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Related Concept Videos

Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Chronic Pancreatitis I: Introduction01:24

Chronic Pancreatitis I: Introduction

The pancreas, an elongated and flat gland situated behind the stomach, serves a vital function in digesting food and managing blood sugar levels.
Pancreatitis is the inflammation of the pancreas, which occurs when the immune system becomes active and causes swelling, pain, and disruptions in organ function. Pancreatitis can manifest as either an acute or chronic condition.
Acute pancreatitis arises suddenly and lasts for a brief duration, while chronic pancreatitis is a long-term affliction...
Acute Pancreatitis II: Clinical Manifestations and Management01:30

Acute Pancreatitis II: Clinical Manifestations and Management

Acute pancreatitis presents a complex medical emergency characterized by rapid onset inflammation of the pancreas, demanding timely diagnosis and management to prevent complications. The condition primarily manifests through severe upper abdominal pain that often radiates to the back. This pain intensifies following the consumption of fatty foods. Accompanying symptoms such as nausea, vomiting, abdominal distention, fever, dyspnea, cyanosis, and jaundice can vary in intensity but significantly...
Acute Pancreatitis I: Introduction01:25

Acute Pancreatitis I: Introduction

Acute pancreatitis is the sudden inflammation of the pancreas caused by the early activation of digestive enzymes, leading to the autodigestion of pancreatic tissue. This results in local inflammation and, in severe cases, systemic complications.EtiologyUnderstanding the underlying causes is crucial, as identifying the etiology guides treatment and anticipates complications. Acute pancreatitis can be triggered by various factors, typically grouped into the following clinical categories.Biliary...

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Updated: Jun 14, 2026

Robotic Enucleation of an Intra-Pancreatic Insulinoma in the Pancreatic Head
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Published on: January 3, 2020

Walled-off pancreatic necrosis.

Michael Stamatakos1, Charikleia Stefanaki, Konstantinos Kontzoglou

  • 14th Department of Surgery, Medical School, University of Athens, Attikon Hospital, Athens, 12462, Greece. stamatakosmih@yahoo.gr

World Journal of Gastroenterology
|April 10, 2010
PubMed
Summary

Walled-off pancreatic necrosis (WOPN) is a rare but lethal complication of acute pancreatitis. Current strategies combine antibiotics with delayed, restricted surgical intervention for better outcomes.

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Retroperitoneal Laparoscopic Debridement and Drainage for Pancreatic Abscess
03:42

Retroperitoneal Laparoscopic Debridement and Drainage for Pancreatic Abscess

Published on: March 15, 2024

Area of Science:

  • Gastroenterology
  • Surgical Pathology

Background:

  • Walled-off pancreatic necrosis (WOPN), previously termed pancreatic abscess, is a severe late complication of acute pancreatitis.
  • While rare, WOPN can be fatal, necessitating a thorough understanding of its management.

Purpose of the Study:

  • To provide a comprehensive review of current knowledge regarding Walled-off pancreatic necrosis.
  • To analyze evolving treatment strategies for WOPN based on recent medical literature.

Main Methods:

  • Critical review of data from Medline and PubMed up to September 2009.
  • Utilized keywords including WOPN, pancreatic abscess, acute necrotizing pancreatitis (ANP), and pancreatitis complications.

Main Results:

  • WOPN develops over 4 weeks after acute necrotizing pancreatitis (ANP), often following pseudocysts.
  • Mortality for WOPN is generally lower than for infected pancreatic necrosis.
  • Percutaneous drainage and ERCP show encouraging results, complementing antibiotics and restricted surgery.

Conclusions:

  • Optimal WOPN management involves early antibiotics and delayed, selective surgical intervention.
  • Minimally invasive techniques like percutaneous drainage and ERCP are valuable in WOPN treatment.
  • This approach reduces the need for early surgery in ANP patients, improving outcomes.