With the increased complexity of managing critically ill patients, it is a valuable exercise to occasionally stop and think about why we use a particular therapy. One such therapeutic intervention is enteral nutrition (EN). Why do we use EN in the intensive care unit (ICU)? Is it to avoid using parenteral nutrition (PN), or is it because there is inherent benefit to EN? Assuming the latter, how do we select an EN product for a critically ill patient? Is it based on cost or on what seems to make sense, or is it based on product-specific data generated in patients similar to the ones we are managing? Providing EN in the early years focused predominantly on delivering adequate calories and protein. EN products have evolved to include more specialized formulations. As more was learned about the altered metabolism seen with organ dysfunction (eg, renal and hepatic) or patient types (eg, diabetic patients and critically ill), newer formulas emerged. Most recently we have EN formulas that contain specific substrates aimed at cellular targets with the potential to alter outcomes. For critically ill patients, these substrate-enriched EN formulas are intended to enhance immune cellularity and function or minimize inflammation. When used this way, for an intended biochemical, physiologic, or clinical outcome, nutrient substrate can be considered pharmacotherapeutic. As such, more questions arise. Which specific patient subgroups benefit from each of the specialized formulations when compared with standard formulations? What therapeutic dose is required for that benefit? When should this specialized intervention be initiated and for how long should it be continued? For specialized EN products that deliver other than the standard macronutrients and micronutrients seen with the first generation products, selection for use should be based on a review of the evidence. In answer to many questions, Russell and Charney provide a superb review in this issue of Nutrition in Clinical Practice on the role of specialized EN formulations in the ICU. They present much of the available evidence and offer clinical suggestions that mostly reflect recent clinical guidelines. Implicit in the article is the extreme heterogeneity of what we refer to collectively as “critically ill patients” whose nutrition support issues are varied. Most of the specialized EN formulas discussed in the review have been administered to patients whether or not they are critically ill. Of particular interest in recent years are the “immune-enhancing” formulations to which I will return to later. Answers to some of the questions posed above are beginning to emerge. The evidence-based scrutiny of PN as a therapeutic modality in recent years is welcome in attempts to define appropriate use. The same analysis is likely to occur for EN. Virtually everyone can agree that while there still remains a role for PN, a functional gastrointestinal (GI) tract in the ICU patient that can be safely accessed should be used for nutrition support (ie, EN) when indicated. There is no question that EN is preferred over PN in practice, with suggestions that EN is better—although for many patient subgroups, this assertion is not yet supported by data. Although access-related complication rates between EN and PN are similar, the therapeutic advantage that may be realized for EN occurs in only a few select patient subgroups, including abdominal trauma. Whether this benefit is due to the route of administration per se, or to the specific substrate by that route is still not entirely clear. Although PN may not necessarily result in the gross mucosal atrophy or bacterial translocation seen in animal models, there seems to be an advantage from the substrate provided through EN products. The presumption of EN s benefit, particularly for critically ill patients, revolves around GI tract function in health and disease. The GI tract serves a central role as both an endocrine and immune organ. That role includes an adaptive (or maladaptive) physiology involved in the injury response of critically ill patients. This is apparent through the influences of gut-associated lymphoid tissue, gut perfusion, the enteral nervous system, and nutrient availability to the intestinal mucosa. Maintaining adequate barrier function to prevent infection or inflammation requires sufficient Correspondence: Joseph Boullata, PharmD, BCNSP, Associate Professor of Pharmacy Practice, Temple University School of Pharmacy, 3307 North Broad St., Philadelphia, PA 19140.
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Apr 3, 2009
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Open Access