Manipulations of the Metabolic Response for Management of Patients with Severe Surgical Illness: Review

Abstract

The metabolic response to severe surgical illness is complex and varied. Much recent laboratory and clinical research has focused on increasing our understanding of the metabolic response and the development of new therapies designed to modify this response. Antiinflammatory agents can target harmful aspects of the metabolic response; the immune system can be stimulated; and anabolic factors can be used in an attempt to enhance recovery. The nutritional support of the surgical patient remains crucial, but the effects of new additives are being studied in a variety of surgical conditions. As yet, few of these "novel" agents have found an established role in the management of surgical patients. This review focuses on many "novel" agents or those that do not yet have a clearly defined role in surgical illness. Clinical trials in the areas of severe sepsis, major surgical trauma, and major elective surgery have been emphasized.

Cytokine Removal with High Cut-Off Membrane: Review of Literature

“…A number of attempts have been made in the past to attenuate the clinical expression of the dysregulation through the suppression of specific mediators implicated in either inflammatory or anti-inflammatory pathways [5]. However, those efforts failed to produce required clinical improvement due to the redundant and pleiotropic effects of the cytokines.…”

Overview of Modern Management of Patients with Critical Injury and Severe Sepsis

“…Much subsequent work has confirmed these findings. Similar protein loss (10 -15% of body protein) occurs under conditions of negative or positive energy balance [7] and in patients treated with modifiers tested to date, including antitumor necrosis factor (anti-TNF) monoclonal antibody in sepsis patients [17] and glutamine supplementation in trauma patients [28]. As this represents a loss of "the structural and functional components of the body, such erosion must be coupled with loss of function" [11].…”

Na+‐dependent Neutral Amino Acid Transporter ASCT2 Is Downregulated in Seriously Traumatized Human Intestinal Epithelial Cells

“…Actually, some metabolic responses such as obligate skeletal muscle proteolysis and resultant negative nitrogen balance are responsible for these clinical signs (2). Any agents and methods are broadly designed to either block the harmful effects of the metabolic response or promote beneficial processes such as boosting the immune system or stimulating protein synthesis (3). Clinically, nutrition support has been an important component of the care of traumatized patients who are unable to accept complete volitional nutrition.…”