Energy Requirement and Consumption in the Critically Ill Patient

Metabolic Response to Critical Illness

In 1932 Cuthbertson was the first to describe the metabolic response to traumatic injury. Later, he divided the response to such injury into two distinct phases. Characteristics of these phases are listed in Table 72.1 . The short-lived “ebb,” or hypometabolic, phase immediately after injury is manifested clinically by cold, clammy extremities and a thready pulse. After adequate resuscitation, the patient warms up and cardiac output increases. The flow, or hypermetabolic, phase is characterized by a rise in energy expenditure that peaks at 5% to 60% above normal, depending on the magnitude of the injury. The duration of this phase depends on the severity of injury and the development of complications. Profound metabolic changes occur during this phase, and the increased oxygen consumption supports these interorgan substrate exchanges.

Metabolism in serious sepsis is similar to that of major traumatic injury. A systemic inflammatory response is induced in patients with sepsis as well as in patients with major traumatic injury, and the two groups of patients also experience similar metabolic sequelae. This generalized response is evident in patients with major burn injury, who may exhibit oxygen consumption rates far in excess of those seen in patients with severe sepsis and major trauma. A high percentage of patients with so-called systemic inflammatory response syndrome (SIRS) develop dysfunction of one or more organ systems. A major cause of acute renal failure in critically ill patients is SIRS with associated organ dysfunction. The hypermetabolism associated with sepsis and the inflammatory response is shown in Fig. 72.1 for patients with and without acute renal failure. These data, derived from Uehara et al., illustrate the similarity in response for both groups of patients, peaking approximately 10 days after admission to an intensive care unit (ICU). The onset of SIRS is the predominant determinant of the degree of hypermetabolism, whereas the development of organ failure portends a prolonged hyperdynamic phase.

Reprioritization of the normal nutritional homeostasis of the body occurs in response to the hypermetabolism and catabolism of the systemic inflammatory response. Marked alterations in carbohydrate, fat, and protein metabolism occur (see Chapter 135, Chapter 136, Chapter 138 ). Hyperglycemia, hypertriglyceridemia, high lactate levels, and high free fatty acid concentrations are characteristic of the critically ill patient and indicate major derangements in intermediary metabolism. Optimal nutritional management of these patients requires an understanding of fuel utilization and the control of energy balance in the flow phase of critical illness.