Nutrition support in critical patients: A review of enteral and parenteral nutrition in patients exhibiting multiple organ dysfunction, hypermetabolism and hypercatabolism

Caitlin Swartz

April 30^th, 2014

Introduction

Nutrition support for critically ill patients encompasses both enteral and parenteral feeding in order to aide in patient survival following life threatening events. Nutrition support is generally practiced by a team of registered dietitian nutritionists, intensive care physicians, nurses, and pharmacists (Association of Parenteral and Enteral Support (A.S.P.E.N), 2014).  Nutrition support practitioners maintain a Nutrition Support Certification through the National Board for Nutrition Support Certification.

Enteral nutrition (EN) is broadly defined as any form of feeding where nutrients pass through the gastrointestinal (GI) system (A.S.P.E.N, 2014). EN in the focus of nutrition support uses catheters to bypass certain areas on the GI system. Nasogastric catheters are inserted in to the stomach via the nasal passages. This form of EN is preferable because it is associated with the lowest risk of complications in addition to using the greatest portion of the GI tract (Mosier, Pham, Klein, Gibran, Arnoldo, Gamelli, Tompkins, & Herndon, 2011). Complications from nasogastric catheters are limited to localized irritation and accidental aspiration that occasionally leads to pneumonia. Jejunostomy is a catheter that is placed directly in to the small intestine via an access point on the patient’s abdomen (A.S.P.E.N, 2014). Bowel strangulation, physical obstruction of blood flow to the bowel caused by the catheter wrapping around the bowel (Merck Manual, 2014), is a rare, but serious complication of jejunostomies (Gerristen, Besselink, Cieslak, Vriens, Steenhagen, van Hillegersberg, Borel Rinkes, & Molenaar, 2012). Complications from EN are generally in the form of intestinal regurgitation resulting from gastroparesis or paralytic ileus. Though, this complication can be avoided with early onset EN (Dissanaike, Pham, Shalhub, Warner, Hennessy, Moore, Maier, O’Keefe, & Cushieri, 2008).

Parenteral nutrition (PN) support is the extraintestinal insertion of a catheter in to a vein (A.S.P.E.N, 2014). A solution of substrates ie. simple carbohydrates, amino acids, short chain fatty acids, vitamins, and minerals is supplied directly to the bloodstream. The use of total parenteral nutrition (TPN) is indicated in patients who cannot tolerate EN. A combination of PN and EN can be used in patients who cannot reach a neutral or positive energy balance via EN alone (Thibault, Pichard, Wernerman, & Bendjelid, 2010).  PN is associated with serious complications including: gut atrophy, sepsis, electrolyte imbalances, hyperglycemia, overfeeding, uremia, metabolic acidosis, and immunosuppression (Varga, Griffiths, Chiolero, Nitenberg, Leverve, Pertkiewicz, Roth, Wernerman, Pichard, & Preiser, 2006). The risks associated with PN outweigh the risks associated with fasting and starvation in cases with a short duration. Therefore, ASPEN recommends delaying PN until eight days following the patient’s admission to the intensive care unit (ICU) (Cove & Pinskey, 2011). Furthermore, EN is always preferred over PN in patients who can tolerate GI feeding (Varga et al., 2006).

The purpose of this paper is to explain the need for nutrition support in ICUs by examining the pathology of multiple organ dysfunction syndrome (MODS), hypermetabolism, and hypercatabolism in patients suffering from severe burns, heart and respiratory failure requiring the use of extracorporeal therapy, and following trauma and major surgery.

Multiple Organ Dysfunction Syndrome Pathology

            There are several factors contributing to the small intestine’s role in MODS. In critically ill patients, the mucosa of the in small intestine begins to atrophy as a result of fasting. In non-critical individuals, the brush boarder secrets intestinal alkaline phosphatase (IAP). IAP neutralizes bacterial lipopolysaccharide (LPS). LPS is an endotoxin which harms human cells. As the mucosa deteriorates in fasting patients, the brush boarder does not regenerate. The excess LPS initiates an immune response from the complement system. Macrophages secret inflammatory interleukins 1 and 6, and tumor necrosis factor alpha. This cytokine action increases GI permeability.

Increased GI permeability leads to bacterial translocation, the movement of normal intestinal bacteria to surrounding sterile mesenteric organs (Berg, 1999). The mesenteric organs include the liver, kidneys, spleen, and mesenteric lymph node complex (MLNC). The liver and MLNC spread bacteria throughout the circulatory system resulting in sepsis.

The small intestine contains the highest concentration of immune tissue relative to the rest of the system. As the GI undergoes atrophy, the immune tissue does not regenerate. This results in an overall decrease in immune function. The patient experiences a decrease in the ability to fight the systemic infection due to a decrease in immunoglobin A secretion.

Finally, during times of metabolic stress, the body adapts by redirecting blood flow to the vital organs including the brain, heart, and lungs. This redirection of blood flow results in bowel ischemia.

EN prevents the initial bowel atrophy by providing activity for intestinal muscles.