Specialized Nutrition in Critically Ill Patients

Sherry A. Brown, PharmD, BCPS


November 30, 2001

In This Article


Free radicals are highly reactive chemical species capable of independent existence that possess 1 or more unpaired electrons in the outer orbit that is responsible for cellular injury. According to Lingtak-Neander Chan, PharmD, BCNSP, Clinical Assistant Professor, College of Pharmacy and Medicine, University of Illinois, Chicago,[10] these free radicals are produced in septic patients via 3 distinct mechanisms: the production of proinflammatory mediators, neutrophil activation, and ischemic-reperfusion injury. Antioxidants are compounds that can be used to prevent free radical-induced oxidative damage by either preventing the generation of free radicals or by intercepting radicals already in existence. A study performed by Dasgupta and colleagues[11] showed that the total antioxidant capacity was significantly lower in critically ill patients when compared with controls. Furthermore, a study performed by Alonso de Vaga and associates[12] demonstrated that nonsurvivors in an intensive care unit had lower total antioxidant capacity when compared with survivors. This is thought to be due to an increase in the production of free radicals by neutrophils, stated Dr. Chan. When looking at the different antioxidant concentrations in plasma, dramatic decreases in alpha-tocopherol, beta-carotene, ascorbate, and selenium were seen in critically ill patients.[13,14,15] Therefore, not only do these patients have total antioxidant capacity depletion, but specific antioxidant levels are diminished.

Selenium, an intracellular cation, is a cofactor for the production of glutathione peroxidase, which acts as a coenzyme in several oxidation-reduction reactions. Selenium-dependent glutathione peroxidase is one of the main scavenger systems responsible for the cleavage of free radicals. Several variables such as albumin, prealbumin, and cholesterol may affect selenium concentrations in the critically ill population. Dr. Chan noted that during acute phase response, serum protein drops, causing a huge shift in transitional cations. Therefore, selenium levels decline during critical illness. Angstwurm and colleagues[16] conducted a controlled, prospective, open-label pilot study involving 42 septic patients who were randomized to either a standard, low dose of selenium or varying, high doses of selenium therapy. Patients treated with the higher doses of selenium therapy had a significantly improved APACHE III score and a decreased need for continuous veno-venous hemodialysis due to acute renal failure. Also, there was a trend toward a reduction in mortality seen in patients treated with higher doses of selenium compared with patients treated with low-dose selenium, 33.5% vs 52%; P = .13, respectively. These data look promising for the use of selenium supplementation in critically ill patients; however, larger studies are needed to specifically address this question.

As mentioned previously, the inflammatory response to critical illness leads to massive production of free radicals. Additionally, we see a significant decrease in the antioxidant levels in these patients. A study performed by Preiser and colleagues[17] randomized 37 critically ill patients to receive either vitamin A, C, and E-enriched enteral feeding or standard enteral therapy. Patients in the enriched enteral therapy group demonstrated significantly higher plasma levels of beta-carotene and alpha tocopherol, with no difference seen between the 2 groups with regard to vitamin A plasma levels. The study also looked at the clinical outcomes of infection, length of intensive care unit stay, and mortality, and found no significant differences between the 2 groups. However, there was a trend toward worse outcomes with the use of the enriched enteral feed formula. According to Dr. Chan, we do not have enough evidence to conclude that antioxidant/vitamin supplementation is improving outcomes in our patients.


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