Related Experiment Video
Updated: Aug 9, 2026

Severe Burn Injury in a Swine Model for Clinical Dressing Assessment
Published on: November 6, 2018
Skin necrosis induced by extravasation of glycerol-containing peripheral parenteral nutrition formulation
1School of Pharmacy, University of Mississippi Medical Center, Jackson, USA.
Abstract:
Administration of parenteral nutrition (PN) via a peripheral vein has gained support over the last decade due to serious complications associated with central venous catheterization. Extravasation and tissue necrosis have been reported with both peripheral and central dextrose-containing PN formulations. The following case report represents the first documented case of skin necrosis due to extravasation of a glycerol-containing PN formulation. Our patient's condition resolved with local therapy such as elevation of the affected extremity and cold compresses. Routine evaluation of proper catheter placement is recommended to prevent this serious morbid event, while various treatment recommendations are outlined for severe injuries that do not respond to general measures such as cold compresses.
Related Concept Videos
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become anucleated and die, but their...
Burn Injuries
The damage results in the death of skin cells, which can lead to a massive loss of fluid. Dehydration, electrolyte imbalance, and renal and circulatory failure follow, which can be fatal. Burn patients are treated with intravenous fluids to offset...
Parentral Nutrition: Centeral and Peripheral Parental Nutrition
PN can be administered through two primary routes:
1. Central Parenteral Nutrition (CPN):
CPN involves delivering a high concentration of nutrients through a large vein. This is typically achieved using a Peripherally Inserted Central Catheter (PICC) or,...
Cellular Injury IV: Necrosis
Diabetic Neuropathy
Acute Pancreatitis II: Pathophysiology

