Format

Send to

Choose Destination
Curr Nutr Rep. 2019 Dec;8(4):363-373. doi: 10.1007/s13668-019-00296-y.

Mitochondrial Dysfunction in Critical Illness: Implications for Nutritional Therapy.

Author information

1
Department of Medicine, University of Louisville School of Medicine, Louisville, KY, USA. samcclave@louisville.edu.
2
Division of Gastroenterology, Hepatology & Nutrition, University of Louisville School of Medicine, 550 South Jackson Street, Louisville, KY, 40202, USA. samcclave@louisville.edu.
3
Department of Anesthesiology, Duke University, Durham, NC, USA.
4
Department of Surgery, University of Louisville School of Medicine, Louisville, KY, USA.
5
Department of Intensive Care Medicine, Gelderse Vallei Hospital, Ede, The Netherlands.

Abstract

PURPOSE OF THE REVIEW:

This paper will review the evidence for mitochondrial dysfunction in critical illness, describe the mechanisms which lead to multiple organ failure, and detail the implications of this pathophysiologic process on nutritional therapy.

RECENT FINDINGS:

Mitochondria are particularly sensitive to increased oxidative stress in critical illness. The functional and structural abnormalities which occur in this organelle contribute further to the excessive production of reactive oxygen species and the reduction in generation of adenosine triphosphate (ATP). To reduce metabolic demand, mitochondrial dysfunction develops (a process likened to hibernation), which helps sustain the life of the cell at a cost of organ system failure. Aggressive feeding in the early phases of critical illness might inappropriately increase demand at a time when ATP production is limited, further jeopardizing cell survival and potentiating the processes leading to multiple organ failure. Several potential therapies exist which would promote mitochondrial function in the intensive care setting through support of autophagy, antioxidant defense systems, and the biogenesis and recovery of the organelle itself. Nutritional therapy should supplement micronutrients required in the mitochondrial metabolic pathways and provide reduced delivery of macronutrients through slower advancement of feeding in the early phases of critical illness. A better understanding of mitochondrial dysfunction in the critically ill patient should lead to more innovative therapies in the future.

KEYWORDS:

Critical illness; Mitochondrial failure; Multiple organ failure; Nutritional therapy

PMID:
31713718
DOI:
10.1007/s13668-019-00296-y

Publication type

Publication type

Supplemental Content

Loading ...
Support Center