Related Experiment Video
Updated: Jul 17, 2026

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
Published on: April 1, 2022
[Artificial nutrition and acute pancreatitis: a review and update]
E Gento Peña1, E Martín de la Torre, A Miján de la Torre
1Servicio de Aparato Digestivo Complejo Asistencial de Burgos, Facultad de Medicina, Universidad de Valladolid.
Abstract:
Most of acute pancreatitis cases present as mild cases for which nutritional support is not recommended provided the patient is able to restart normal oral intake within 5- days. By contrast, severe pancreatitis associates metabolic stress and requires early nutritional support. In these cases, enteral nutrition is recommended, which should be supplemented with parenteral nutrition if needed. Recent studies indicate that enteral nutrition may improve the course of severe acute pancreatitis, reduce its complications and promote a quicker improvement from the disease. Most of the patients tolerate oligomeric nutrition administered as continuous infusion distally to the Treitz' s angle. Recent studies show, however, that intragastric perfusion is safe and may be an adequate therapeutic option in particular patients with acute severe pancreatitis. Besides, specific agents added to the nutrition (immunomodulators and probiotics) seem to reduce hospital stay and infectious and non-infectious complications of acute pancreatitis.
Related Concept Videos
Acute Pancreatitis II: Clinical Manifestations and Management
Acute Pancreatitis I: Introduction
Acute Pancreatitis I: Introduction
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
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Assessment:
Acute Pancreatitis II: Pathophysiology
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