Purpose of review Assess current potential catabolism-biomarkers to characterize patients developing prolonged critical illness.
Recent findingsA raised urea-to-creatinine ratio (UCR) during critical illness is negatively associated with muscle mass with greater increases in UCR seen patients developing persistent critical illness. Similarly, sarcopenia index (a ratio of creatinine to cystatin-c concentrations) correlates well to muscle mass in intensive care populations. Elevated growth/differentiation factor-15 (GDF-15) has been inconsistently associated with muscle loss. Although GDF-15 was a poor marker of feeding tolerance, it has been associated with worse prognosis in intensive care.
SummaryUCR is an available and clinically applicable biomarker of catabolism. Similarly, sarcopenia index can be used to assess muscle mass and indirectly measure catabolism based on readily available biochemical measurements. The utility of novel biomarkers, such as GDF-15 is less established.
Metabolic dysfunction, and its associated muscle atrophy, remains the most common complication of critical care. At the center of this is mitochondrial dysfunction, secondary to hypoxia and systemic inflammation. This leads to a bioenergetic crisis, with decreased intramuscular adenosine triphosphate content and a reduction in the highly energy‐dependent process of protein synthesis. Numerous methods have been studied to try and reduce these effects, with only limited success. Trials investigating the use of increased energy and protein administration have instead found a decrease in relative lean body mass and a potential increase in morbidity and mortality. Ketone bodies have been proposed as alternative substrates for metabolism in critical illness, with promising results seen in animal models. They are currently being investigated in critical care patients in the Alternative Substrates in the Critically Ill Subjects trial (ASICS). The evidence to date suggests that individualized feeding regimens may be key in the nutrition approach to critical illness. Consideration of individual patient factors will need to be combined with personalized protein content, total energy load received, and the timing of such feeds. This review covers mitochondrial dysfunction in critical illness, how it contributes to muscle wasting and the resultant morbidity and mortality, and the scientific basis of why current nutrition approaches to date have not been successful in negating this effect. These two factors underpin the need for consideration of alternative nutrition strategies in the critically ill patient.
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