Date: Written March 31, 2011; updated January 7, 2013; updated December 3, 2014
Key words: Malnutrition, protein, glucose, starvation, catabolism, glutamine, arginine
Although conventional veterinary medicine ignored the nutritional needs of critically ill patients for many years, exotic animal veterinarians have never had that luxury. Small animal size and rapid metabolic rate have meant that many of our patients require rapid and intensive nutritional support to survive.
Recent advances in human and veterinary medicine have confirmed what zoological medicine has always stressed: Nutritional support is an important part of successful supportive care and management of disease (Fig 1). Research in intensive care patients has found that those suffering from under-nutrition have inferior clinical outcomes (Griffiths 2005, Giner 1996). By the same token, enhanced delivery of nutritional support can translate into improved clinical outcome (Martin 2004).
The use of enteral nutrition, as opposed to parenteral nutrition results in a signficant decrease in the incidence of complications and can also be less costly. Providing adequate nutrition, especially when administered enterally, can be a powerful tool in managing critically ill patients (Larsen, 2012). Enteral nutrition should be the first choice for nutritional support in the critically ill (Gramlich 2004).
Malnutrition is believed to increase patient morbidity and mortality through a multitude of effects (Table 1) (Burns 2012). Even a brief period of critical illness can cause rapid loss of skeletal muscle. In fact, in human patients rapid loss of lean body mass is considered a predictor of mortality. Loss of muscle means loss of protein, which increases the risk of wound dehiscence and post-operative infections. Protein malnutrition can also alter drug metabolism causing unexpected changes in therapeutic effect.
Table 1. Documented effects of malnutrition in various species
Gastrointestinal tract ↑GI transit time
↓ Absorption of nutrition Villous atrophy
↑ Risk of bacterial translocation
Urinary tract ↑ Excretion of urinary calcium and phosphorus
↓ Excretion of acid
↓ Glomerular filtration rate
Immunity ↓ Humoral immunity
↓ Barrier function decreases (skin, mucosal surfaces)
↓ Inflammatory response
↓ Leukocyte motility
↓ Bactericidal activity
Lungs ↓ Lung elasticity
↓ Production of secretions
↓ Response to hypoxia
↓ Tidal volume
Heart ↑ Incidence of arrhythmias
↓ Heart muscle weight
Skeletal muscle ↑ Risk of surgical dehiscence
↑ Post-operative infection
Metabolism during critical illness
Critical illness is associated with a host of physiologic changes caused by the stress response (Martindale 2002):
- –Increased sympathetic tone
- –Tachycardia and increased cardiac output
- –Sodium and water retention
- –Protein catabolism
Glucose is an initial source of energy
Alterations in carbohydrate metabolism have been documented in the critically ill patient. Glucose initially serves as the primary fuel source for the central nervous system, bone marrow, and injured tissue.
Glycogen stores are rapidly exhausted, particularly in strict carnivores. If the patient is not provided with dietary carbohydrates, new glucose is derived from gluconeogenesis via the breakdown of muscle protein. Additional alterations in carbohydrate metabolism include:
- Enhanced peripheral glucose uptake and utilization
- Increased glucose production
- Depressed glycogenesis
- Glucose intolerance
- Insulin resistance
These changes can result in stress hyperglycemia.
Proteolysis is another major metabolic alteration associated with critical illness
Marked skeletal muscle catabolism is required during critical illness to provide adequate substrate for the acute phase inflammatory response, gluconeogenesis, tissue repair, and immune function. Marked proteolysis exceeds protein synthesis in critical illness and is in itself an energy-consuming process. This is in stark contrast to the catabolism of starvation where reductions in protein synthesis result in a net protein loss (Box 1) (Martindale 2002; Saker & Remillard, 2010).
Fat serves as a source of energy in simple starvation, but not critical illness
During simple starvation, but NOT critical illness, a metabolic shift occurs within days that allows fat depots to serve as a preferential source of energy. This allows lean muscle tissue to be spared. In diseased states, the inflammatory response triggers alterations in cytokines and hormone levels that rapidly shift metabolism towards a catabolic state (Box 1). The rates of fatty acid oxidation also increase in critically ill patients (Martindale 2002).
Box 1. Definitions
Simple starvation Healthy animals primarily lose fat when deprived of the necessary calories
Sick or traumatized patients catabolize mean body mass when deprived of the necessary calories
Patients that present on an emergency basis may be suffering from chronic illness and poor nutrition prior to admission. What is the best way to evaluate your patient’s nutritional state?
- –Obtain a detailed history covering medical as well as husbandry. What food is the pet offered and in what proportions? What does the pet actually eat?
- –Perform a careful physical examination
- –Include careful evaluation of fat and muscle stores to assess the patient’s body condition. Obesity is not a contraindication for nutritional support.
What is nutrition for critical care?
Nutritional support provided for recovery or maintenance is different than nutrition for critical care. Nutrition for critical care is…
- Calorie-rich: Critical illness is often associated with hypermetabolism (Monk 1996; Saker & Remillard, 2010). The systemic inflammatory response seen with sepsis or major trauma will increase the basal metabolic rate usually proportional to the degree of insult (Griffiths 2005).
- Nutrient-rich containing adequate levels of protein: Critical illness can lead to malnutrition (Martin 2004, Monk 1996). Catabolic depletion of protein reserves is one of the most striking features of the critically ill patient; therefore the supply of protein is the most critical nutrient (Griffiths 2005).
- Supplemented with glutamine and arginine: Depletion of these critical amino acids is common during periods of starvation and catabolic stress (Oehler 2002).
- Critical illness leads to a marked deficiency in glutamine that is correlated with mortality in the intensive care unit setting (Wischmeyer 2007), and supplementation of glutamine has been shown to improve patient outcome (Oehler 2002, Labow 2000, Neu 1996; Saker & Remillard, 2010).
- Arginine is an important precursor for hepatic gluconeogenesis, particularly during periods of hypermetabolic stress.
Recent studies showed that the use of an enteral diet or parenteral nutrition that contains immune nutrients enhances the recovery of critically ill patients (de Aguilar 2012).
- Started as soon as enteral feeding is safe and practical: If enteral nutrition is indicated, it is usually preferable, to begin as soon as possible (Martin 2004). In one study evaluating human ICU patients, early enteral nutrition was associated with a significantly lower incidence of infections and a reduced length in hospital stays (Marik 2001).An increase in positive incomes with early enteral nutrition has even been documented in conditions previously thought to require “gut rest”, like pancreatitis and parvovirus enteritis (McClave 2006, Qin 2002, Mohr 2003).What exactly does “early enteral nutrition” mean?
- In dogs and cats, nutritional support is instituted at the latest after 3 days of anorexia or when the patient is not expected to eat within 2 to 3 days.
- Of course with many tiny exotic animal patients, anorexia lasting < 8-12 hours is cause for alarm. Each species and individual patient must be evaluated separately, and this assumes one knows how long the patient has gone without food. Obviously in many wildlife patients this information is not available.
- Challenging!: It’s never enough just to select a quality critical care product because regular assessment of your patient is key for a positive clinical outcome. Equations used to estimate energy requirements provide relatively unreliable predictions of patient need—particularly in exotic species where little clinical data is available (Griffiths 2005). Nevertheless a good rule of thumb is to meet at least 75% to 80% of calculated requirements by 72 hours post-presentation.
Cautions or potential complications
As with any intervention in critically ill animals, nutritional support carries some risk. The risk of complications increases with the severity of disease (Burns 2012).
Is the patient cardiovascularly stable?
To minimize risk, the patient must be stable before nutritional support is initiated. To maintain adequate perfusion of the key organs like the heart, brain, and lungs, perfusion of the gastrointestinal tract is reduced. In turn, processes like gastrointestinal motility, digestion, and assimilation of nutrients are altered, increasing the risk of complications in affected patients such as functional or even mechanical obstructions, and/or delayed crop or gastric emptying.
Have fluid and electrolyte deficits been addressed?
Enteral feeding should also be delayed until preexisting fluid and electrolyte abnormalities are corrected. Deficits can exacerbate problems associated with suboptimal gastrointestinal function, and can also promote hypophosphatemia and hypokalemia associated with “refeeding syndrome” (Burns 2012).
Refeeding syndrome occurs during the reintroduction of nutrients after a period of starvation. The sudden influx of carbohydrates stimulates insulin release. The subsequent uptake and utilization of glucose by cells is also associated with an intracellular shift of potassium, phosphorus, magnesium, and thiamine from serum. . These metabolic changes can result in potentially profound hypokalemia, hypophosphatemia, hypomagnesemia, and thiamine deficiency.
How high is the risk of aspiration?
Can the patient protect the airway? Enteral feedings should be avoided in patients with…
- Uncontrolled vomiting or regurgitation
- Reduced level of consciousness
- Reduced gag reflex
- A need for frequent sedation or general anesthesia
How to accomplish enteral feeding
Each case is different and the best method for administering food will vary:
- Voluntary intake, which often must be encouraged and closely monitored
- Coax or hand feeding
- “Assisted” or syringe feeding
- An enteral feeding tube, such as a nasogastric tube or esophagostomy tube is often a good choice to reduce stress in the hospitalized patient or for long-term management of select patients. Overall feeding tubes insure that the nutrients are getting into the patient and is considered to be the best route for administering nutrients to the patient.
Parenteral nutrition may be indicated for patients at significant risk for complications with enteral feeding.
Nutritional support in the critically ill patient is aimed at enhancing the rate of recovery and minimizing the impact of malnutrition. Malnutrition causes metabolic derangements and catabolism of lean body tissue, which has negative effects on wound healing, immune function, strength of skeletal and respiratory muscles, and ultimately overall prognosis.
References and recommended reading
Burns KM. Nutrition for the critically ill. Proc VECCS 2012. Pp. 513-516.
Chan DL. Revisiting nutritional controversies. Proc IVECCS 2012. Pp. 663-666.
Chan DL. The role of nutrients in modulating disease. J Small Anim Pract. 49(6):266-271, 2008.
Chan DL, Freeman LM. Nutrition in critical illness. Vet Clin North Am Small Anim Pract. 36(6):1225-1241, 2006.
Gallagher-Allred CR, Voss AC, Finn SC, McCamish MA. Malnutrition and clinical outcomes: the case for medical nutrition therapy. J Am Diet Assoc 96(4):361-366, 1996.
Giner M, Laviano A, Meguid MM, et al. In 1995 a correlation between malnutrition and poor outcome in critically ill patients still exists. Nutr 12(1):23-29, 1996.
Gramlich L, Kichian K, Pinilla J, et al. Does enteral nutrition compared to parenteral nutrition result in better outcomes in critically ill adult patients? A systematic review of the literature. Nutrition 20(10):843-848, 2004.
Griffiths RD, Bongers T. Nutrition support for patients in the intensive care unit. Postgrad Med J 81:629-636, 2005.
Griffiths RD. Specialized nutrition support in critically ill patients. Curr Opin Crit Care 9:249-259, 2003.
Labow BI, Souba WW. Glutamine. World J Surg 24(12):1503-1513, 2000.
Larsen JA. Enteral nutrition and tube feeding. In: Fascetti AJ, Delaney SJ (eds). Applied Veterinary Clinical Nutrition. Wiley-Blackwell: Ames, Iowa, 2012. Pp. 329-352.
Marik PE Zaloga GP. Early enteral nutrition in acutely ill patients: A systematic review. Critical Care Med 29(12):2264-2270, 2001.
Martin CM, Doig GS, Heyland DK, et al. Multicentre, cluster-randomized clinical trial of algorithms for critical-care enteral and parenteral therapy (ACCEPT). CMAJ 170(2):197-204, 2004.
Martindale RG, Shikora SA, Nishikawa R, Siepler JK. In: American Society for Parenteral and Enteral Nutrition (ed). Nutritional Considerations in the Intensive Care Unit: Science, Rationale, and Practice. City, State: Kendall/Hunt Publishing Company; 2002.
McClave SA, Heyland DK. The physiologic response and associated clinical benefits from provision of early enteral nutrition. Nutr Clin Pract. 24(3):305-315, 2009.
Mohr AJ, Leisewitz AL, Jacobson LS, et al. Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 17(6):791-798, 2003.
Monk DN, Plank LD, Franch-Arcas G, et al. Sequential changes in the metabolic response in critically injured patients during the first 25 days after blunt trauma. Ann Surg 223:395-405, 1996.
Orosz SE. Perioperative nutrition for birds. Proc Annu Conf Assoc Avian Vet; 2009. Pp. 37-44.
Qin HL, Su ZD, Gao Q, Lin QT. Early intrajejunal nutrition: Bacterial translocation and gut barrier function of severe acute pancreatitis in dogs. Hepatobiliary Pancreat Dis Int 1(1):150-154, 2002.
Saker KE, Remillard RL. Critical Care Nutrition and Enteral-Assisted Feeding. In Small Animal Clinical Nutrition, 5th ed. Hand M, Thatcher C, Remillard RL, Roudebush P, Novotny B. eds. 2010. MMI, Topeka, KS.
Written by Christal Pollock, DVM, Dipl. ABVP-Avian; Lafeber Company veterinary consultant.
Updated by Kara M. Burns, MS, MEd, LVT, VTS (Nutrition): Lafeber Company consultant.