Patients of any age may become malnourished from inadequate nutrient intake while in our care.
Malnutrition is not fully appreciated by most clinicians because it does not appear as a number on your laboratory data or physical exam. Hospitalized veterinary patients are more commonly malnourished due to a decreased total food intake.
The major consequences of malnutrition in sick or injured patients are decreased immunocompetence, decreased tissue synthesis and repair and altered drug metabolism. You can help heal the patient by feeding it.
The reciprocal relationship between nutrition and immunity has been recog-nized for centuries. A malnourished animal is more susceptible to infections, and a septic patient is more likely to be anorectic, which results in malnutrition.
Nutrient imbalances suppress immune function, which increases the risk of disease; conversely, certain diseases alter some nutrient requirements. Protein and (or) calorie malnutrition causes progressively poor responses in several components of the immune system, including significantly impaired cell-mediated responses, secretory IgA production, phagocytosis, complement function, antibody affinity and cytokine production.
Studies have shown that protein deficiencies that limit amino acid and nucleotide substrates for cell proliferation result in reduced numbers of circulating T lymphocytes, helper and suppressor cells.
Malnutrition also decreases immune function of existing cells through reduced complement secretions, less effective macrophage function and decreased killer-cell activity. Cytokine production and release are independently impaired in protein-calorie malnutrition.
The good news is that numbers of T4 helper cells and T8 cytotoxic suppressor cells in malnourished patients return to normal quickly with refeeding. Immunoglobulins and circulating antibodies are maintained at relatively low levels during malnutrition, but are highly responsive to appropriate refeeding stimuli.
Tissue synthesis and repair
Local tissue synthesis and wound healing depend on whole body nutrition. On the cellular level, amino acids and carbohydrates are needed for collagen and ground-substance synthesis. Fibroblasts require energy to synthesize the RNA, DNA and ATP necessary for protein anabolism. Migration of fibroblasts, epithelial and endothelial cells also requires energy.
The liver requires energy and protein specifically for synthesis of fibro-nectin, complement and glucose. The bone marrow requires nutrients for production of platelets, leukocytes and monocytes. On the organ level, transportation of these necessary components, plus oxygen to wound sites, require the muscular activities of respiration and cardiac work.
Tissue trauma and healing alter the normal cycle of protein turnover (synthesis and degradation) in the body. Protein turnover in perioperatively fed people had a 91 percent increase in protein synthesis with only a 10 percent increase in protein degradation (net gain), while perioperatively starved people had only a 50 percent increase in protein synthesis with a 79 percent increase in protein degradation (net loss).
Cellular activities are dependent upon, and regulated by, the coordinated actions of peptides, lipids, vita-mins and minerals as substrates, enzymes, coenzymes and cofactors of intermediary metabolism.
In short, all nutrients are essential for the maintenance of normal cellular structure and function.
Nutrient deprivation alters the normal metabolic synergy responsible for ion gradients, membrane potentials, production of high-energy phosphate compounds and antioxidant defenses. Protein-calorie deficiencies result in decreased:
1) hepatic biotransformation of certain antibiotics
2) concentrations of serum proteins that bind and transport drugs throughout the body
3) renal blood flow, which decreases the rate of drug elimination, increasing the possibility of drug toxicity.
Therefore, protein-calorie malnutrition may alter the normal or expected metabolism of certain drugs, which may in turn increase or decrease their therapeutic effect even when given at recommended dosages.
Animals receiving sufficient calories and protein are expected to have better, or near normal, drug distribution, meta-bolism and elimination than animals with protein-calorie malnutrition.
Patients with disease have decreased metabolic rates and therefore energy requirements less than those of comparable healthy individuals. Hospitalized veterinary patients are assumed to be similar to ill people and their daily energy requirements (DER) are very near their resting energy requirements (RER).
Results of a few preliminary respiration calorimetry measurements in dogs with specific disease conditions support the idea because most had 24-hour energy requirements near RER. Hospitalized veterinary patients should be fed at their calculated RER, realizing their actual energy requirement is likely to increase with recovery. Therefore, initially feeding patients at RER, or at least 50 percent of RER, is a rational, safe recommendation that decreases the probability of metabolic and surgical complications.
There are exceptions when the caloric requirement will be greater than RER. For example, according to indirect respiration calorimetry, people with severe closed-head and brain injury have energy requirements 40 percent to 60 percent above their calculated RER.
Brain injury apparently increases oxygen consumption and acute-phase protein synthesis, which increase patients' caloric and protein requirements significantly above RER. Energy requirements of twice RER appear to be the upper limit in the most severe head injuries.
Energy expenditure may be 30 percent to 50 percent above RER in patients with multisystem trauma.
Severely burned patients also have energy and protein requirements 80 percent to 100 percent above RER, relative to the extent of skin damage and surface area exposed because the body loses heat, moisture and proteins through wounds that have little or no epithelial covering.
Hence, severely traumatized patients' actual metabolic rate is related to the degree of trauma and can only be approximated in a clinical setting. These are rare cases, whereas the majority of hospitalized veterinary patients can be safely fed at RER.
Protein in the body is always in a flux between synthesis and breakdown. Protein synthesis requires that amino acids be present within cells at the correct time and ratio so that a protein may be constructed successfully. Protein degradation involves the release of amino acids, and if the amino acid is deaminated, the ketoacid analog is converted to glucose or fat for energy and the amino group enters the hepatic urea cycle and is ultimately excreted in the urine.
Dietary protein provided to animals in catabolic states spares the breakdown of skeletal muscle protein and supplies essential amino acids for acute-phase protein synthesis and a robust immune response.
Protein administration should complement the calorie intake because amino acids will be oxidized for energy when and if the patient's total energy need has not been first met with fat or glucose. Sufficient calories must be available from fat and/or glucose before amino acids will be used for tissue synthesis and repair.
On the other hand, excessive protein feeding requires energy expenditure to rid the body of the excess nitrogen, which, in certain patients, may not be handled well by the liver (urea cycle) and kidneys. The result may be hyper-ammonemia with accompanying clinical signs of encephalopathy.
Commercial products intended for enteral support of critically ill patients provide between 5.5 g and 14.3 g protein/100 kcal. Due to a lack of evidence to the contrary and because these products appear to work well in canine and feline patients, a range of 5.5 g to 9.0 g protein/100 kcal is recommended for foods for canine patients and 7.5 g to 9.0 g protein/100 kcal is recommended for foods for feline patients.
Because of the overlap of these recommendations, several commercial products intended for nutritional support are designated for use in both dogs and cats (e.g., Canine/Feline CliniCare by Abbott).
Arginine has a marked immuno-preserving effect in the face of immunosuppression induced by protein malnutrition and cancer. In postsurgical patients, arginine supplementation enhances T-lymphocyte response and augments T-helper cell numbers, with a rapid return to normal T-cell function postoperatively, compared with controls.
These findings suggest that arginine supplementation may increase or preserve immune function in high-risk surgical patients and theo-retically enhance their capacity to resist infection. Numerous studies in a variety of animal models demon-strated the efficacy of arginine-supplemented foods in reducing the catabolic response to major trauma and sepsis and injury. Arginine is an essential amino acid in dogs and cats. Therefore, most pet foods meeting AAFCO nutrient concentrations will contain arginine.
Glutamine is another hot-topic amino acid that plays an important role in many cellular processes but has been considered a nonessential amino acid in dogs and cats. However, studies suggest that glutamine concentrations in whole blood and skeletal muscle decrease following injury and other catabolic states, thus making it "conditionally" essential.
Replicating cells such as fibroblasts, lymphocytes and intestinal epithelial cells consume primarily glutamine after injury. These findings may be important for patients with large wounds or inflammation associated with infection. There is considerable evidence that glutamine is important in stimulating immune function, possibly through an effect on gut-associated lymphoid tissue or through stimulation of macrophage function. At least 80 percent of the published data in animals demonstrate a positive effect with glutamine-enriched feedings because it is the preferred fuel for rapidly dividing tissues such as white blood cells and intestinal mucosa.
Most diets contain some protein-bound glutamine, and some even have free glutamine added. The glutamine content often is stated on the label although the optimal concentration of glutamine for different disease states is still uncertain.
Subclinical malnutrition in people is associated with prolonged ventilatory dependence and increased complication rates, with longer hospital stays and higher associated costs. Similarly in veterinary patients, protein-calorie malnutrition is thought to increase morbidity and mortality.
In summary, diseased and debilitated patients require nutrients daily to maintain optimal immune function, tissue synthesis and repair, and drug metabolism.
The patient that has not consumed its minimum daily caloric need (resting energy requirements RER) is subclinically malnourished and is drawing on skeletal muscle for protein.
On a cellular level, the starved patient's ability to have a competent immune response, repair tissue and metabolize medications as expected is decreased.
Surely every clinician strives to provide their patients the best possible chance of recovery. Hence, feeding your patient early (rather than waiting until it goes home) will significantly improve the odds that the pet will go home.