased cytokine production, sympathetic excitation (massive release of catecholamines), and more catabolic hormones than synthetic hormones (glucocorticoids, glucagon, thyroxin) as same as a result of trauma, infection, and shock. Patients in a high catabolic state usually present with accelerated glycogen breakdown, enhanced gluconeogenesis, and accelerated breakdown of skeletal muscle proteins and cellular structural proteins. The hypercatabolic state produces large amounts of endogenous calories; thus, the addition of SPN in this phase can easily lead to overfeeding.
Recent studies and guidelines favor late administration of SPN, suggesting initiating SPN when EN does not meet 60% of the target requirement in 1 week; earlier SPN can be given for patients with high nutritional risk., Early implementation of SPN could be given to patients at high nutritional risk with NRS 2002 ≥5 or NUTRIC score ≥6 and if EN cannot meet 60% of target energy and protein requirements within 48–72 h. Although the debate on the timing of adding PN will remain, ultimately, the clinical workup will be individualized based on the patient's pathophysiology and metabolic changes, balancing nutritional risks and benefits.
| Conclusion|| |
Nutritional support is an important part of SAP treatment, and EN is preferred to PN; early tube feeding for SAP, both gastric and postpyloric, is optional. EN should be implemented as early as possible (within 48 h), but gastrointestinal function needs to be monitored closely. SPN needs to be added if EN cannot meet the target energy intake, and the timing needs to be combined with the nutritional risk assessment, usually after 7 days, but can be advanced for those with high nutritional risk.
Financial support and sponsorship
The study was supported by Excellent Researcher Training Program of Dongcheng District, Beijing (BJ-2020-023).
Conflicts of interest
There are no conflicts of interest.
| References|| |
Dutta AK, Goel A, Kirubakaran R, Chacko A, Tharyan P. Nasogastric versus nasojejunal tube feeding for severe acute pancreatitis. Cochrane Database Syst Rev 2020;3:CD010582.
Talukdar R, Vege SS. Acute pancreatitis. Curr Opin Gastroenterol 2015;31:374-9.
Banks PA, Bollen TL, Dervenis C, Gooszen HG, Johnson CD, Sarr MG, et al.
Classification of acute pancreatitis-2012: Revision of the Atlanta classification and definitions by international consensus. Gut 2013;62:102-11.
Boxhoorn L, Voermans RP, Bouwense SA, Bruno MJ, Verdonk RC, Boermeester MA, et al.
Acute pancreatitis. Lancet 2020;396:726-34.
Schepers NJ, Bakker OJ, Besselink MG, Ahmed Ali U, Bollen TL, Gooszen HG, et al.
Impact of characteristics of organ failure and infected necrosis on mortality in necrotising pancreatitis. Gut 2019;68:1044-51.
Biczo G, Vegh ET, Shalbueva N, Mareninova OA, Elperin J, Lotshaw E, et al.
Mitochondrial dysfunction, through impaired autophagy, leads to endoplasmic reticulum stress, deregulated lipid metabolism, and pancreatitis in animal models. Gastroenterology 2018;154:689-703.
Gukovskaya AS, Gukovsky I, Algül H, Habtezion A. Autophagy, inflammation, and immune dysfunction in the pathogenesis of pancreatitis. Gastroenterology 2017;153:1212-26.
Lugea A, Waldron RT, Mareninova OA, Shalbueva N, Deng N, Su HY, et al.
Human pancreatic acinar cells: Proteomic characterization, physiologic responses, and organellar disorders in ex vivo
pancreatitis. Am J Pathol 2017;187:2726-43.
Pan LL, Li J, Shamoon M, Bhatia M, Sun J. Recent advances on nutrition in treatment of acute pancreatitis. Front Immunol 2017;8:762.
Lee PJ, Papachristou GI. New insights into acute pancreatitis. Nat Rev Gastroenterol Hepatol 2019;16:479-96.
Trikudanathan G, Wolbrink DR, van Santvoort HC, Mallery S, Freeman M, Besselink MG. Current concepts in severe acute and necrotizing pancreatitis: An evidence-based approach. Gastroenterology 2019;156:1994-2007.e3.
Song J, Zhong Y, Lu X, Kang X, Wang Y, Guo W, et al.
Enteral nutrition provided within 48 hours after admission in severe acute pancreatitis: A systematic review and meta-analysis. Medicine (Baltimore) 2018;97:e11871.
Lankisch PG, Apte M, Banks PA. Acute pancreatitis. Lancet 2015;386:85-96.
Yasuda H, Horibe M, Sanui M, Sasaki M, Suzuki N, Sawano H, et al.
Etiology and mortality in severe acute pancreatitis: A multicenter study in Japan. Pancreatology 2020;20:307-17.
Saluja A, Dudeja V, Dawra R, Sah RP. Early intra-acinar events in pathogenesis of pancreatitis. Gastroenterology 2019;156:1979-93.
Watanabe T, Kudo M, Strober W. Immunopathogenesis of pancreatitis. Mucosal Immunol 2017;10:283-98.
Wen L, Voronina S, Javed MA, Awais M, Szatmary P, Latawiec D, et al.
Inhibitors of ORAI1 prevent cytosolic calcium-associated injury of human pancreatic acinar cells and acute pancreatitis in 3 mouse models. Gastroenterology 2015;149:481-92.e7.
McClave SA. Nutrition support in acute pancreatitis. Gastroenterol Clin North Am 2007;36:65-74, vi.
Aghdassi AA, John DS, Sendler M, Weiss FU, Reinheckel T, Mayerle J, et al.
Cathepsin D regulates cathepsin B activation and disease severity predominantly in inflammatory cells during experimental pancreatitis. J Biol Chem 2018;293:1018-29.
Hietaranta AJ, Saluja AK, Bhagat L, Singh VP, Song AM, Steer ML. Relationship between NF-kappaB and trypsinogen activation in rat pancreas after supramaximal caerulein stimulation. Biochem Biophys Res Commun 2001;280:388-95.
Hegyi P, Rakonczay Z. Insufficiency of electrolyte and fluid secretion by pancreatic ductal cells leads to increased patient risk for pancreatitis. Am J Gastroenterol 2010;105:2119-20.
Dawra R, Sah RP, Dudeja V, Rishi L, Talukdar R, Garg P, et al.
Intra-acinar trypsinogen activation mediates early stages of pancreatic injury but not inflammation in mice with acute pancreatitis. Gastroenterology 2011;141:2210-7.e2.
Lugli AK, Carli F, Wykes L. The importance of nutrition status assessment: The case of severe acute pancreatitis. Nutr Rev 2007;65:329-34.
Wang W, Huang Y, Lan Y, Wang L. The application of a structural nutritional care management model in severe acute pancreatitis patients undergoing early enteral nutrition via nasal jejunal nutrition tubes. Am J Transl Res 2021;13:8200-6.
Windsor AC, Kanwar S, Li AG, Barnes E, Guthrie JA, Spark JI, et al.
Compared with parenteral nutrition, enteral feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. Gut 1998;42:431-5.
Pisters PW, Ranson JH. Nutritional support for acute pancreatitis. Surg Gynecol Obstet 1992;175:275-84.
Marik PE. What is the best way to feed patients with pancreatitis? Curr Opin Crit Care 2009;15:131-8.
Gupta R, Patel K, Calder PC, Yaqoob P, Primrose JN, Johnson CD. A randomised 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 (APACHE II>or=6). Pancreatology 2003;3:406-13.
Eckerwall G, Olin H, Andersson B, Andersson R. Fluid resuscitation and nutritional support during severe acute pancreatitis in the past: What have we learned and how can we do better? Clin Nutr 2006;25:497-504.
Haney JC, Pappas TN. Necrotizing pancreatitis: Diagnosis and management. Surg Clin North Am 2007;87:1431-46, ix.
Nathens AB, Curtis JR, Beale RJ, Cook DJ, Moreno RP, Romand JA, et al.
Management of the critically ill patient with severe acute pancreatitis. Crit Care Med 2004;32:2524-36.
Wang G, Liu Y, Zhou SF, Qiu P, Xu L, Wen P, et al.
Effect of somatostatin, ulinastatin and gabexate on the treatment of severe acute pancreatitis. Am J Med Sci 2016;351:506-12.
Kalfarentzos FE, Karavias DD, Karatzas TM, Alevizatos BA, Androulakis JA. Total parenteral nutrition in severe acute pancreatitis. J Am Coll Nutr 1991;10:156-62.
Li W, Liu J, Zhao S, Li J. Safety and efficacy of total parenteral nutrition versus total enteral nutrition for patients with severe acute pancreatitis: A meta-analysis. J Int Med Res 2018;46:3948-58.
Wu P, Li L, Sun W. Efficacy comparisons of enteral nutrition and parenteral nutrition in patients with severe acute pancreatitis: A meta-analysis from randomized controlled trials. Biosci Rep 2018;38:BSR20181515.
Janisch N, Gardner T. Recent advances in managing acute pancreatitis. F1000Res 2015;4:F1000 Faculty Rev-1474.
Janisch NH, Gardner TB. Advances in management of acute pancreatitis. Gastroenterol Clin North Am 2016;45:1-8.
Peng L, Wu LG, Li B, Zhao J, Wen LM. Early enteral nutrition improves intestinal immune barrier in a rat model of severe acute pancreatitis. J Hepatobiliary Pancreat Sci 2016;23:681-7.
Li JY, Yu T, Chen GC, Yuan YH, Zhong W, Zhao LN, et al.
Enteral nutrition within 48 hours of admission improves clinical outcomes of acute pancreatitis by reducing complications: A meta-analysis. PLoS One 2013;8:e64926.
Singer P, Blaser AR, Berger MM, Alhazzani W, Calder PC, Casaer MP, et al.
ESPEN guideline on clinical nutrition in the Intensive Care Unit. Clin Nutr 2019;38:48-79.
Bengmark S. Bio-ecological control of acute pancreatitis: The role of enteral nutrition, pro and synbiotics. Curr Opin Clin Nutr Metab Care 2005;8:557-61.
Crockett SD, Wani S, Gardner TB, Falck-Ytter Y, Barkun AN, American Gastroenterological Association Institute Clinical Guidelines Committee. American Gastroenterological Association Institute guideline on initial management of acute pancreatitis. Gastroenterology 2018;154:1096-101.
Yao H, He C, Deng L, Liao G. Enteral versus parenteral nutrition in critically ill patients with severe pancreatitis: A meta-analysis. Eur J Clin Nutr 2018;72:66-8.
Petrov MS, Whelan K. Comparison of complications attributable to enteral and parenteral nutrition in predicted severe acute pancreatitis: A systematic review and meta-analysis. Br J Nutr 2010;103:1287-95.
Flint RS, Windsor JA. The role of the intestine in the pathophysiology and management of severe acute pancreatitis. HPB (Oxford) 2003;5:69-85.
Oláh A, Romics L Jr. Enteral nutrition in acute pancreatitis: A review of the current evidence. World J Gastroenterol 2014;20:16123-31.
Al-Omran M, Albalawi ZH, Tashkandi MF, Al-Ansary LA. Enteral versus parenteral nutrition for acute pancreatitis. Cochrane Database Syst Rev 2010;1:CD002837.
Guo ZZ, Wang P, Yi ZH, Huang ZY, Tang CW. The crosstalk between gut inflammation and gastrointestinal disorders during acute pancreatitis. Curr Pharm Des 2014;20:1051-62.
Lodewijkx PJ, Besselink MG, Witteman BJ, Schepers NJ, Gooszen HG, van Santvoort HC, et al.
Nutrition in acute pancreatitis: A critical review. Expert Rev Gastroenterol Hepatol 2016;10:571-80.
Shen QX, Xu GX, Shen MH. Effect of early enteral nutrition (EN) on endotoxin in serum and intestinal permeability in patients with severe acute pancreatitis. Eur Rev Med Pharmacol Sci 2017;21:2764-8.
McClave SA. Factors that worsen disease severity in acute pancreatitis: Implications for more innovative nutrition therapy. Nutr Clin Pract 2019;34 Suppl 1:S43-8.
McClave SA, Heyland DK. The physiologic response and associated clinical benefits from provision of early enteral nutrition. Nutr Clin Pract 2009;24:305-15.
Zhang J, Yu WQ, Wei T, Zhang C, Wen L, Chen Q, et al.
Effects of short-peptide-based enteral nutrition on the intestinal microcirculation and mucosal barrier in mice with severe acute pancreatitis. Mol Nutr Food Res 2020;64:e1901191.
Yong L, Lu QP, Liu SH, Fan H. Efficacy of glutamine-enriched nutrition support for patients with severe acute pancreatitis: A meta-analysis. JPEN J Parenter Enteral Nutr 2016;40:83-94.
Cao Y, Xu Y, Lu T, Gao F, Mo Z. Meta-analysis of enteral nutrition versus total parenteral nutrition in patients with severe acute pancreatitis. Ann Nutr Metab 2008;53:268-75.
Schörghuber M, Fruhwald S. Effects of enteral nutrition on gastrointestinal function in patients who are critically ill. Lancet Gastroenterol Hepatol 2018;3:281-7.
Moron R, Galvez J, Colmenero M, Anderson P, Cabeza J, Rodriguez-Cabezas ME. The importance of the microbiome in critically ill patients: Role of nutrition. Nutrients 2019;11:3002.
Andersen S, Banks M, Bauer J. Nutrition support and the gastrointestinal microbiota: A systematic review. J Acad Nutr Diet 2020;120:1498-516.
Ma Y, Yang X, Chatterjee V, Wu MH, Yuan SY. The gut-lung axis in systemic inflammation. Role of mesenteric lymph as a conduit. Am J Respir Cell Mol Biol 2021;64:19-28.
Hui L, Zang K, Wang M, Shang F, Zhang G. Comparison of the preference of nutritional support for patients with severe acute pancreatitis. Gastroenterol Nurs 2019;42:411-6.
Bai X, Jin M, Zhang H, Lu B, Yang H, Qian J. Evaluation of Chinese updated guideline for acute pancreatitis on management of moderately severe and severe acute pancreatitis. Pancreatology 2020;20:1582-6.
Wu LM, Sankaran SJ, Plank LD, Windsor JA, Petrov MS. Meta-analysis of gut barrier dysfunction in patients with acute pancreatitis. Br J Surg 2014;101:1644-56.
McClave SA, Taylor BE, Martindale RG, Warren MM, Johnson DR, Braunschweig C, et al.
Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr 2016;40:159-211.
Arvanitakis M, Ockenga J, Bezmarevic M, Gianotti L, Krznarić Ž, Lobo DN, et al.
ESPEN guideline on clinical nutrition in acute and chronic pancreatitis. Clin Nutr 2020;39:612-31.
Marik PE, Zaloga GP. Meta-analysis of parenteral nutrition versus enteral nutrition in patients with acute pancreatitis. BMJ 2004;328:1407.
Petrov MS, Pylypchuk RD, Uchugina AF. A systematic review on the timing of artificial nutrition in acute pancreatitis. Br J Nutr 2009;101:787-93.
Yi F, Ge L, Zhao J, Lei Y, Zhou F, Chen Z, et al.
Meta-analysis: Total parenteral nutrition versus total enteral nutrition in predicted severe acute pancreatitis. Intern Med 2012;51:523-30.
Liu M, Gao C. A systematic review and meta-analysis of the effect of total parenteral nutrition and enteral nutrition on the prognosis of patients with acute pancreatitis. Ann Palliat Med 2021;10:10779-88.
Kaushik N, Pietraszewski M, Holst JJ, O'Keefe SJ. Enteral feeding without pancreatic stimulation. Pancreas 2005;31:353-9.
Vege SS, DiMagno MJ, Forsmark CE, Martel M, Barkun AN. Initial medical treatment of acute pancreatitis: American Gastroenterological Association Institute technical review. Gastroenterology 2018;154:1103-39.
Nally DM, Kelly EG, Clarke M, Ridgway P. Nasogastric nutrition is efficacious in severe acute pancreatitis: A systematic review and meta-analysis. Br J Nutr 2014;112:1769-78.
Zhu Y, Yin H, Zhang R, Ye X, Wei J. Nasogastric nutrition versus nasojejunal nutrition in patients with severe acute pancreatitis: A meta-analysis of randomized controlled trials. Gastroenterol Res Pract 2016;2016:6430632.
Chang YS, Fu HQ, Xiao YM, Liu JC. Nasogastric or nasojejunal feeding in predicted severe acute pancreatitis: A meta-analysis. Crit Care 2013;17:R118.
Piciucchi M, Merola E, Marignani M, Signoretti M, Valente R, Cocomello L, et al.
Nasogastric or nasointestinal feeding in severe acute pancreatitis. World J Gastroenterol 2010;16:3692-6.
Bakker OJ, van Brunschot S, van Santvoort HC, Besselink MG, Bollen TL, Boermeester MA, et al.
Early versus on-demand nasoenteric tube feeding in acute pancreatitis. N Engl J Med 2014;371:1983-93.
Jiang K, Chen XZ, Xia Q, Tang WF, Wang L. Early nasogastric enteral nutrition for severe acute pancreatitis: A systematic review. World J Gastroenterol 2007;13:5253-60.
Eatock FC, Chong P, Menezes N, Murray L, McKay CJ, Carter CR, et al.
A randomized study of early nasogastric versus nasojejunal feeding in severe acute pancreatitis. Am J Gastroenterol 2005;100:432-9.
Kumar A, Singh N, Prakash S, Saraya A, Joshi YK. Early enteral nutrition in severe acute pancreatitis: A prospective randomized controlled trial comparing nasojejunal and nasogastric routes. J Clin Gastroenterol 2006;40:431-4.
Singh N, Sharma B, Sharma M, Sachdev V, Bhardwaj P, Mani K, et al.
Evaluation of early enteral feeding through nasogastric and nasojejunal tube in severe acute pancreatitis: A noninferiority randomized controlled trial. Pancreas 2012;41:153-9.
Hegazi RA, DeWitt T. Enteral nutrition and immune modulation of acute pancreatitis. World J Gastroenterol 2014;20:16101-5.
Qi D, Yu B, Huang J, Peng M. Meta-analysis of early enteral nutrition provided within 24 hours of admission on clinical outcomes in acute pancreatitis. JPEN J Parenter Enteral Nutr 2018;42:1139-47.
Casaer MP, Van den Berghe G. Nutrition in the acute phase of critical illness. N Engl J Med 2014;370:2450-1.
Leppäniemi A, Tolonen M, Tarasconi A, Segovia-Lohse H, Gamberini E, Kirkpatrick AW, et al.
2019 WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg 2019;14:27.
Nakashima I, Horibe M, Sanui M, Sasaki M, Sawano H, Goto T, et al.
Impact of enteral nutrition within 24 hours versus between 24 and 48 hours in patients with severe acute pancreatitis: A multicenter retrospective study. Pancreas 2021;50:371-7.
Forsmark CE, Vege SS, Wilcox CM. Acute pancreatitis. N Engl J Med 2016;375:1972-81.
Reignier J, Boisramé-Helms J, Brisard L, Lascarrou JB, Ait Hssain A, Anguel N, et al.
Enteral versus parenteral early nutrition in ventilated adults with shock: A randomised, controlled, multicentre, open-label, parallel-group study (NUTRIREA-2). Lancet 2018;391:133-43.
Piton G, Le Gouge A, Brulé N, Cypriani B, Lacherade JC, Nseir S, et al.
Impact of the route of nutrition on gut mucosa in ventilated adults with shock: An ancillary of the NUTRIREA-2 trial. Intensive Care Med 2019;45:948-56.
Smit M, Buddingh KT, Bosma B, Nieuwenhuijs VB, Hofker HS, Zijlstra JG. Abdominal compartment syndrome and intra-abdominal ischemia in patients with severe acute pancreatitis. World J Surg 2016;40:1454-61.
Doty JM, Oda J, Ivatury RR, Blocher CR, Christie GE, Yelon JA, et al.
The effects of hemodynamic shock and increased intra-abdominal pressure on bacterial translocation. J Trauma 2002;52:13-7.
Cheng J, Wei Z, Liu X, Li X, Yuan Z, Zheng J, et al.
The role of intestinal mucosa injury induced by intra-abdominal hypertension in the development of abdominal compartment syndrome and multiple organ dysfunction syndrome. Crit Care 2013;17:R283.
Leng Y, Zhang K, Fan J, Yi M, Ge Q, Chen L, et al.
Effect of acute, slightly increased intra-abdominal pressure on intestinal permeability and oxidative stress in a rat model. PLoS One 2014;9:e109350.
Jin M, Zhang H, Lu B, Li Y, Wu D, Qian J, et al.
The optimal timing of enteral nutrition and its effect on the prognosis of acute pancreatitis: A propensity score matched cohort study. Pancreatology 2017;17:651-7.
Bakker OJ, van Brunschot S, Farre A, Johnson CD, Kalfarentzos F, Louie BE, et al.
Timing of enteral nutrition in acute pancreatitis: Meta-analysis of individuals using a single-arm of randomised trials. Pancreatology 2014;14:340-6.
Li X, Ma F, Jia K. Early enteral nutrition within 24 hours or between 24 and 72 hours for acute pancreatitis: Evidence based on 12 RCTs. Med Sci Monit 2014;20:2327-35.
Feng P, He C, Liao G, Chen Y. Early enteral nutrition versus delayed enteral nutrition in acute pancreatitis: A PRISMA-compliant systematic review and meta-analysis. Medicine (Baltimore) 2017;96:e8648.
Sun JK, Li WQ, Ke L, Tong ZH, Ni HB, Li G, et al.
Early enteral nutrition prevents intra-abdominal hypertension and reduces the severity of severe acute pancreatitis compared with delayed enteral nutrition: A prospective pilot study. World J Surg 2013;37:2053-60.
Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, et al.
Intra-abdominal hypertension and the abdominal compartment syndrome: Updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med 2013;39:1190-206.
Reintam Blaser A, Starkopf J, Alhazzani W, Berger MM, Casaer MP, Deane AM, et al.
Early enteral nutrition in critically ill patients: ESICM clinical practice guidelines. Intensive Care Med 2017;43:380-98.
Oshima T, Heidegger CP, Pichard C. Supplemental parenteral nutrition is the key to prevent energy deficits in critically ill patients. Nutr Clin Pract 2016;31:432-7.
Casaer MP, Mesotten D, Hermans G, Wouters PJ, Schetz M, Meyfroidt G, et al.
Early versus late parenteral nutrition in critically ill adults. N Engl J Med 2011;365:506-17.
Fraipont V, Preiser JC. Energy estimation and measurement in critically ill patients. JPEN J Parenter Enteral Nutr 2013;37:705-13.
Singer P, Berger MM, Van den Berghe G, Biolo G, Calder P, Forbes A, et al.
ESPEN guidelines on parenteral nutrition: Intensive care. Clin Nutr 2009;28:387-400.
[Table 1], [Table 2], [Table 3]