Nutritional Support


Nutritional Support



Much of the application of nutritional principles comes from provision of essential nutrients in support of animal maintenance and productive functions (see Chapter 9). It is assumed that sufficient supply and appropriate balance of all essential nutrients will provide some level of disease prevention, or the converse, imbalance in nutrient delivery results in specific disease conditions (see Chapter 13).1,2 Although specialized nutritional supplementation methods in support of sick animals have been known for over 30 years, practical application has only recently been incorporated into veterinary practice beyond referral institutions. Llamas and alpacas are predisposed to hepatic lipidosis and hypoalbuminemia secondary to a range of disease conditions.3,4 Any llama or alpaca presenting with reduced feed intake (i.e., hyporexia) broaching on anorexia (e.g., absence of feed intake) is a good candidate to receive supportive nutrition. Camelid anatomy and unique glucose metabolism provide some challenges in directly applying commonly used enteral and parenteral supportive methods for other species. This chapter will address the role and methods of supportive nutrition, either delivered enteral or parenteral, on disease mitigation and recovery in llamas and alpacas.



Role of Supportive Nutrition in Disease


The physiologic ebb and flow metabolic response to disease or traumatic insult is well recognized in human and veterinary medicine.57 Immediately following an insult, the body responds by reducing the blood flow and slowing the metabolism (shock response) in an effort to “minimize the damage.” Following this response, the body initiates the flow phase as part of the recovery response. Recovery is characterized by a state of hypermetabolism proportional to the severity of the insult in an effort to repair the body from the disease state.78 Although this metabolic response targets a recovery process, it may become exaggerated and place the animal at high risk for malnutrition and deleterious health consequences. The animal’s nutritional status prior to the insult greatly influences case outcome, so nutritional intervention strategies should be guided by the interactions among insult severity, animal nutritional status, and ability to consume and assimilate nutrient sources.



Characterizing the Hypermetabolic State


In response to traumatic or thermal injuries, sepsis, or other inflammatory insults, the body’s physiologic response is to stimulate a state of hypermetabolism in an effort to recover and repair tissue damage. The hypermetabolic response to disease (e.g., stressed starvation) is quite different from the metabolic response in healthy animals (adapted starvation) to inadequate nutrition (Table 33-1).5,6 In both situations, glucose is preferentially metabolized initially to support energy needs, with rapid depletion of hepatic glycogen reserves in the face of inadequate energy intake. Body protein, primarily skeletal muscle, is degraded to release amino acids in providing substrate for hepatic gluconeogenesis. In adapted starvation, energy metabolism ultimately switches from glucose to fatty acids and ketone bodies as fuel resources in all but obligate glucose-utilizing tissues. The basal metabolic rate (BMR) is lowered and the rate of gluconeogenesis is slowed dramatically to conserve body protein. These adaptive responses are specifically directed to minimize body protein wastage.8



In contrast to these survival adaptations, the hypermetabolic state is differentially characterized by increased metabolic rate fueled predominately by glucose via continued gluconeogenesis from mobilized amino acids.9 Increased protein degradation, coupled with moderately decreased protein synthesis, culminates in extensive skeletal myofibril degradation.7,10 Increased energy metabolism is sustained in an effort to support tissue repair, immune function, and inflammatory responses at the expense of body protein wastage. Although insulin, glucagon, catecholamines, and glucocorticoids are the primary regulatory hormones controlling metabolic adaptations in both instances, hypermetabolism is uniquely characterized by high concentrations of inflammatory cytokines (e.g., Interleukin (IL)-1, IL-6, tumor necrosis factor alpha [TNF-α]), which promote this metabolic dysfunction of exaggerated proteolysis and increased basal metabolic rate.7,10 Insulin resistance relative to control over gluconeogenesis is suggested by the lack of responsiveness to insulin or glucose infusions, yet tissue glucose utilization is near maximum.8 Fatty acids are readily oxidized, but body fat mobilization is limited as a result of a hyperglycemia-induced state of hyperinsulinemia. Affected animals may effectively retain body fat deposits at the expense of lean body loss. Although the role of increased inflammatory mediators is well recognized as part of the exaggerated hypermetabolic response, the exact mechanism is not understood and most likely is not a consequence of a single mediator.5,8



Consequences of Hypermetabolism


The primary goal of the hypermetabolic response is to provide substrate in support of the reparative process. The hypermetabolic state provides substrate to increase body temperature in an effort to combat pathogens. For every 1°C increase in body temperature, the BMR is increased by 10% to 15%.9 Mobilization of amino acids from body protein provides not only substrate for the gluconeogenic process but also amino acids for hepatic acute phase protein synthesis and for tissue repair. Additional amino acids may be made available to the liver from decreased synthesis of constitutive proteins (e.g., albumin, retinol-binding protein, apoproteins). Laboratory findings of hyperglycemia, hyperlactatemia, hypoalbuminemia, and azotemia are indicators of these metabolic adaptations. Collectively, these responses help support the body’s immune response to the insult, as evidenced by observed leukocytosis and increased mediators of the inflammatory process.


Although the hypermetabolic response is to facilitate recovery, the response is graded along a continuum and may become detrimental if prolonged or exaggerated. Severity of the hypermetabolic state is proportional to the insult and coupled with the stress hormonal milieu as influenced by local and systemic inflammatory mediator and growth factor responses.8,9 With increased energy expenditure, body fuel resources are diminished. Mobilization of body protein results in varying degrees of muscle weakness, fatigue, and atrophy.7,10 Secondary complications of respiratory distress and thromboembolic risks may manifest following muscle demise. As body protein degradation continues, the state of malnutrition ensures that those tissues dependent on active protein synthesis are most severely affected. As a consequence, wound healing, immune response, and integrity of the intestinal mucosal barrier may be compromised. Failure of the mucosal barrier results in bacterial translocation from the gut lumen to the vascular space, which leads to bacterial septicemia. Multiple organ failure and death are the most common sequelae to septicemia in such compromised patients.5



Clinical Assessment for Nutritional Support


Any camelid presenting with inadequate nutritional status or potential for continued compromise in nutrient intake or assimilation should be considered for nutritional support. The goal for nutritional support is to minimize development of malnutrition from hypermetabolism and to provide key substrates in support of nutrient deficiencies and tissue repair. A primary goal is to maintain nitrogen balance in the patient. This may be particularly important in camelids given the unique arrangement of their metabolism. A key issue is determining which patients would best respond to nutritional support. It must be remembered that nutritional support does have potential risk for complications, especially in severely compromised patients, though the best opportunity for benefit in these patients also exists. Additionally, it should be recognized that mitigating any current disease process is far more important than nutritional support in correcting the underlying problem of malnutrition.11 The key factors to assess in determining the appropriate candidate to receive nutritional support are discussed below.



History and Signalment of Problem


The duration and severity of the insult should be considered relative to the initiation of nutritional support, primarily in assessing the length of time the animal has not consumed food and the potential for ongoing nutrient losses. Large open wounds or effusive disease with continuous drainage increase protein losses above and beyond those from hypermetabolism. Anorexia for more than 5 to 7 days in adult animals or 1 to 2 days in neonatal animals would warrant initiation of support. The extent of any preexisting conditions such as cardiac, renal, or hepatic disease that may affect nutritional support decisions must be determined. Animals should be cardiovascularly stable before enteral support is initiated, as the gut may be poorly perfused in lieu of perfusion to other essential organs. Underlying issues of dehydration, acid–base deficits, and electrolyte imbalances need to be evaluated and addressed independent of nutritional support. Historical information should be used to assess potential changes in body weight or body condition score (BCS) over time prior to presentation. The history should also ascertain the current physiologic state of the patient as it would relate to ongoing nutrient requirements.



Determination of Intake Ability


The patient’s ability to consume food determines the appropriate method of nutritional support. If the underlying problem impairs the animal’s ability to chew or swallow, enteral support options may be limited to tube feeding. Camelids are obligate nasal breathers and are highly stressed with orogastric tube placement, thus potentially limiting the extent to which enteral support may be used. Disease conditions of the mandible or the maxilla, fractures, tooth abscesses, inflammatory conditions of the mouth or pharynx, and neurologic conditions may impede the animal’s ability to chew and swallow food. These processes may also impede the camelid’s ability to regurgitate and remasticate C1 contents. Renal or hepatic failure may diminish the animal’s desire to eat.




Nutritional Status


Methods to assess nutritional status of an individual are detailed elsewhere (see Chapter 12). Readily available objective measures of body composition and energy expenditure are not currently available in veterinary medicine. The simplest measure of nutritional status is a current body weight and some assessment of body weight change over time. Greater than 10% unintentional body weight loss over a period of days to weeks would be of concern in camelids. A study showed that feed-restricted llamas that lost 15% to 20% of body weight over a 1- to 2-week period were more predisposed to hepatic lipidosis.13 Lactating females may lose upward of 20% of body weight over the first month of milk production. Neonates losing greater than 5% body weight should be evaluated for nutritional support. The BCS may be used to assess degree of fat reserves as well as body protein, although current systems have not been validated relative to protein changes per unit of BCS. Lower body condition scores (<3 on a 1-to-5 scale) indicate lower subcutaneous body fat deposits but also suggest a loss in skeletal muscle mass as bony processes become more evident. These changes may be seen by using ultrasonographic measures of fat and muscle thickness.


Additional subjective criteria in assessing nutritional status might include a poor-quality hair coat or unexplained fleece loss in camelids. Indications of poor wound healing may also suggest an inadequate nutritional state.


Beyond physical measures of nutritional status, blood analyte concentrations or other blood parameters may be used for secondary assessment of nutritive status. Hypoalbuminemia (<2.0 grams per deciliter [g/dL]) is often considered an indicator of malnutrition, although this often may result from diseases inducing increased blood protein losses. Lymphopenia, although not a specific indicator of nutritional state, is associated with animals in poor nutritional status or under stress. In camelids, other blood analytes such as nonesterified fatty acids (NEFA; >0.8 milliequivalents per liter [mEq/L; >0.8 millimoles per liter [mmol/L]) and β-hydroxybutyrate (BHB; >5 milligrams per deciliter [mg/dL; >0.48 mmol/L]) are indicators of risk for metabolic or energy-related problems.4 Other blood analyte indicators of camelid nutritional status have yet to be identified and validated.



Enteral Nutritional Support


Provision of nutrients to the gut may be accomplished via voluntary intake or via forced feeding. Methods to stimulate appetite or the desire to eat provide the simplest way of promoting nutrient intake. Forced feeding is a much greater challenge in camelids and may be reserved for only targeted cases in which the stress induced is a lesser problem than the inadequacy of nutrient intake. As a result of orogastric tubing concerns, approach to nutritional support in camelids may best be a balance between stimulating intake coupled with support of foregut fermentation activity and some degree of partial parenteral nutrition.



Rationale for Use


A cardinal rule of nutrition is “If the gut works, use it.” Providing nutrients via the gastrointestinal tract is more physiologic and may minimize potential complications related to mucosal barrier dysfunction and impaired local immune response. Most data suggest a reduction in mortality in critically ill patients supported by enteral nutrition through a reduction in septic complications leading to death.8 Enteral nutrition provides direct nutritional support to enterocytes, which may maintain the physical barrier, as well as having indirect trophic effects.7,8 Enteral nutrition may also improve mesenteric blood flow and autonomic stimulation, thus improving gut function and activity. Supportive enteral nutrition is critical to maintaining normal functionality to the forestomach fermentation vat.



Appetite Stimulation


A simple approach to improving nutrient intake is to stimulate appetite. Various techniques to increase appetite exist, although these methods are not well understood and documented in camelids.14 Options include increasing feed palatability or variety, limiting environmental stress factors, pharmacologic stimulation, foregut transfaunation, and provision of a stimulating feeding environment. All of these may have some applicability, with the basic caveat that an intervention should do more good than harm. It should be remembered that correction of dehydration and underlying metabolic abnormalities is the top priority in stimulating intake.


Although many feed characteristics to promote improved palatability are known for companion animals (e.g., moisture, temperature, fat or protein content), extrapolation to camelids may not be appropriate.14 In our clinical experience, providing a variety of feedstuffs has been the most useful method of stimulating intake. Alfalfa leaves, fresh grass clippings, and blackberry leaves or any other browse material are among the best feeds to help stimulate feed intake.


Environmental factors to consider are freshness of offered feed and availability of water resources. Feed should be available as often as possible, and feeding should not be associated with administration of pharmacologic agents in treating underlying disease. Buddy animals are helpful in some cases, but allowing an animal to eat without competition is often better. A positive environment for feed consumption should be maintained. This may require elevating the feed to facilitate access.


Use of direct fed microbial (DFM) products (“probiotics”) may not be appropriate as compared with transfaunation of rumen juice from another animal. Microbial populations associated with most DFM products include a number of lactobacilli, which are not really desired bacterial species, as they produce lactic acid as a primary fermentation end product. These microbes are more desirable as colonies populating the intestinal tract rather than the forestomach. Rumen juice has the better range of desired microbial populations. Some benefit may be achieved by providing yeast-based products, either live cultures or yeast extracts. Most commercial yeast products are derived from cultures of Saccharomyces cerevisiae. A number of probiotic products may also contain yeast components as well as live bacterial cultures. Yeast products have been shown to generate metabolic derivatives that promote forestomach bacterial growth and subsequently increase dry matter intake and fiber digestibility.15,16 Improving fiber digestibility results in greater volatile fatty acid production in support of energy needs as well as increasing rate of particulate passage allowing for increased intake capability.


Pharmacologic stimulation of appetite is generally of short duration and variable efficacy. Diazepam (0.05 milligrams per kilogram [mg/kg], intravenously [IV]) works very well in some camelids but not at all in others. B-vitamin injections are supposed to stimulate appetite and improve glucose utilization. Analgesic agents may also be effective when pain is inhibiting appetite. Efficacy of other compounds is not well characterized in camelids.

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Mar 27, 2017 | Posted by in GENERAL | Comments Off on Nutritional Support

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