The Evolution of Nutrition in Different Phases of Critical Illness

Abstract

Survival is only the first part of the battle that confronts critically ill patients. There is increased recognition that loss of skeletal muscle mass and muscle weakness in the ICU is an enormous issue for patients and the whole healthcare system. Using the theoretical construct of allostasis, critical illness can be understood as consisting of 4 distinct stages: acute critical illness (ACI), prolonged acute critical illness (PACI), Chronic critical illness (CCI), and recovery from critical illness (RCI) . Each of these stages has a unique pathophysiological state with metabolic targets, interventions, and end points. Acute critical illness is initiated following a physiologic insult to homeostasis, The mediators of allostasis are responsible for the “stress response,” and they include hormones of the hypothalamic-pituitary-adrenal (HPA) axis, catecholamines, cytokines, glucagon, growth hormone (GH), and vasopressin. Organs and processes that are not immediately necessary for survival are suppressed, while critical ones are enhanced . In PACI, the allostatic load still present and inflammation fails to down-regulate, even in the absence of the initial insult. Features of PACI can be recognized after approximately 3-10 days of ACI and reflect a dramatic change in neuroendocrine physiology. CCI commences at the time of tracheotomy, which is typically performed after 10–14 days of ventilator dependence, signifying the ICU team's subjective view that the patient will not die or be weaned from the ventilator in the near future. CCI is an allostatic overload state . The RCI stage begins with liberation from mechanical ventilation and can follow ACI, PACI, or CCI, with a gradual shift from catabolism to anabolism, reflected by an overt rise in serum albumin and prealbumin (primarily due to down-regulation of inflammation) and decrease in the urinary urea nitrogen (UUN) excretion rate. Therapeutic efforts are focused on building lean mass with increased provision of nutrition and use of anabolic agents if needed. The basic evolutionary reason for feeding the ill or injured patient is to prevent loss of body mass and provide essential nutrients for basic biologic function. For ICU patients with a stay of 24 to 48 hours, our short-term protein and lean body mass stores are probably sufficient. However, patients that stay 3 to 7 days may lose large amounts of protein. This loss is due to muscle disuse, stress/cortisol-induced catabolism, insulin resistance, and other metabolic changes. For long-stay patients, perhaps more than 7 to 10 days , cumulative energy and protein balance may become quite severe and have been shown to effect morbidity and mortality . The acute phase may be a period when a reducednonprotein-calorie, high-protein delivery (1.5 to 2.0 g/kg/day) may be optimal. In the chronic phase of critical illness (CCI), energy expenditure as measured by calorimetry increases significantly and thus increased non protein calories should be delivered and sufficient protein (1.5 to 2.0 g/kg/day) should continue to be given. In this phase, administration of glutamine has been shown to reduce mortality in critically patients. In the recovery phase, when C-reactive protein and other markers of inflammation are often much decreased, continued protein and calories are required to continue the recovery of lean body mass and physical function required for independent living and quality of life. In this period, perhaps stronger consideration should be given to anabolic agents .