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Propofol-Related Infusion Syndrome: A Clinical Review

Propofol-related infusion syndrome (PRIS) is a lethal condition characterized by multiple organ system failures. It can occur due to prolonged administration of propofol (an anesthetic) in mechanically intubated patients. The main presenting features of this condition include cardiovascular dysfunct...

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Autores principales: Singh, Aayushi, Anjankar, Ashish P
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9671386/
https://www.ncbi.nlm.nih.gov/pubmed/36407194
http://dx.doi.org/10.7759/cureus.30383
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author Singh, Aayushi
Anjankar, Ashish P
author_facet Singh, Aayushi
Anjankar, Ashish P
author_sort Singh, Aayushi
collection PubMed
description Propofol-related infusion syndrome (PRIS) is a lethal condition characterized by multiple organ system failures. It can occur due to prolonged administration of propofol (an anesthetic) in mechanically intubated patients. The main presenting features of this condition include cardiovascular dysfunction with particular emphasis on impairment of cardiovascular contractility, metabolic acidosis, lactic acidosis, rhabdomyolysis, hyperkalaemia, lipidaemia, hepatomegaly, acute renal failure, and eventually mortality in most cases. The significant risk factors that predispose one to PRIS are: critical illnesses, increased serum catecholamines, steroid therapy, obesity, young age (significantly below three years), depleted carbohydrate stores in the body, increased serum lipids, and most importantly, heavy or extended dosage of propofol. The primary pathophysiology behind PRIS is the disruption of the mitochondrial respiratory chain that causes inhibition of adenosine triphosphate (ATP) synthesis and cellular hypoxia. Further, excess lipolysis of adipose tissue occurs, especially in critically ill patients where the energy source is lipid breakdown instead of carbohydrates. This process generates excess free fatty acids (FFAs) that cannot undergo adequate beta-oxidation. These FFAs contribute to the clinical pathology of PRIS. It requires prompt management as it is a fatal condition. The clinicians must observe the patient's electrocardiogram (ECG), serum creatine kinase, lipase, amylase, lactate, liver enzymes, and myoglobin levels in urine, under propofol sedation. Doctors should immediately stop propofol infusion upon noticing any abnormality in these parameters. The other essentials of management of various manifestations of PRIS will be discussed in this article, along with a detailed explanation of the condition, its risk factors, diagnosis, pathophysiology, and presenting features. This article aims to make clinicians more aware of the occurrence of this syndrome so that better ways to manage and treat this condition can be formulated in the future.
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spelling pubmed-96713862022-11-18 Propofol-Related Infusion Syndrome: A Clinical Review Singh, Aayushi Anjankar, Ashish P Cureus Anesthesiology Propofol-related infusion syndrome (PRIS) is a lethal condition characterized by multiple organ system failures. It can occur due to prolonged administration of propofol (an anesthetic) in mechanically intubated patients. The main presenting features of this condition include cardiovascular dysfunction with particular emphasis on impairment of cardiovascular contractility, metabolic acidosis, lactic acidosis, rhabdomyolysis, hyperkalaemia, lipidaemia, hepatomegaly, acute renal failure, and eventually mortality in most cases. The significant risk factors that predispose one to PRIS are: critical illnesses, increased serum catecholamines, steroid therapy, obesity, young age (significantly below three years), depleted carbohydrate stores in the body, increased serum lipids, and most importantly, heavy or extended dosage of propofol. The primary pathophysiology behind PRIS is the disruption of the mitochondrial respiratory chain that causes inhibition of adenosine triphosphate (ATP) synthesis and cellular hypoxia. Further, excess lipolysis of adipose tissue occurs, especially in critically ill patients where the energy source is lipid breakdown instead of carbohydrates. This process generates excess free fatty acids (FFAs) that cannot undergo adequate beta-oxidation. These FFAs contribute to the clinical pathology of PRIS. It requires prompt management as it is a fatal condition. The clinicians must observe the patient's electrocardiogram (ECG), serum creatine kinase, lipase, amylase, lactate, liver enzymes, and myoglobin levels in urine, under propofol sedation. Doctors should immediately stop propofol infusion upon noticing any abnormality in these parameters. The other essentials of management of various manifestations of PRIS will be discussed in this article, along with a detailed explanation of the condition, its risk factors, diagnosis, pathophysiology, and presenting features. This article aims to make clinicians more aware of the occurrence of this syndrome so that better ways to manage and treat this condition can be formulated in the future. Cureus 2022-10-17 /pmc/articles/PMC9671386/ /pubmed/36407194 http://dx.doi.org/10.7759/cureus.30383 Text en Copyright © 2022, Singh et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Anesthesiology
Singh, Aayushi
Anjankar, Ashish P
Propofol-Related Infusion Syndrome: A Clinical Review
title Propofol-Related Infusion Syndrome: A Clinical Review
title_full Propofol-Related Infusion Syndrome: A Clinical Review
title_fullStr Propofol-Related Infusion Syndrome: A Clinical Review
title_full_unstemmed Propofol-Related Infusion Syndrome: A Clinical Review
title_short Propofol-Related Infusion Syndrome: A Clinical Review
title_sort propofol-related infusion syndrome: a clinical review
topic Anesthesiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9671386/
https://www.ncbi.nlm.nih.gov/pubmed/36407194
http://dx.doi.org/10.7759/cureus.30383
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