Page 438 - Small Animal Clinical Nutrition 5th Edition

452 Small Animal Clinical Nutrition

as neuronal dysfunction, neuronal death or cerebral infarction cations. Intracellular tight junctions maintain the intestinal
VetBooks.ir (Gandhi et al, 2007). In contrast, partial or complete cessation epithelial barrier. Formation of dysfunctional tight junctions
after stressful events such as surgery, contribute to postsurgical
of nutrition has been identified to be one of the major risk fac-
complications and delayed recovery (Bouritius et al, 2008).
tors for developing hypoglycemia (Elia and De Silva, 2008). A
low-carbohydrate food can amplify the onset of the hypo- Adequate intestinal blood flow along with the mononuclear
glycemic state, particularly in small-breed dogs. phagocytic system, located predominately in the liver, work in
Diarrhea appears to be a common problem in critically ill tandem to protect against bacterial translocation. Studies have
patients during refeeding. Malabsorption of dietary carbohy- indicated that glucose supplementation increases intestinal
drate or fat, hyperosmolar formulas (generally high carbohy- blood flow and that hepatic glycogen content contributes to
drate content), and feeding high volumes of enteral fluid have increased survival rate by maintaining the liver system.
all been reported as causal factors (Mutlu et al, 2001). Com- Clinically these findings were substantiated when rats receiving
plications of diarrhea include effects on hydration, acid/base a carbohydrate drink consisting of glucose, maltose and poly-
status, mineral balance, contamination of wounds, decreased saccharides (12 g carbohydrate/100 ml) for six days before
colonic fermentation and reduced butyric acid production major abdominal surgery retained intestinal barrier function
(Thaklar et al, 2005; Kien et al, 1999). Traditional attempts to and were protected from translocation of bacteria to distant
minimize the osmotic diarrhea, believed due to carbohydrate organs compared to cohorts not fed carbohydrates (Bouritius et
malabsorption, have focused on limiting the dietary carbohy- al, 2008). Based on these studies, dietary carbohydrates main-
drate intake (Kein et al, 2004). Small intestinal carbohydrate tain the mucosal barrier, hasten tissue healing, minimize com-
malabsorption (breath H ) and colonic fermentation, stool vol- plications and shorten hospital stays.
2
ume and total enteral fluid volume were measured in burn The dietary carbohydrate level in the initial refeeding of
patients receiving a high carbohydrate (Vivonex TEN) enteral critically ill patients should be based on patient assessment
food over a four-week period. Although all patients had diar- and timing. Dampening the body’s natural response of hyper-
rhea over several weeks, the lack of correlation of either carbo- glycemia to illness/stress may not be as beneficial as previous-
hydrate intake or breath H with stool volume suggested diar- ly thought; carbohydrates in various forms have metabolic and
2
rhea was due to factors other than carbohydrate malabsorption physiologic value to patients. Conversely, promotion of a
(Thaklar et al, 2005). Notwithstanding, prevention and possi- severe hyperglycemic state in these patients is contraindicated
bly treatment of osmotic diarrhea has been addressed by deliv- to recovery. On average, “recovery” type foods provide 2 to 4
ery of lower osmolarity nutrient solutions. g carbohydrate/100 kcal, with increased fat and/or protein
The value of dietary carbohydrate in maintaining an ade- content; this appears to be a safe starting point for refeeding.
quate and healthy population of gut microbiota cannot be Then, consider transitioning to a higher carbohydrate food (6
overlooked.The intestinal microflora has been proposed as an to 10 g/100 kcal) and evaluating the insoluble carbohydrate
environmental factor responsible for control of body weight (fiber) source three to four days into the refeeding process,
and energy metabolism. Fermentation of non-digestible based on patient reassessment.
dietary fiber (insoluble carbohydrate) and resistant starches
(oligosaccharides) along with numerous other mechanisms Protein
are linked to the health of gut microflora and energy metab- Protein in the body is always in flux between synthesis and
olism.The major part of the microbiota is present in the colon breakdown. Protein synthesis requires that amino acids be pres-
where food products have escaped digestion, so the biologic ent within cells at the correct time and ratio so that a protein
functions controlled by this microflora seem to relate to effec- may be constructed successfully. Protein degradation involves
tiveness of bacteria to harvest energy that has been ingested, the release of amino acids, and if the amino acid is deaminated,
but not digested, by the patient. Human and rodent studies the ketoacid analog is converted to glucose or fat and the amino
similarly conclude that microbiota can extract energy from group enters the hepatic urea cycle and is ultimately excreted in
non-digestible carbohydrate based on species (Turnbaugh et the urine. Under most circumstances, about 15% of the RER
al, 2006; Ley et al, 2006), suggesting a benefit of providing comes from the oxidation of amino acids (Kinney, 1988).
adequate insoluble carbohydrate in the diet of critically ill Providing a dietary protein source to patients in catabolic states
patients. Additionally, fructooligosaccharides taken in the diet spares endogenous skeletal muscle protein and supplies essen-
(5 to 20 g/day) improved mucosal barrier function, improved tial amino acids and amino groups for acute-phase proteins and
glucose tolerance and insulin homeostasis in human patients the immune response. Excessive dietary protein should be
and rodents (Cani and Delzenne, 2007). Another study fur- avoided in patients with kidney or liver disease (Chapters 37
ther highlights the value of resistant starches and dietary fiber and 68). However, high dietary protein intakes are handled well
as sources of short-chain fatty acids in critically ill/injured by most canine and feline critical care patients to replace dietary
patients. Increased short-chain fatty acids, in particular carbohydrate when carbohydrates are not well tolerated.
butyrate, significantly enhanced colonic anastomosis healing Protein administration should complement nonprotein calo-
and increased intestinal bursting pressure postoperatively in ries because amino acids will be oxidized for energy when a
rats (Campos et al, 2008). patient’s total energy need has not been met first. Sufficient
Perioperative carbohydrates minimize postoperative compli- calories must be available from fat and/or glucose before ingest-