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| CASE REPORT |
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| Year : 2014 | Volume
: 4
| Issue : 3 | Page : 185-187 |
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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 2021 Sep 22];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
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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
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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.
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[Figure 1], [Figure 2]
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