Arginine Immunonutrition in Critically Ill Patients: A Clinical Dilemma

Joyce K. Stechmiller, PhD, ARNP; Beverly Childress, MSN; Tricia Porter, BSN


Am J Crit Care. 2004;13(1) 

In This Article

Immune Response in Critical Illness

Mediators of shock and inflammation known as cytokines are important in the pathogenesis of critical illness.[47] Two cytokines, tumor necrosis factor α (TNF-α) and IL-1, are produced by macrophages and are considered the main mediators of shock, sepsis, and multiple organ failure syndrome.[47] Macrophages are triggered to produce TNF-α by a variety of inflammatory stimuli, including bacteria and other cytokines. TNF-α has many functions: It stimulates white blood cells to release IL-1, IL-6, IL-8, platelet activating factor, leukotrienes, thromboxanes, and prostaglandins. It also stimulates the production and activity of polymorphonuclear leukocytes and promotes adhesion of immune cells to the endothelium. It activates the coagulation and complement systems. It depresses myocardial contractility, and it stimulates fever production by the hypothalamus.[47] As these observations suggest, any interventions that stimulate the synthesis or activity of mediators such as TNF-α and IL-1 can exacerbate the pathogenesis of shock and sepsis and thus should be avoided.[47]

Systemic inflammatoryresponse syndrome (SIRS) is an abnormal host response characterized by generalized inflammation caused by infectious or noninfectious entities. SIRS is defined by the presence of 2 or more of the following: (1) body temperature greater than 38 C or less than 36 C (2) heart rate greater than 90/min; (3) respirations greater than 20/min or PaCO2 less than 32 mm Hg, and (4) white blood cell count greater than 12 x 109/L, less than 4 x 109/L, or more than 0.10 band cells.[48] These signs provide a framework for assessing the cellular and immunologic mechanisms that cause sepsis and organ dysfunction.[47]

Multiple organ failure syndrome is defined as the progressive failure of 2 or more organ systems associated with a hypermetabolic systemic inflammatorystate. The syndrome is preceded by a variety of events, including shock, sepsis, hemorrhage, burns, trauma, ischemia, pancreatitis, and major surgery. The systemic response to shock follows a sequential course once initiated. A relative state of stability lasting 48 to 72 hours is followed by a state of hypermetabolism that typically peaks in 3 to 4 days and resolves in 2 weeks. However, often the initial response may lead to a progressive series of complications resulting in a persistent state of hypermetabolism and the development of multiple organ system failure, which is now the leading cause of death in patients with sepsis, trauma, and burns.[47]


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