Metabolism of Proteins and Amino Acids in Critical Illness: From Physiological Alterations to Relevant Clinical Practice

Abstract

The clinical impact of nutrition therapy in critically ill patients has been known for years, and relevant guidelines regarding nutrition therapy have emphasized the importance of proteins. During critical illness, such as sepsis or the state following major surgery, major trauma, or major burn injury, patients suffer from a high degree of stress/inflammation, and during this time, metabolism deviates from homeostasis. The increased degradation of endogenous proteins in response to stress hormones is among the most important events in the acute phase of critical illness. Currently published evidence suggests that adequate protein supplementation might improve the clinical outcomes of critically ill patients. The role of sufficient protein supplementation may even surpass that of caloric supplementation. In this review, we focus on relevant physiological alterations in critical illness, the effects of critical illness on protein metabolism, nutrition therapy in clinical practice, and the function of specific amino acids.

Energy requirements for critically ill patients with COVID‐19

“…These changes include growth hormone resistance, increased levels of glucagon and cortisol, decreased levels of insulin and testosterone, and sympathetic‐induced release of catecholamines, all of which contribute to a net catabolic state. 16 , 20 , 21 …”

“… 20 There are high‐circulating levels of glucagon and catecholamines and a high rate of endogenous energy production primarily via catecholamine‐induced glycogenolysis. 21 After the early acute phase, the patient transitions to a late acute phase (traditionally referred to as the “flow” phase), which may last up to 7 days. 21 The late acute phase is characterized as a hypermetabolic state with increased VO 2 and increased cardiac output.…”

“… 21 After the early acute phase, the patient transitions to a late acute phase (traditionally referred to as the “flow” phase), which may last up to 7 days. 21 The late acute phase is characterized as a hypermetabolic state with increased VO 2 and increased cardiac output. 20 A higher severity of illness is associated with a greater increase in energy expenditure.…”

“…The early acute phase (traditionally referred to as the “ebb” phase) lasts roughly 24–48 h and is characterized as a relatively hypometabolic state with decreased VO 2 and decreased cardiac output 20 . There are high‐circulating levels of glucagon and catecholamines and a high rate of endogenous energy production primarily via catecholamine‐induced glycogenolysis 21 . After the early acute phase, the patient transitions to a late acute phase (traditionally referred to as the “flow” phase), which may last up to 7 days 21 .…”

“…These changes include growth hormone resistance, increased levels of glucagon and cortisol, decreased levels of insulin and testosterone, and sympathetic-induced release of catecholamines, all of which contribute to a net catabolic state. 16,20,21 The metabolic response to critical illness is characterized by an early acute phase followed by a late acute phase. 11 The early acute phase (traditionally referred to as the "ebb" phase) lasts roughly 24-48 h and is characterized as a relatively hypometabolic state with decreased VO 2 and decreased cardiac output.…”