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neonatal foals, are intolerant of even a conservative rate of dextrose because of insulin resistance. Foals with persistently increased values, above 10–11 mmol/l for greater than 4–6h, may benefit from exogenous insulin therapy. It has been described that hypoglycaemia and hyperglycaemia are common in critically ill foals and oftentimes are associated with poor outcome thus significant variations in blood glucose should be avoided (Krause and McKenzie 2007; Hollis et al. 2008a,b). Sepsis has been documented in 50% of foals less than
30 days of age with diarrhoea (Hollis et al. 2008a,b). Since clearance of lipids can be impaired with Gram-negative sepsis monitoring the serum triglyceride value is important. Triglyceride concentrations of >2.3 mmol/l were associated with nonsurvival in both man and foals receiving i.v. nutrition (Heyland et al. 1998; Myers et al. 2009). Thus lipid administration should be discontinued if the triglyceride value is persistently elevated. Since electrolyte abnormalities are a common occurrence in patients with diarrhoea, frequent monitoring of electrolytes should be performed. Hypokalaemia is common in foals receiving i.v. nutrition because glucose and insulin administration reduce extracellular potassium concen trations. Metabolic acidosis can occur due to gastrointestinal loss of bicarbonate ions. In certain instances a constant rate of infusion of fluids
and parenteral nutrition is not feasible and fluids will need to be bolused. Depending on the foal and severity of the diarrhoea the fluids can be administered every 2–6 h over a period of 30 min. Once the foal has been stabilised, the amount of fluids to administer at each bolus can be calculated by estimating the total volume the foal would receive in a 24 h period and dividing by the frequency of administration. Fluid therapy for a foal with diarrhoea typically consists of maintenance rate combined with an estimate of ongoing losses. The volume will need to be changed daily as the foal’s condition improves or worsens. In this instance to provide extra calories, dextrose can be added to the fluids. In order to prevent significant hyperglycaemia, a 1–2.5% dextrose solution in isotonic polyionic fluids can be administered slowly over a period of 20–30 min. Based on this author’s experience, this amount of dextrose will not result in significant hyperglycaemia.
Enteral nutrition
Results from numerous animal and human studies support that enteral nutrition is superior to parenteral nutrition. Food in the gastrointestinal tract has an important role in preserving normal physiology, especially related to immune function and systemic inflammation. Animal models have demonstrated that enteral nutrition lowers the risk of infection by preserving the gastrointestinal tract integrity and enhancing its ability to provide an immunocompetent barrier to prevent invasion by pathogenic microorganisms. Rats fed enterally demonstrated better lymphocyte function and better survival when subjected to bacterial challenge than those receiving only total parenteral nutrition (TPN) (Birkhahn and Renk 1984). The intestinal barrier is maintained by the enterocytes which play a major role in digestion and immunological protection. Enterocytes are responsible for brush border digestion and absorption of nutrients. Virtually all nutrients enter the body by crossing the enterocytes by active transport or diffusion. Amino acids, specifically glutamine, are the enterocytes main
source of fuel, but glucose and fatty acids can also be utilised by enterocytes. Enterocytes, which are joined together by tight junctions, also provide a barrier against microbial translocation across the bowel wall into the systemic circulation (Alverdy 1994). Enterocytes constitute more than a physical barrier against foreign substances from the gut as they are capable of reacting to the heavy antigenic load of the gastrointestinal tract. Through their direct receptors, antimicrobial peptides and regulatory cytokines enterocytes are true immune competent cells (Alverdy 1994). Enterocytes can take up and process antigens which are then presented directly to T cells (Snoeck et al. 2005). Production of secretory IgA, the principle immunoglobulin in the lumen of the gastrointestinal tract, is influenced by enterocytes (Miron and Cristea 2012). Rats fed enterally maintained secretory IgG levels better than rats fed the same nutrients i.v. (Alverdy et al. 1985). Studies have shown that after just a few days of complete
bowel rest, progressive atrophy of the intestinal tract occurs. There is loss of villi, decreased disaccharide activity, malabsorption of sugars, decreased absorption and disruption of barrier protective functions (Johnson 1988; Mainous and Deitch 1994). The lack of food produces a state of ‘luminal starvation’ that adversely affects the enterocytes (Strodtbeck 2003). The consequences of enterocyte starvation are characterised by intestinal mucosal atrophy, decreased absorption of nutrients, loss of tight junctions between enterocytes and impaired immune functions (Johnson 1988; Mainous and Deitch 1994). The risk for translocation of bacteria is increased due to loss of gut integrity. Rats fed only parenteral nutrition for 2 weeks had a 66% incidence of positive cultures in mesenteric lymph nodes whereas those fed enterally had no evidence of bacterial translocation (Alverdy et al. 1988). Translocation of bacteria across the gastrointestinal mucosa has been documented during periods of bowel rest in intensive care patients. Enteral nutrition helps to maintain the functional integrity of the bowel, prevent translocation of bacteria and subsequent sepsis. Therefore, even if the gastrointestinal tract cannot be used to meet complete needs, small amounts of enteral feeding may be helpful. Numerous studies with preterm human infants have documented the beneficial outcomes of minimal enteral feedings. These studies noted decreased hospitalisation, faster transition to complete oral feedings, fewer infants with feeding intolerance and a reduction in sepsis (Berseth 1992; Dallas et al. 1998; Shulman et al. 1998). In mice an experimental study noted that small amounts of enteral nutrition paired with parenteral nutrition prevented and reversed some of the changes in the gastrointestinal mucosa that are typically noted with lack of enteral nutrition (Ikezawa et al. 2008). It has been well documented that fresh mare’s milk is the
preferred source of enteral nutrition in the neonatal foal. Advantages of this source of enteral feeding include physiological stimulation leading to normal metabolic regulation, preservation of gastrointestinal mucosa integrity and important trophic substances (including epidermal growth factor and insulin-like growth factors) which stimulate normal growth and development. If fresh mare’s milk is not available, frozen mare’s milk is the next best alternative followed by milk replacer. Milk from another species can be used if there are no other options. Goat’s milk is higher in fat, total solids and gross energy than mare’s milk and easier to
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