Page 431 - Small Animal Clinical Nutrition 5th Edition
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Enteral-Assisted Feeding      445


                  and are more dependent on proteolysis than are patients that  cial to the patient because it ensures an energy source in the
        VetBooks.ir  are simply food deprived.The hypermetabolic state that results  face of hypoperfusion or poorly perfused organs (Daley and
                                                                      Bistrian, 1994). General feelings of malaise and anorexia sig-
                  from illness and anorexia is generated by general neuroen-
                                                                      nal the patient to reduce activity of skeletal muscle and signal
                  docrine responses and local mediators common to stressful
                  stimuli. The specific hormonal and subsequent physiologic  the GI tract to conserve energy for essential tissue mainte-
                  changes that occur in a stressed patient are unique to that dis-  nance and repair. Although in the short-term, hyperglycemia
                  ease condition, the time course of the disease process and other  appears to benefit the patient, maintaining this state is not
                  complicating diseases or conditions. The metabolic responses  conducive to recovery. Thus, the acute phase is characterized
                  have best been characterized in conditions with a known acute  by decreased exogenous nutrients in the face of increased
                  onset such as trauma or infection (sepsis) (Cuthbertson, 1979).  energy demands (hypermetabolic state) and a net negative
                  The response has been described as having an acute (ebb) phase  energy balance. Breakdown or catabolism of protein and fat
                  followed by an adaptive (flow) phase (Popp and Brennan,  stores is necessary to address this imbalance between expen-
                  1983).These phases can vary in duration and intensity depend-  diture and intake.
                  ing on the severity of the condition. Duration is usually short-  This catabolic phase will continue until the neuroendocrine
                  er with trauma as compared to infection during which the acute  stimuli and cytokine mediators are removed. During severe
                  phase remains until the infection has been eliminated.  head trauma, burns, multiple trauma and sepsis, lean tissue loss
                    The acute phase is characterized by catabolism and general-  and overall body weight loss are rapid and unremitting in the
                  ly occurs within the first 24 to 72 hours. As mentioned, the  absence of feeding. It is difficult to reverse the ongoing catabo-
                  hypermetabolic state that occurs results from a milieu of neu-  lism and achieve nitrogen balance in patients with these injuries
                  roendocrine and locally activated mediators stimulated by the  and conditions. The goal in providing nutrition to these
                  sympathetic nervous system as part of the stress response. As in  patients is to feed the catabolism with exogenous sources of
                  simple starvation, glucose use is somewhat reserved; however,  protein and fat while sparing endogenous sources. The latter is
                  part of this reservation is by consequence of increased cortisol  critical because loss of 25 to 30% of body protein stores has
                  levels  perpetuating insulin resistance and hyperglycemia.  been associated with reduced heart muscle mass and function,
                  Simultaneous sympathetic nervous system stimulation and  decreased pulmonary function, diminished respiratory drive,
                  release of catecholamines, cortisol, adrenocorticoids, glucagon,  compromised immune function and therefore mortality
                  growth hormone and antidiuretic hormone induce metabolic  (Matthews and Fong, 1993).
                  and physiologic responses including:                  There is a definite turning point in which clinicians note a
                    • Insulin antagonism leading to insulin resistance.  subjective improvement in their patients. This noted improve-
                    • Hyperglycemia from glycogenolysis and gluconeogenesis,  ment is associated with the adaptive phase in which net
                     which provides an energy source for the “fight or flight”  anabolism occurs. The adaptive phase is characterized by
                     phenomenon.                                      increased metabolic rate, nitrogen gain and normal body tem-
                    • Increased lipolysis to provide fatty acids and glycerol for  perature and may last for several days, weeks or years (Daley and
                     glucose and energy production.                   Bistrian, 1994). The convalescent anabolic phase rebuilds dam-
                    • Increased proteolysis and net protein catabolism from albu-  aged and catabolized lean tissue and therefore requires exoge-
                     min and skeletal muscle sources to supply gluconeogenic  nous energy and protein sources. RQ values determined in rest-
                     amino acids for glucose production and hepatic and  ing postoperative and severely traumatized dogs were 0.76, indi-
                     immune cell proteins.                            cating that fat was the preferred energy fuel, while dietary pro-
                    • Increased rate and depth of respiration and increased cardiac  tein is used for anabolic processes (Walton et al, 1996).
                     work to maintain perfusion to muscles and wound sites.  In the catabolic and adaptive phases, fat and protein will
                    These responses are amplified in infection in which a toxic  more effectively address nutrient needs of the patient.
                  response results from invasive organisms and resorption of  Therefore, provision of dietary carbohydrates should be mini-
                  necrotic tissue. The amplification is caused by release of chem-  mized, whereas fat and protein calories are maximized in
                  ical mediators and lysosomal enzymes including histamine,  refeeding formulas (provided there is no contraindication).
                  kinins, prostaglandins, cytokines and serotonin. Interleukin-1  Increased food carbohydrate fractions may lead to electrolyte
                  induces fever, which increases energy expenditure 10 to 13%  disturbances and hyperglycemia, though the latter happens
                  per degree Celsius increase in body temperature. Endotoxins  rarely in dogs. Cats, however, have very low glucokinase activi-
                  released from dying gram-negative bacteria trigger coagulation  ty and cannot effectively transport glucose into hepatic cells
                  cascades that profoundly affect carbohydrate metabolism and  given high intravenous and occasionally high enteral concen-
                  cytokines stimulate production of hepatic acute-phase proteins.  trations (Table 25-2). Subsequently, hyperglycemia is a com-
                  The net result is a hypermetabolic state with increased energy  monly observed phenomenon during refeeding of cats.
                  requirements that if not met, result in catabolism of endoge-  Additionally, specific disease states will affect the type and/or
                  nous fat and protein stores.                        degree of metabolic and hormonal alterations in the patient,
                    In the acute phase, glucose is the preferred fuel; however,  which subsequently influence substrate usage. In consideration
                  muscles are insulin resistant and hyperglycemia is maintained  of these factors, the recovery phase is patient dependent, which
                  for net immune and hepatic tissue anabolism. This is benefi-  underscores the need for continual and consistent reassessment
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