ABSTRACT. Background: In the late course of chronic pancreatitis (CP), weight loss is often seen because of reduced caloric intake and a reduction of pancreatic enzyme secretion, resulting in maldigestion. Most of these patients can be managed by dietary recommendations and pancreatic enzyme supplementation. However, approximately 5% of these patients are reported to be candidates for enteral nutrition support during their course of CP. Although small bowel access for enteral feeding can be easily obtained by percutaneous endoscopic gastrojejunostomy (PEG/J) or direct percutaneous endoscopic jejunostomy (DPEJ), to date there are no data regarding clinical outcome and safety of long-term jejunal feeding in CP. Methods: From January 1999 to October 2002, 57 patients receiving enteral nutrition by PEG/J or DPEJ were retrospectively analyzed during a follow-up period of 6 months. There were 38 females and 19 males, with an average age of 46.6 years. Results: Small-bowel access was obtained by PEG/J in 53 patients and by DPEJ in 4. Duration of enteral feeding was 113 days. Average body weight significantly increased from 64.8 kg at day 1 to 69.1 kg at day 180 (p
Chronic pancreatitis (CP) causes many digestive and metabolic disturbances and a progressive degradation of a patient’s nutritional state. The relationship between nutrition and CP is bilateral: nutrition is one of the factors involved in the onset of CP, whereas poor food intake is one of its consequences and is one of the major predictors of poor outcome. The onset of malnutrition in CP is late in the disease course. Only after 80% to 90% loss of exocrine function will signs of malabsorption occur.1 The principal mechanisms of malnutrition in CP are a reduction in nutrient intake, a reduction in nutrient absorption, and an increased metabolic activity.
Pain of varying severity and duration is a leading clinical symptom in up to 90% of patients with CP.^sup 2^ Because of food intake-related abdominal pain, patients often eat too little.3
Gastroparesis, reported in up to 44% of patients with small-duct CP, may lead to nausea and vomiting and therefore further contribute to poor oral food intake and clinical decline.4 Patients with CP often display an elevated basal metabolic rate of approximately 110% of baseline (35 kcal/kg/24 hours) as a result of the chronic inflammation.5 This, in combination with poor oral food intake, accounts for the initial 10% to 20% loss of body weight.6
The onset of diabetes mellitus is reported in 60% to 70% of CP patients, and the probability of endocrine insufficiency progressively increases within 10 years after the diagnosis of CP.7 Steatorrhea is observed in about 30% of all cases, resulting in further weight loss.8-10 In this stage, the nutritional status of the patient can be greatly disturbed.
Before the initiation of nutrition support, nutritional risk should be assessed. Many nutrition screening tools exist. Kondrup et al11 developed a screening tool that includes measurements of undernutrition and disease severity in order to evaluate if a patient is at risk for malnutrition. In addition, patients may be evaluated using the subjective global assessment of Detsky et al.12 This approach classifies patients subjectively according to data obtained from their history and physical examination.
Nutrition support in CP patients is an ongoing challenge for clinicians. Although most of these patients can be managed by dietary recommendations and pancreatic enzyme supplementation, approximately 5% had severe and ongoing malnutrition and maldigestion. In these patients, enteral nutrition should be recommended. Enteral feeding beyond the ligament of Treitz is preferred over parenteral nutrition because enteral nutrition is less costly and has the advantages of reduced infectious and metabolic complications.13 In addition, enteral feeding maintains gut integrity and is fundamental in supporting the gut immune system, important for the at-risk patient.14 Further, enteral feeding beyond the ligament of Treitz allows the pancreatic gland to rest and minimizes pancreatic secretion, which may result in a reduction of abdominal pain.15 Additionally, jejunal feeding during acute flares of CP can reduce the incidence of nosocomial infections and the duration of systemic inflammatory response and severity.16,17
Endoscopie small-bowel access may be obtained by 2 methods. The first method, percutaneous endoscopic gastrojejunostomy (PEG/J), has been reported with a 100% success rate and no major complications.18 In this method, a PEG tube is used as a conduit to place a jejunal feeding tube with an over-the-guidewire method. The second method, direct percutaneous endoscopie jejunostomy (DPEJ), directly places a jejunal tube into the small bowel by using an enteroscope or pediatric colonoscope to reach the puncture site beyond the ligament of Treitz. Good results with only minor complications have been reported by Shike et al.19
Patients with a severe course of CP who have recurrent flares with abdominal pain, poor oral food intake, and whose illness cannot be controlled by oral dietary recommendations may benefit from long- term nutrition support by jejunal feeding. Unfortunately, there are no controlled data available from patients with CP using enterai feeding protocols. Current outcome data are based solely on case reports.
The aim of this current study was to analyze the safety and clinical outcome in patients receiving longterm nutrition support by PEG/J or DPEJ feeding during their course of CP.
MATERIALS AND METHODS
Patients
From January 1999 to October 2002, 57 patients with CP referred to the nutrition service of the Medical University of South Carolina were retrospectively evaluated. All patients were hospitalized at the time of tube placement because of an acute flare-up of CP. Nutritional status in all patients was assessed by using the Subjective Global Assessment (SGA) score. Nutrition support was delivered either by PEG/J or DPEJ.
Endoscopic Procedures
Endoscopic placement of a percutaneous tube system (DPEJ or PEG/ J) was usually performed under the use of conscious sedation and local anesthesia at the skin puncture site. Procedures were performed either in the intensive care units, at the bedside, or in the endoscopy suite. All patients were given cefazolin 1 g IV as single dose prophylaxis against infection before the endoscopie procedure.
PEG/J
A Wilson-Cook 24 Fr tulip-tip PEG or Boston Scientific (Natrick, MA) 24 Fr PEG was inserted with the standard push or pull technique. The endoscope was then reinserted and the internal bumper of the PEG tube located. A grasping forceps was placed through the endoscope and the PEG tube was cannulated by pushing the grasping forceps through the PEG to the outside of the patient. A flexible, 0.035 guidewire is grasped by the forceps and pulled back through the PEG into the stomach and advanced under direct endoscopie visualization into the fourth portion of the duodenum. The grasping forceps and guidewire were then advanced another 8-10 cm beyond the tip of the endoscope under direct visualization. A 12 Fr J-tube was then threaded over the guidewire and advanced to the proximal jejunum. The guidewire and forceps are removed and the endoscope was then withdrawn by gently rotation. If a large loop of J-tube was visualized within the stomach, the J-tube placement was repeated.18
Direct Percutaneous Endoscopic Jejunostomy
A standard, commercially available, pull-type 20 Fr PEG kit (Microinvasive Endoscopy; Boston Scientific Corp) was used for the DPEJ procedure. After insertion of the endoscope to the jejunum, a skin puncture site was determined by using abdominal wall transillumination and abdominal wall finger palpation with endoscopie gastric mucosal visualization. A 19-gauge needle was passed into the bowel through the abdominal wall. To fix the small bowel wall against the abdominal wall, the 19-gauge needle was grasped with a snare passed through the endoscope. An incision of 1 cm at the skin puncture site of the needle was made. An introducer cannula with a plastic outer sheath was then passed through the abdominal wall into the jejunum just adjacent to the 19-gauge needle. The snare was released from the 19-gauge needle and placed \around the cannula to stabilize it within the small bowel. The guidewire was passed through the plastic sheath, grasped with the snare and pulled with the endoscope out through the patient’s mouth. A standard PEG tube was attached to the guidewire and then pulled through the skin incision site in the abdominal wall. The final position of the DPEJ was confirmed endoscopically.20
Feeding
All patients were able to begin tube feeding within 12 hours after enterai access was obtained. A standard polypeptide diet (SD) was administrated by initially using a continuous 24-hour feeding regimen. The volume and rate of jejunal feeding were adjusted, depending on individual tolerance of the feeding formula. The feeding rate was increased with the goal of reaching the full caloric requirement on day 3. The total daily caloric requirement was calculated using the HarrisBenedict formula, individually adjusted to the patient’s clinical course and physical activity. An elemental diet (ED) was only administrated in patients with suspected intolerance to the SD. In addition, patients were allowed to consume clear liquids orally if tolerated. Patients took their medications orally. Patients were converted routinely to an overnight cyclic feeding regimen. The characteristics of the enteral feeding formulas are summarized in Table I.
TABLE I
Type and composition of tube feeding
Data Collection and Statistical Analysis
Institutional review board approval for the research project was obtained before the data collection. Data were collected retrospectively from the patient’s hospital and clinic medical records. Abdominal pain and gastrointestinal symptoms (nausea, vomiting, diarrhea) were evaluated by questioning patients during their hospitalization for enterai tube placement (day 0) and again during their regular follow-up consultations at days 90 and 180. All hospitalizations and not routinely planned physician visits related to CP were further recorded. The type and amount of narcotic drug intake were also analyzed. Follow-up data that were not documented in the medical records are indicated as not reported. Statistical analysis was performed using Intercooled STATA 8.0 for Windows (2003, STATA Corporation, College Station, TX). Because some continuous variables within the dataset were not normally distributed, we performed a nonparametric test for matched pairs of observations, using the Wilcoxon matched-pairs signed-ranks test. The null hypothesis (H0) is that both observation groups come from the same distribution; the alternative (H1) is that 2 groups do not come from the same distribution. Test results with p values of ≤0.05 were considered significant.
RESULTS
The etiologies for CP in our patient group were secondary to alcohol consumption (n = 16; 28%), papillary stenosis (n = 10; 17%), pancreas divisum (n = 9; 16%), papillary dysfunction (n = 5; 9%), gallstones (n = 5; 9%), metabolic disorders (n = 2; 4%), and idiopathic pancreatitis (n = 10; 17%). The majority of patients had ongoing weight loss with moderate to severe malnutrition. All patients had previously received dietary recommendations, attempts at oral nutritional supplementation, analgesia, enzyme supplementation, and insulin if required. Eight patients (17%) with moderate to severe malnutrition (SGA category: 4 patients B and 4 patients C) who were candidates for elective pancreatic surgery and who failed to thrive with an adequate dietary regimen also received long-term enteral feeding before surgery. The characteristics of the 57 patients are shown in Table II.
Small bowel access was obtained by PEG/J in 53 patients (93%) and by DPEJ in the remaining 4 patients (7%). Twenty-three patients (40%) had an average weight loss of 13.5 kg (range, 4-35) during the previous 6 months before small bowel feeding was initiated. The average enteral feeding time was 113 days (range, 3-180). In 1 patient, tube removal at day 3 was related to a colon mesentery injury after DPEJ-tube placement, necessitating emergency laparotomy. Elective pancreatic surgery was undertaken in 8 patients: there were 6 distal pancreatectomies, 1 lateral pancreaticojejunostomy (Partington-Rochelle) and 1 pancreaticoduodenectomy (Whipple). Before patients underwent elective surgery, enterai feeding was provided for an average of 76.8 days (range, 46-111). All patients who underwent either emergency or elective surgery were excluded from further data collection and analysis.
Body Weight
The patient’s average weight before initiation of enterai feeding was 64.8 kg (range, 36-108.5). After 90 days of follow-up, the overall mean body weight significantly increased to 67.7 kg (range, 39.5-113.5; p
TABLE II
Patient characteristics (n = 57)
FIG. 1. Patient’s average body weight over 6 months (kg).
SGA
SGA is a tool to determine nutritional status, thus predicting the degree of malnutrition. The SGA data before and after treatment initiation are shown in Table III.
Pain, Pain Medication, and Gastrointestinal Symptoms
Initially, 55 patients (96%) presented with abdominal pain. Pain medication consisted of regular intake of nonsteroidal antiinflammatory drugs (NSAID) in 3 patients (5.3%), opiate derivatives in 23 patients (44%), and a combination of opiate derivatives with NSAID or antidepressants in 26 (45.6%) cases. Further, 51 patients (90%) had gastrointestinal symptoms such as vomiting or nausea (n = 38; 74.5%), diarrhea and vomiting (n = 10; 19.6%), and diarrhea (n = 3; 5.9%). After 90 days, only 27 patients (48%; p
TABLE III
Subjective Global Assessment (SGA)
Laboratory Analysis, Physician Visits, and Rehospitalizations
Albumin levels increased from 2.9 g/dL at initiation to 3.2 g/dL (p .05), although a continuous decline was observed (Figs. 3-5).
On average, patients required 3.6 physician visits (range, 1-12) and underwent 1.8 rehospitalizations (range, 0-5) over the next 6 months (Table VI).
Feeding
In all patients, tube feeding with a SD was introduced within 12 hours after tube placement. The full nutritional goal was reached after 5 days in 84% of patients. One patient underwent emergency laparotomy because of a colon mesentery injury at day 3, and intolerance to enterai feeding was observed in another 8 patients (14%). A switch to an ED in these 8 patients was beneficial in 4 of them (7%), allowing their full caloric needs to be delivered by enterai feeding. The 4 remaining patients had intolerance to jejunal feeding, with no clinical progress and ongoing abdominal pain, abdominal cramps, and diarrhea. In these patients, the feeding devices were removed after an average feeding period of 81 days (range, 30-148).
Complications
Ten patients had complications related to the tube or tube feeding. These complications include tube dislodgement (6 patients), tube obstruction (2 patients), and wound infection (1 patient). Whereas the wound infection was treated conservatively, tube dislodgement and obstruction required ambulatory endoscopic reintervention. One patient (1.7%) had a major complication: 3 days after DPEJ-tube placement, emergency laparotomy was required because of a colon mesentery injury (Table VII).
Abdominal Pain, GI-Symptoms and Narcotic Use
FIG. 2. Abdominal pain, GI symptoms, and narcotic use over 6 months (% of patients).
TABLE IV
Abdominal pain, GI symptoms, and narcotic use
TABLE V
Type of GI symptoms, type of narcotics
DISCUSSION
Approximately 75% of patients with a chronic underlying gastroenterological disease are reported to have protein-energy malnutrition.21 This number may be higher in patients with CP. In CP, approximately 80% of patients can be managed through dietary recommendations, but approximately 5% to 10% are reported to need parenteral nutrition (PN) or enterai tube feeding during their course of CP.22 In the past, nutrition support in CP was synonymous with PN. However, increased cost, the high rate of septic complications, and other associated morbidities with this route of therapy have led to questions about the overall appropriateness of parenteral nutrition support in CP.23
A favorable impact on patient outcomes with enterai tube feeding compared with PN has been shown in several prospective, randomized controlled trials in a variety of disease processes ranging from trauma and head injury to acute pancreatitis.2 Unfortunately, there are little captured data available regarding the utility of enterai feeding into the jejunum in patients with CP. Currently, the literature is established solely according to case reports.
In our series, small-bowel feeding delivered by PEG/J or DPEJ over an average feeding \time of 113 days (range, 3-180) resulted in a statistically significant (p
FIG. 3. Average patient albumin level over 6 months (G/DL).
It is evident from these data that long-term jejunal feeding in CP significantly increases a patient’s weight and improves their nutritional status. Therefore, this therapy may help to minimize malnutrition-related morbidity and mortality.31 In addition, analysis of plasma albumin levels after 6 months also showed significant improvement from 2.6 g/dL to 3.4 g/dL (p
FIG. 4. Average patient serum amylase over 6 months (IU/L).
Pain in CP is by far the most common and recalcitrant indication for medical treatment. However, pain is difficult to quantify. The assessment of its significance may be clouded by a patient’s addiction to alcohol and narcotic analgesics. The mechanism of pain in CP is incompletely understood and perhaps multifactorial. The view that chronic pain will subside as the disease progresses to the point of organ failure (burnout) has been widely accepted.34 However, that process may take an unpredictable number of years or may never occur. Some studies suggest that the likelihood of spontaneous pain relief is low.35 In addition, our data also suggest that jejunal feeding provides a clinical benefit in terms of reducing abdominal pain and gastrointestinal side effects. Although 96% of patients initially had abdominal pain and 90% had gastrointestinal side effects such as nausea, vomiting, and diarrhea, only 23% reported ongoing abdominal pain after 6 months. Also, the percentage of patients regularly using narcotic drugs dropped to 27%, and the percentage of patients with gastrointestinal side effects declined continuously to 14.6%.
FIG. 5. Average patient serum lipase over 6 months (IU/L).
There are several theories about the etiology of pain in CP. The one likely etiology may be elevated cholecystokinin levels secondary to pancreatic protease deficiency.36,37 Feeding low in the gastrointestinal tract invokes a degree of pancreatic gland stimulation that differs little from parenteral nutrients.38 Decreasing pancreatic stimulation to subclinical levels of secretion is thought to relieve abdominal pain and might explain the reduction in abdominal pain observed during longterm jejunal feeding in our study.39 The benefit of jejunal feeding on gastrointestinal side effects might be further explained by the fact that gastroparesis in small duct pancreatitis is seen in up to 44% of patients, with associated symptoms such as nausea, vomiting, and abdominal pain.4
Patients with CP frequently undergo diagnostic or therapeutic endoscopy of the upper gastrointestinal tract. Small-bowel access for feeding can be easily obtained in almost all cases during such interventions without requiring additional endoscopic interventions. CP often presents with intermittent inflammatory flares, often requiring hospitalization for pain management and rehydration. PEG/ J and DPEJ tubes can also be used as small-bowel decompression devices to reduce abdominal distention, nausea, and vomiting during such acute episodes. NPO periods can therefore be shortened, and oral feeding can often be reinstated earlier, without the need for temporary or long-term TPN.
TABLE VI
Physician visits, rehospitalizations
The answer to the question of whether efficacy of jejunal feeding in CP is affected by the cause of the CP remains speculative. However, in our series all patients (n = 4; 8%) with ongoing weight loss (3.7 kg; range, 2-5.5) had nonalcoholic pancreatitis. The failure of treatment in this group of patients is further underlined by the fact that they also needed a higher number of physician visits (7; range, 1-12) because of abdominal pain and gastrointestinal side effects. The switch to an ED did not influence their poor clinical course.
All patients were initially fed with a SD, which was well tolerated in 86%. Only 4 patients (7%) of 8 (14%) receiving an ED tolerated the ED better than the SD. Therefore, we conclude that small-bowel feeding in CP with a SD is safe, cost efficient, and, in most cases, well tolerated.
According to the literature, between 58% and 67% of patients need surgery during their course of CP.40 In our series with a follow-up period of 180 days, elective surgery was undertaken in 8 patients (14%) with moderate to severe malnutrition (SGA category: 4 patients B and 4 patients C) resistant to dietary recommendations. Before undergoing elective surgery, they received jejunal feeding for an average of 76.8 days (range, 46-111), resulting in an average weight gain of 3.1 kg (range, 2-10). According to our findings, moderately or severely malnourished patients scheduled for major pancreatic surgery may be candidates for longterm jejunal feeding delivered before their operative procedure to reduce malnutrition-associated perioperative risks.41
During the follow-up, the mean number of CP-related emergency physician visits (3.6) and rehospitalizations (1.8) was low compared with our clinical experience with this difficult patient group. The patients treated in this study represent a subgroup of patients with severe CP who had ongoing weight loss or severe malnutrition in spite of the best standard of supportive medical care.
TABLE VII
Complications
In our series, complications related to jejunal feeding were managed by upper gastrointestinal endoscopy (n = 8), conservatively by local wound infection (n = 1), or by emergency laparotomy in a case of abdominal pain with colon mesentery injury (n = 1).
We feel that jejunal access and jejunal feeding in CP can be considered safe, with a major complication rate of approximately around 1.8% and zero mortality in experienced hands.
CONCLUSIONS
After reviewing the findings in this retrospective study, we are convinced that the use of jejunal feeding in patients with chronic, recurrent pancreatitis is an important interventional approach, with evidence for decreasing stimulation and inflammation of the pancreas. There was clear evidence in our study of a decrease in associated clinical symptoms, including weight loss, abdominal pain, nausea, and vomiting. Indirectly, those results are confirmed by the reduction in our patients’ use of narcotics and by the favorable nutrition therapy outcomes, including weight gain, malnutrition rate, and increases in serum albumin levels. In addition, jejunal feeding significantly improves nutritional outcomes in malnourished CP patients.
There are limitations to this study. The major limitations are the retrospective nature of the study and the lack of a control group. A further limitation is the fact that there was no follow-up of the gastrointestinal symptoms, abdominal pain, or anthropomtrie parameters after the feeding tubes were removed. In addition, we have only assessed the abdominal pain as subjective specification and not according to a standardized questionnaire or a systematic objective method such as the visual analog scale.
We are planning to conduct a prospective study that is designed to address these limitations and to define the extent to which long- term enterai tube feeding enhances nutritional status, reduces abdominal pain, gastrointestinal symptoms, and other health care resource use in patients with chronic, recurrent pancreatitis.
REFERENCES
1. Del Prato S, Tiengo A. Pancreatic diabetes. Diabetes Rev. 1993; 1:260-285.
2. Ammann RW, Muellhaupt B. The natural history of pain in alcoholic chronic pancreatitis. Gastroenterology. 1999;116:11321140.
3. Shea JC, Hopper IK, Blanco PG, Freedman SD. Advances in nutritional management of chronic pancreatitis. Curr Gastroenterol Rep. 2000;2:232-236.
4. Chowdhury RS, Forsmark CE, Davis RH, Toskes PP, Verne GN. Prevalence of gastroparesis in patients with small duct chronic pancreatitis. Pancreas. 2003;26:235-238.
5. Hebuterne X, Hastier P, Peroux JL, Zeboudj N, Delmont JP, Rampal P. Resting energy expenditure in patients with alcoholic chronic pancreatitis. Dig Dis Sci. 1996;41:533-539.
6. Twersky Y, Bank S. Nutritional deficiencies in chronic pancreatitis. Gastroenterol Clin North Am. 1989;18:543-565.
7. Prato SD, Tileng A. Diabetes secondary to acquired disease of the pancreas. In: Alberti KGMM, Zimmet P, Defronzo RA, eds. International Textbook of Diabetes Mellitus. 2nd ed. Chichester: John Wiley & Son; 1999:189-212.
8. Scolapio JS, Malhi-Chowla N, Ukleja A. Nutrition supplementation in patients with acute and chronic pancreatitis. Gastroenterol Clin North Am. 1999;28:695-707.
9. Nakamura T, Tando Y, Yamada N, et al. Study on pancreatic insufficiency (chronic pancreatitis) and steatorrhea in Japanese patients with low fat intake. Digestion. 1999;60:93-96.
10. Apte MV, Keogh GW, Wilson JS. Chronic pancreatitis: complications and management. J Clin Gastroenterol. 1999;29:225240.
11. Kondrup J, Rasmussen HH, Hamberg O, Stan\ga Z. Nutritional risk screening (NRS 2002): a new method based on an analysis of controlled clinical trials. Clin Nutr. 2003;22:321-336.
12. Detsky AS, Mc Laughlin JR, Baker JP. What is subjective global assessment of nutritional status? JPEN J Parenter Enteral Nutr. 1987;11:8-13.
13. Kudsk KA, Croce MA, Fabian TC, et al. Enteral versus parenteral feeding: effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg. 1992;215:503-511.
14. DeWitt RC, Kudsk KA. The gut’s role in metabolism, mucosal barrier function, and gut immunology. Infect Dis Clin North Am. 1999;13:465-481.
15. Bodoky G, Harsanyi L, Pap A, Tihanyi T, Flautner L. Effect of enteral nutrition on exocrine pancreatic function. Am J Surg. 1991;161:144-148.
16. McClave SA, Greene LM, Snider HL, et al. Comparison of the safety of early enteral vs parenteral nutrition in mild acute pancreatitis. JPEN J Parenter Enteral Nutr. 1997;21:14-20.
17. Hamvas J, Schwab R, Pap A. Jejunal feeding in chronic pancreatitis with severe necrosis. J Pancreas. 2001;2:112-116.
18. DeLegge MH, Patrick P, Gibbs R. Percutaneous endoscopic gastrojejunostomy with a tapered tip, nonweighted jejunal feeding tube: improved placement success. Am J Gastroenterol. 1996;91: 1130- 1134.
19. Shike M, Berner YN, Gerdes H, et al. Percutaneous endoscopic gastrostomy and jejunostomy for long-term feeding in patients with cancer of the head and neck. Otolaryngol Head Neck Surg. 1989;101:549-554.
20. Varadarajulu S, Delegge MH. Use of a 19-gauge injection needle as a guide for direct percutaneous endoscopic jejunostomy tube placement. Gastrointest Endosc. 2003;57:942-945.
21. Papini-Berto SJ, Dichi JB, Dichi I, Victoria CR, Burini RC. Protein-energy malnutrition as a consequence of the hospitalization of gastroenterologic patients. Arq Gastroenterol. 1997;34: 13-21.
22. Meier R. Nutrition in chronic pancreatitis. In: Buechler M, Friess H, Uhl W, Malfertheiner P, eds. Chronic Pancreatitis. Berlin: Blackwell Science; 2002:421-427.
23. Koretz RL. Nutritional supplementation in the ICU: how critical is nutrition for the critically ill? Am J Respir Crit Care Med. 1995;151:570-573.
24. Charash WE, Kearney PA, Annus KA, et al. Early enteral feeding is associated with attenuation of the acute phase/cytokine response and improved outcome following multiple trauma. J Trauma. 1994;37:1015-1018.
25. Moore FA, Moore EE, Jones TN, McCroskey BL, Peterson VM. TEN versus TPN following major abdominal trauma: reduced septic morbidity. J Trauma. 1989;29:916-923.
26. Moore EE, Jones TN. Benefits of immediate jejunostomy feeding after major abdominal trauma: a prospective, randomized study. J Trauma. 1986;26:874-881.
27. Suchner U, Senftleben U, Eckart T, et al. Enteral versus parenteral nutrition: effects on gastrointestinal function and metabolism. Nutrition. 1996;12:13-22.
28. Young B, Ott L, Twyman D, et al. The effect of nutritional support on outcome from severe head injury. J Neurosurg. 1987; 67:668-676.
29. Windsor AC, Kenwar S, Li AG, et al. Compared with parenteral nutrition, enterai feeding attenuates the acute phase response and improves disease severity in acute pancreatitis. Gut. 1998; 42:431- 435.
30. Kalfarentzos F, Kehagias J, Mead N, Kokkinis K, Gogos CA. Enterai nutrition is superior to parenteral nutrition in severe acute pancreatitis: results of a randomized prospective trial. Br J Surg. 1997;84:1665-1696.
31. Klein S, Kinney J, Jeejeebhoy KJ, et al. Nutrition support in clinical practice: review of published data and recommendations for future research directions: National Institutes of Health, American Society for Parenteral and Enteral Nutrition, and American Society for Clinical Nutrition. JPEN J Parenter Enteral Nutr. 1997;21:133- 156.
32. Grant JR. Nutritional assessment in clinical practice. Nutr Clin Pract. 1986;1:3-11.
33. Fleck A. Acute phase response: implications for nutrition and recovery. Nutrition. 1988;4:109-117.
34. Ammann RW, Akovbiantz A, Largiader F, Schueler G. Course and outcome of chronic pancreatitis. Gastroenterology. 1984;86: 820- 888.
35. Lankisch PG, Seidensticker F, Lohr-Happe A, Otto J, Creutzfeldt W. The course of pain is the same in alcohol- and non alcohol-induced chronic pancreatitis. Pancreas. 1995;10: 338-341.
36. AGA technical review: treatment of pain in chronic pancreatitis. Gastroenterology. 1998;115:765-776.
37. Toskes PP. Update on diagnosis and management of chronic pancreatitis. Curr Gastroenterol Rep. 1999;1:145-153.
38. Corcoy R, Martin-Sanchez J, Domingo P, et al. Nutrition in the patient with severe acute pancreatitis. Nutrition. 1988; 4:269- 275.
39. Helton WS. Intravenous nutrition in patients with acute pancreatitis. In: Rombeau JL, ed. Clinical Nutrition: Parenteral Nutrition. Philadelphia, PA: WB Saunders; 1990:442-461.
40. Levy P, Milan C, Pignon JP, Baetz A, Bernades P. Mortality factors associated with chronic pancreatitis: unidimensional and multidimensional analysis of a medical-surgical series of 240 patients. Gastroenterology. 1989;96:1165-1172.
41. McClave SA, Schnider HL, Spain DA. Preoperative issues in clinical nutrition. Chest. 1999;115(Suppl):64S-70S.
Zeno Stanga, MD*[double dagger]; Urs Giger, MD*[dagger]; Arthur Marx, MD; and Mark H. DeLegge, MD, FACG, CNSP*
From the * Section of Nutrition, Digestive Disease Center, Medical University of South Carolina, Charleston, South Carolina; [dagger] Department of General Surgery, Kantonsspital Fribourg, Fribourg, Switzerland; [double dagger] Division of Endocrinology and Diabetes, University Hospital Bern, Bern, Switzerland; and the Department of Internal Medicine and Social and Preventive Medicine, University of Bern, Bern, Switzerland
Received for publication February 18, 2004.
Accepted for publication October 1, 2004.
Correspondence: Mark H. DeLegge, MD, FACG, CNSP, Section of Nutrition, Digestive Disease Center, Medical University of South Carolina (MUSC), 96 Jonathan Lucas St, Ste 210, Charleston, SC 29425. Electronic mail may be sent to [email protected].
Copyright American Society for Parenteral and Enteral Nutrition Jan/ Feb 2005
Comments