Nutrition
support in critical patients: A review of enteral and parenteral nutrition in
patients exhibiting multiple organ dysfunction, hypermetabolism and
hypercatabolism
Caitlin
Swartz
April
30th, 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.