|
 |
| CASE REPORT |
|
| Year : 2014 | Volume
: 4
| Issue : 3 | Page : 185-187 |
|
Acute necrotizing pancreatitis: Worthy impact of total parenteral nutrition on the disease progression
Raksha Goyal1, Rakesh Shivhare2, Manish Khasgiwale2, Sanjay Dhanuka3, Rekha Jamdagni2, Vishwesh Mehta3
1 Department of Dietetics, Synergy Hospital, Indore, Madhya Pradesh, India
2 Department of Gastroenterology, Synergy Hospital, Indore, Madhya Pradesh, India
3 Department of Critical Care, Synergy Hospital, Indore, Madhya Pradesh, India
| Date of Submission | 30-Dec-2013 |
| Date of Acceptance | 11-Feb-2014 |
| Date of Web Publication | 16-May-2014 |
Correspondence Address:
Raksha Goyal
Scheme No. 74 C, Sector B, Vijay Nagar, Indore 452 010, Madhya Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/2231-0738.132679
 Abstract | | |
We report the case of a 23-year-old male with severe acute pancreatitis. In this case report we discuss the desirable effects of parenteral nutrition and the importance of nutritional support at patients with severe necrotizing pancreatitis. Severe acute pancreatitis is usually accompanied by systemic inflammatory response syndrome which results in hypermetabolism with prominent protein catabolism. Providing nutrition to these patients is of paramount importance. An adequate nutritional support is crucial in patients with severe and complicated pancreatitis. Keywords: Acute necrotizing pancreatitis, hyper catabolism, hypermetabolism, parenteral nutrition
How to cite this article:
Goyal R, Shivhare R, Khasgiwale M, Dhanuka S, Jamdagni R, Mehta V. Acute necrotizing pancreatitis: Worthy impact of total parenteral nutrition on the disease progression. Int J Nutr Pharmacol Neurol Dis 2014;4:185-7 |
How to cite this URL:
Goyal R, Shivhare R, Khasgiwale M, Dhanuka S, Jamdagni R, Mehta V. Acute necrotizing pancreatitis: Worthy impact of total parenteral nutrition on the disease progression. Int J Nutr Pharmacol Neurol Dis [serial online] 2014 [cited 2022 May 16];4:185-7. Available from: https://www.ijnpnd.com/text.asp?2014/4/3/185/132679 |
| Introduction | |  |
The Atlanta Conference [1] in 1992 defined pancreatic necrosis as diffuse or focal area (s) of nonviable pancreatic parenchyma typically associated with peripancreatic fat necrosis. The necrosis is either sterile or infected depending on the presence of infection.
Acute pancreatitis occurs in different clinical patterns ranging from a mild and mostly self-limiting to severe necrotizing disease with local and systemic complications. [2] Specific and nonspecific metabolic changes occur during acute pancreatitis. A variety of proinflammatory cytokines increase the basal metabolic rate. [3],[4] Severe acute pancreatitis is a very catabolic state, with 80% of patients exhibiting increased energy expenditure and accelerated protein catabolism. [5],[6]
Patients with acute pancreatitis are at risk for malnutrition due to hypermetabolism and increased catabolism associated with acute pancreatitis. Those with acute pancreatitis may be unable to eat for a prolonged period of time because of abdominal pain, nausea, and vomiting that are exacerbated upon eating. [4] Malnutrition can worsen, or if not already present, develop due to the increased catabolism. [6],[7] Nutritional support in severe necrotizing pancreatitis is essential because these patients develop rapidly nutritional deficiencies. A prolonged negative nitrogen balance determines negative clinical outcome. [5],[8]
| Case report | | |
A 23-year-old male diagnosed as acute necrotizing pancreatitis 5 days back was referred to our hospital with the symptoms of abdominal pain, anorexia, nausea, vomiting, and fever 101°C.
According to contrast-enhanced computed tomography (CECT) scan, the patient had moderate hepatomegaly, mild splenomegaly, bulk pancreatic with multiple necrotic area within it associated with extensive peripancreatic inflammatory changes with moderate peripancreatic fluid collection, mild ascites, retroperitoneal intraperitoneal inflammation changes, bilateral pleural effusion, and acute necrotizing pancreatitis [Figure 1]. The Ranson's score was 5 and Acute Physiology and Chronic Health Evaluation II (APACHE II) score was 21. | Figure 1: Computed tomography (CT) scan of acute necrotizing pancreatitis showing near total necrosis with bleed in necrotic area
Click here to view |
The patient was shifted to intensive care unit (ICU), put on ventilator support, and managed as per the protocol. A nasogastric tube was inserted for enteral feeding with semi elemental substitutes. However, enteral feeding became difficult in view of continuous distension of the abdomen and high gastric residual volume, so the patient was placed on the total parenteral nutrition (TPN). He was on hemodialysis due to decreased urine output. He slowly weaned off the ventilator support and initially treated symptomatically to avoid early surgical intervention as per the protocols. He was shifted to ward in the stable condition and enteral nutrition was gradually increased.
After 18 days of hospitalization, he suddenly developed abdomen distension and hypotension in ward; so, immediately shifted to ICU for management. Elective exploratory laparotomy necrosectomy was done after a CT scan abdomen with angio. After 3 days of exploratory laparotomy he developed distension of abdomen, hence reexploration with removal of pad was done [Figure 2]. Patient still did not tolerate the enteral nutrition, hence managed on TPN. | Figure 2: Postoperative CT scan of acute necrotizing pancreatitis showing no bleed in necrotic area
Click here to view |
Patient started continuous enteral nutrition via a jejunal tube with semi-elemental diet along with TPN. As he tolerated the feed, quantity had been increased up to 2.5-3 l and simultaneously decreased the TPN and shifted to ward in stable condition. Gradually patient had been started oral diet with semi-elemental and medium chain triglyceride (MCT) supplements. After 10 weeks of hospitalization, he lost about 15% of his weight (9 kg). After 70 days of hospitalization, the clinical situation was good and the patient was discharged.
| Discussion | | |
Between 10 and 20% of patients with acute pancreatitis developed severe pancreatitis with associated necrosis. This complication produces mortality rates of 10-25%. [9] Mortality increases to 40-70% when infection develops, requiring surgical debridement and prolonged medical and surgical management. [9]
For nutritional support, it is therefore necessary to assess the severity of acute pancreatitis and the nutritional status at the time of admission and during the course of the disease. Both factors are necessary to plan nutrition interventions in patients with acute pancreatitis. This patient had severe acute pancreatitis, which worsened, so we established a plan for nutritional support.
Patients with severe acute pancreatitis are hypermetabolic. There is increased protein catabolism, characterized by an inability of exogenous glucose to inhibit gluconeogenesis, increased energy expenditure, increased insulin resistance, and increased dependence on fatty acid oxidation to provide energy substrates. [10] The more severe acute pancreatitis is, the more excessive is hypermetabolism. If the disease is complicated by sepsis or multiorgan failure, the resting energy expenditure (REE) is significantly increased. These patients have increased nutrient requirement because of increased rate of REE and protein breakdown. A negative nitrogen balance has been associated with an adverse clinical outcome.
In patients with severe necrotizing pancreatitis, the full amount of nutrient delivery by the enteral route is not always possible. Complications of acute pancreatitis such as persisting ileus, large pseudocysts, intestinal and pancreatic fistula, intestinal edema, retroperitoneal edema, pancreatic ascites, pancreatic or peripancreatic collections, and infected necrosis may sometimes make enteral feeding difficult to conduct and tolerate, and parenteral nutrition should be instituted along with appropriate treatment for these conditions. [11] Usually, the combined nutritional support allows that the patient reach the nutritional goals. Our patient had initially some of the complications mentioned above. These complications made impossible the administration of enteral nutrition, so the patient was placed on TPN. Eighty percent of patients with severe necrotizing pancreatitis are over catabolic and everyday lose more than 40 g of proteins which give negative balance and is adverse to the disease recovery. [12],[13] Therefore, nutrition support must be guaranteed; if not in time, denutrition will get the condition worse. [13]
| Conclusion | | |
In conclusion we can say that despite of the severity of the disease, nutrition support is expected to positively affect the course of the disease and improves the outcome. In severe acute pancreatitis, evaluation of body's metabolism should be the first consideration and then gradually combined treatment of parenteral nutrition with enteral nutrition should be used as routine therapy. This cannot only improve the natural history of pancreatitis, but also can reduce the incidence of complication and mortality. Any nutritional therapy for patient admitted for severe acute pancreatitis is better than no nutritional support.
| References | | |
| 1. | Washington W Jr, Allen S, Janda W, Koneman E, Procop G, Shrecksenberger P, et al. In: Koneman's Color Atlas and Textbook of Diagnostic Microbiology. 6 th ed. Philadelphia: Lipincott Williams and Wilkins; 2006. p. 909-23. 
|
| 2. | Banks PA, Freeman ML. Practice Parameters Committee of the American College of Gastroenterology. Practice guidelines in acute pancreatitis. Am J Gastroenterol 2006;101:2379-400.
|
| 3. | Meier R, Sobotka L. Nutritional support in acute and chronic pancreatitis. In: Sobotka L, Allison S, Forbes A, Ljungqvist O, Meier R, Pertkiewicz, et al., editors. Basics in clinical nutrition. 4 th ed. Prague: Galen; 2011. p. 494-508.
|
| 4. | Borto D. Acute and chronic pancreatitis. In: Annalynn S, editor. Dietitian's Handbook of Enteral and Parenteral Nutrition. 3 rd ed. Sudbury: Jones and Bartlett Publishers; 2011. p. 134-44.
|
| 5. | Meier R, Ockenga J, Pertikiewicz M, Pap A, Milinic N, MacFie J, et al. ESPEN guidelines on enteral nutrition; Pancreas. Clin Nutr 2006;25:275-84.
|
| 6. | Dickerson RN, Vehe KL, Mullen JL, Feurer ID. Resting energy expenditure in patients with pancreatitis. Crit Care Med 1991;19:48490.
|
| 7. | Bouffard YH, Delafosse BX, Annat GJ, Viale JP, Bertrand OM, Motin JP, et al. Energy expenditure during severe acute pancreatitis. J Paren Enteral Nutr 1989;13:26-9.
|
| 8. | Sitzmann JV, Steinborn PA, Zinner MJ, Cameron JL. Total parenteral nutrition and alternate energy substrates in treatment of severe acute pancreatitis. Surg Gynecol Obstet 1989;168:311-7.
|
| 9. | Greenberger NJ, Toskes PP. Acute and chronic pancreatitis. In: Kasper DL, et al., editors. Harrison's Principles of Internal Medicine. 16 th ed. New York: McGraw-Hill; 2005. p. 1895-906.
|
| 10. | Whitcomb DC. Clinical practice: Acute pancreatitis. N Engl J Med 2006;354:2142-50.
|
| 11. | Dellinger RP, Levy MM, Carlet JM, Bion J, Parker MM, Jaeschke R, et al., International Surviving Sepsis Campaign Guidelines Committee, American Association of Critical-Care Nurses, American College of Chest Physicians, American College of Emergency Physicians, Canadian Critical Care Society, European Society of Clinical Microbiology and Infectious Diseases, et al. Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008;36:296-327.
|
| 12. | Meier RF, Beglinger C. Nutrition in pancreatic diseases. Best Pract Res Clin Gastroenterol 2006;20:507-29.
|
| 13. | O'Keefe SJ, McClave SA. Feeding the injured pancreas. Gastroenterology 2005;129:1129-30.
|
[Figure 1], [Figure 2]
|
