Vol.18, No.

12 December 1996

HEINZ SYMPOSIUM 1996

Continuing Education Article

FOCAL POINT #Nutritional intervention is seldom

addressed early enough in the management of sick or injured patients.

Nutritional Needs of Critically Ill Patients

Virginia Tech

Craig D. Thatcher, DVM, PhD

norexia is a common problem in veterinary patients, especially among the critically ill. Many animals that are presented to the veterinarian may not have eaten properly for a prolonged period. Nutrition for critically ill or injured animals should be addressed early in case management. With all the concern about diagnostics, fluid therapy, and therapeutic regimens, it is easy to overlook the animals need for nutritional support at first. Nevertheless, early attention to the patients nutritional needs can have an important impact on outcome. There are several pressing reasons to emphasize nutritional support. One of the most important is ethical: The veterinarian is deciding whether to support the patient nutritionally or to let it continue to be anorectic. Veterinarians have an ethical responsibility to ensure that hospitalized patients are properly fed. Nutritional support of human patients has been shown to contribute dramatically to the medical outcome of a case.1,2 The earlier the intervention, the better the outcome usually is. Finally, many types of nutritional supporteven most methods of tube feedingare easy and practical. Some can become routine in a hospital setting. Others, especially parenteral nutrition, are somewhat more difficult. Nevertheless, many veterinarians could institute parenteral feeding in a practice setting. Providing such services could represent an opportunity for practice growth and additional practice income. Nutritional support includes assessment of the animals nutritional requirements relative to its physiologic state and assessment of the current diet, including intake and feeding method. The nutritional plan involves not only the diet to be fed and the amount to be fed but also the route of administration. If the animal will not eat, the practitioner must decide whether the nutrients will be provided enterally through a tube or via a parenteral route.

KEY FACTS
I Metabolic rate slows during protracted simple starvation, but critically ill patients are typically in a hypermetabolic state. I Sepsis may cause critical illness or result from the accompanying atrophy of the gastrointestinal tract and translocation of bacteria. I Critically ill patients may have hyperinsulinemia despite glucose intolerance in tissue. I Critically ill patients should not be allowed to lose weight, even if they are obese. I Veterinarians should be more concerned about the energy needs of critically ill patients and less concerned about vitamins and minerals.

MALNUTRITION VERSUS STARVATION Much of the information on the nutritional status of hospitalized animals has been extrapolated from studies of humans. Nevertheless, many of the findings have been successfully applied to the care of dogs, cats, and other veterinary species. Between 30% and 50% of hospitalized human patients are

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malnourished.3,4 The incidence of malnutrition among hospitalized veterinary patients is probably also high. The box lists disorders that may increase the risk of malnutrition. Malnutrition is common in hospitalized patients because metabolism is altered as a result of disease. Malnutrition worsens infection as well as surgical complications. 2,510 Thus, malnutrition increases morbidity and Disorders That May Increase the Risk of mortality rates among human patients and probably Malnutrition does so among veterinary patients. Disorders That Alter Malnutrition has many Loss of Protein and causes. Nutrient intake may Electrolytes be altered; and the animal I Vomiting may be less able to digest, I Draining wounds absorb, or metabolize nutriI Burns ents. The animals ability to eliminate wastes may also be I Ileus impaired. Nutrient requireI Diarrhea ments are different for critI Abscesses ically ill animals than for I Malassimilation healthy dogs and cats.11 The nutritional status and nutriDisorders That Alter ent intake of high-risk hosNutrient Requirements pitalized patients should be I Trauma monitored. Their intake I Blood loss must be compared with their I Liver disease nutritional requirements. Many hospitalized patients I Sepsis have no oral intake of food, I Drugnutrient and others eat less than usuinteractions al. Sick animals may be selecI Burns tive in what they will eat and I Multiple surgical therefore may eat inapproprocedures priate, unbalanced diets (e.g., a patient that will only I Chronic renal disease eat cooked chicken). A paI Fever tients nutrient stores can I Cancer rapidly be depleted if the patients intake is not meeting its requirements. The veterinarian must estimate the patients nutritional requirements and its nutrient intake and develop a plan to address the deficit. The nutritional intervention must then be implemented and adapted as the animals condition changes. Malnutrition can impair humoral and cell-mediated immunity.12 Cutaneous hypersensitivity reactions are delayed. The complement cascade and the opsonic function of plasma can be affected, as can the function of polymorphonuclear lymphocytes. Malnutrition can also delay wound healing or cause organ dysfunc-

tion.13,14 Nutritional intervention is intended to prevent these problems. Again, much of this information has come from the human medical literature. Nevertheless, the same effects are probably occurring in veterinary patients.

Simple Starvation Glucose Homeostasis Simple starvation differs somewhat from the metabolism that occurs in critically ill animals.15 During starvation, the animal initially tries to maintain its blood glucose levels. The first metabolic consequence of simple starvation is therefore increased hepatic glycogenolysis and increased gluconeogenesis. Glycogen stores, however, are depleted within 24 hours.16 Hormonal changes that accompany food deprivation include a change in insulin response.17 As simple starvation progresses, the blood glucose level decreases. Insulin secretion decreases initially because of the low blood glucose. The increase in glycogenolysis implies increased glucagon secretion; low blood glucose increases glucagon production, thus stimulating glycogenolysis and gluconeogenesis. So in simple starvation, glucagon increases initially in an attempt to maintain blood glucose levels. As glucagon increases, lipolysis (the breakdown of body fat) increases. This increases levels of glycerol, free fatty acid, and ketone bodies. As starvation proceeds, more ketone bodies (e.g., -hydroxybutyrate) are produced, thus resulting in mild acidosis. During prolonged starvation in humans, ketones are utilized as an energy source by the brain.17 Free fatty acids increase and eventually level off. Glucose concentration should also stabilize over time. Metabolic Changes In simple starvation, the animal down-regulates its metabolism and becomes hypometabolic to conserve its body stores of protein and fats. Therefore, the basal metabolic rate decreases in starving animals.1719 In simple starvation, hepatic gluconeogenesis increases. After hepatic glycogen is depleted, amino acids are used for gluconeogenesis.18,2023 These amino acids are derived from the breakdown of both skeletal muscle and visceral body proteins, many of which have very short half-lives (e.g., prealbumin, retinal binding protein, fibronectin, and transferrin).18,20 The levels of these proteins might become valuable in monitoring the nutritional status of critically ill animals. However, these tests are not routinely available in veterinary medicine. Currently, serum albumin is used to aid in the monitoring of nutritional status; but serum levels of proteins

UNBALANCED DIETS I IMMUNE FUNCTION I GLUCAGON

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with short half-lives might provide better information. Hepatic gluconeogenesis also uses secretory proteins (e.g., immunoglobulins and lymphokines).11,20 Thus, these proteins eventually become depleted in starving animals. As mentioned, the metabolic rate decreases with chronic starvation. Conversion of thyroxine (T4) to triiodothyronine (T3) decreases. Consequently, the active T3 level decreases and oxygen consumption declines.17 As starvation progresses, fat oxidation increases and protein breakdown decreases because of the decreased metabolic rate. The brain adjusts by using ketone bodies for energy because the glucose requirements of the central nervous system decrease.20 As starvation continues, the site of gluconeogenesis shifts from the liver to the kidneys.17,18 In cases of prolonged simple starvation, ketosis occurs. Ketone bodies accumulate in the blood, and metabolic acidosis results. Much of the information on the metabolic changes described above was derived from studies of humans. Dogs and cats show somewhat different responses. Dogs show a milder ketosis. Fat mobilization progresses more slowly in dogs than in humans. 24 Cats have increased fat metabolism compared with dogs. This difference is important because starving cats with enhanced fat oxidation may be predisposed to hepatic lipidosis.2527

Critical Illness Although metabolic rate decreases in starving animals, critically ill or injured animals are typically in a hypermetabolic state. The consequences are somewhat different from those of simple starvation. Hypermetabolism In hypermetabolic states, the neuroendocrine system is typically activated because of local tissue injury or changes in homeostasis. Many critically ill animals have had some local tissue injury and may also have hypovolemia because of intractable vomiting, diarrhea, dehydration, or other problems. Hypoglycemia and acidosis progress rapidly in critically ill animals because of activation of the neuroendocrine pathway. Such stress has many metabolic consequences.12,15,20,28,29 When the neuroendocrine system is activated by critical illness or acute injury, the sympathetic nervous system responds. Epinephrine and norepinephrine are released. The stimulation of the sympathetic nervous system is positively correlated with the severity of the stressor.18,20 The more severe the stress, the greater the stimulation of the sympathetic nervous system and consequently the greater the hypermetabolism. Simultaneously, there is an increase in the counter-

regulatory hormones: Glucagon is released, and cortisol levels increase.28 The increases in these counterregulatory hormones have several results.28,30 The animal may rapidly deplete its nitrogen and therefore enter negative nitrogen balance. Potassium levels will also be depleted. Because of the cortisol response, the animal becomes glucose intolerant; hyperinsulinemia occurs despite the glucose intolerance in tissue. Consequently, ill or injured animals are in a hypermetabolic state and have marked nitrogen losses (which will result in a negative nitrogen balance). The body is in negative nitrogen balance when nitrogen losses (e.g., via urine, feces, and skin) exceed dietary nitrogen intake. Nitrogen balance reflects the bodys protein balance. Protein losses are also proportional to the stress that the animal has received. Researchers in human medicine have estimated the increase in metabolic rates in humans with various disorders.31 Humans with long-bone fractures have an increase in metabolic rate of somewhere between 15% and 30%. The metabolic rate may be increased by up to 50% if the person has multiple injuries. Burn patients exhibit the highest increase in metabolic rate sometimes as high as 100%. Critically ill animals probably have similar increases in metabolic rate.12,32 The hypermetabolic state in humans depends on mediators of inflammation as well as on hormonal responses. Both components must be present for hypermetabolism.33 Documented mediators of inflammation include interleukin-1 and tumor necrosis factor.33,34 Both are probably increased when an animal is in a hypermetabolic state.

Sepsis Sepsis, which is common in critically ill animals, may have a serious impact on metabolism. In particular, oxygen consumption, metabolic rate, and cardiac index are higher in septic humans than in nonseptic patientsand the respiratory quotient is lower. The lower respiratory quotient means that fat is being used as the primary energy source. Respiratory quotient reflects the relative quantity of energy produced by carbohydrate, fat, and protein.17,35 When critically ill patients have sepsis, their risk of multiple organ failure may be increased. Sepsis may cause critical illness, but prolonged anorexia may also contribute to sepsis. When a hypermetabolic critically ill animal is not receiving nutritional support, the gastrointestinal tract atrophies and its walls become thinner. Thus, the gastrointestinal walls become more permeable to bacteria and toxins that are normally present in the lumen. The bacteria and toxins can then translocate into the bloodstream; thus, they

FAT MOBILIZATION I NITROGEN BALANCE I RESPIRATORY QUOTIENT

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may contribute to sepsis.36 Other factors related to critical illness, such as decreased immune response, may also contribute.11,20 Nutritional support of critically ill animals may be important in preventing sepsis. Enteral nutritional support helps to protect the integrity of the gastrointestinal tract.37 The animal should be fed enterally if possible. Even a small amount of enteral feeding can have an important protective effect in the gastrointestinal tract. Protein intake is crucial for maintaining the integrity of the gastrointestinal tract. Protein deficiency decreases bowel weight, increases epithelial perforation, and decreases crypt depth in the gastrointestinal tract.38 These changes are related to atrophy of the gastrointestinal tract.

on its physiologic state. Body weight is an important indicator of the need for nutritional support. Nutritional support is indicated if the patient has recently lost more than 10% of usual or optimum body weight. This indication applies to animals that are ill from any cause, not just to critically ill animals. Even if a patient is obese, it should not be placed on a weight-reduction diet when it is critically ill. Obesity should only be addressed after the critical illness has resolved. Body weight of critically ill patients should be monitored daily. Monitoring body weight can aid in evaluating the success of nutritional intervention. An animal that is receiving nutritional support to meet its nutritional requirements should not continue to lose body weight. Nevertheless, body weight is only one indicator of the animals nutritional status.

ASSESSMENT All too often, veterinarians wait to address the critically ill patients nutritional status until the animal has been ill for several days. The earlier that nutritional intervention is undertaken, the better the outcome will be. Currently, veterinarians can use many sources of information when assessing an animals nutritional status.32,39,40 Assessment of the nutritional status of dogs and cats is a structured process that includes review of the history and medical record, physical examination, laboratory evaluation, and an estimation of nutritional allowances based on physiologic status. Sometimes the decision to institute nutritional support is based on clinical impression rather than objective data. The first step is to obtain as much information as possible on the animals history. The veterinarian should ask the owner not only about medical history, but also about dietary history, including the animals usual diet and eating habits. The medical records should also provide some important objective information that may provide clues to the animals current nutritional status. Physical examination and laboratory evaluation can certainly be helpful. All of the foregoing information helps in assessing the animals nutritional requirements. If a diagnosis of illness is made, it can also help guide nutritional intervention, especially if the animal can benefit from a diet with an altered nutrient profile. Once the initial assessment is complete, the veterinarian must formulate a nutritional plan. The plan then must be implemented and monitored and the client educated. Body Weight An animals nutritional requirements depend largely

Clinical Condition Restricted food intake for 3 days is not cause for much concern. However, animals that have been anorectic for longer than 3 days may benefit from nutritional intervention. So do animals with illnesses that result in nutrient loss. Chylothorax, for example, can cause tremendous losses of protein into the thorax. Animals that are receiving antinutrients (i.e., medications that interfere with nutrient absorption or metabolism) or catabolic drugs can also benefit from nutritional intervention. Nutritional support may be indicated if the patient has received intravenous fluids for longer than 3 days if therapy that causes catabolism, anorexia, or dysphagia is required. Some illness and treatment regimens (e.g., some cancer chemotherapies) predictably cause anorexia. In these cases, the veterinarian should anticipate the need for nutritional support. Other indicators of the animals nutritional status include muscle mass and the condition of haircoat, claws or nails, and skin. Thin, dry, and scaly skin and easily depilated haircoat may indicate undernutrition. The practitioner should examine each body system to identify any problems related to nutrition. Body condition scoring, which is a subjective evaluation of the animals fat cover, may suggest that an animal needs nutritional support. The animals fat cover is scored from one to five: 1 is very thin and 5 is grossly obese. A score of 3 represents the optimum body condition. The fat over the ribs, down the topline or over the spinous processes, and over the lumbar transverse process is visually assessed and palpated. The area over the tuber coxi and tuber ischii is also evaluated. Fat tends to accumulate around the tailhead in dogs. Obesity is also typically evident in the animals ventral silhouette.

GASTROINTESTINAL INTEGRITY I MONITORING I BODY CONDITION

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Laboratory Assessment No single diagnostic or laboratory test accurately depicts the nutritional status of dogs and cats, but a combination of tests can provide additional information. Chronically ill animals typically are hypoalbuminemic. Animals with hypoalbuminemia generally benefit from nutritional support. Lymphocyte count and packed cell volume may serve as objective indicators of nutritional status. Serum glucose is important in the assessment of hypercatabolic, severely stressed animals. Serum alkaline phosphatase, hemoglobin levels, and biochemical profiles indicative of liver, kidney, or other organ problems can be helpful in assessing the animals nutritional status. Low serum albumin may indicate depletion of visceral protein; however, serum albumin levels change slowly (i.e., over days) because of that proteins long halflife. Tests for the levels of proteins with very short half-lives are currently used to monitor nutritional status and the effects of nutritional support in human medicine. These levels may, however, reflect the primary disease process rather than nutrient depletion. The tests to monitor levels of proteins with very short halflives are not yet available for veterinary use. In human patients, hypoalbuminemia correlates with increased morbidity and mortality rate and longer hospital stays. Hypoalbuminemia also correlates with a higher incidence of infection and lower body cell mass.41 Similar relationships probably occur in veterinary patients. The diagnosis of hypoalbuminemia can aid in the selection of patients that are at high risk for malnutrition. Certainly, animals that have protein-losing enteropathy or nephropathy and are losing large amounts of protein may benefit from nutritional intervention. REQUIREMENTS The practitioner must consider the patients physiologic state, the nature of the disease or injury, and environmental factors in determining the animals nutrient requirements. After deciding that a critically ill patient might benefit from nutritional support, the veterinarian estimates the patients nutrient requirements.12,32,39 Water is the nutrient that has the highest priority for the animal. Next is energy, especially in the form of fat and carbohydrate. Protein can certainly contribute to meeting the animals caloric requirements but is also essential for wound healing and tissue repair. The requirements for vitamins and minerals are the least urgent, yet these requirements are often the first ones addressed by the veterinarian. Critically ill patients have lower metabolic rates and energy requirements than those of healthy dogs and

cats. The caloric requirements are less, primarily because critically ill patients have decreased physical activity. A summary of the various equations that have been used to calculate the energy requirements of sick dogs and cats has been published.12 The resting energy requirement (RER) is calculated as follows: RER (kcal) = 30 (body weight [kg]) + 70 Another formula is as follows: RER (kcal) = 70 (body weight [kg])0.75 The energy requirements of critically ill animals are at or greater than RER but rarely exceed maintenance energy requirements. Factors to multiply RER for estimating energy requirements in a wide variety of illnesses have been extrapolated from human respiration calorimetry studies for use in veterinary patients.39 After estimating the animals requirements, the veterinarian must choose the diet to be fed and the method of nutrient delivery. Whenever enteral feeding is possible, it is preferable to parenteral nutrition. Enteral nutrition is more physiologic, less expensive, and easier to accomplish than parenteral delivery. Sometimes, however, the animal can only be supported through the parenteral routes. The veterinary literature describes numerous techniques for enteral and parenteral nutrition.32,39,42,43 For enteral feeding, food dosage (g/day) is determined by the daily caloric requirement of the patient (kcal/day) divided by the caloric density of the diet (kcal/g): Food dosage = Total daily energy requirement Diet caloric density Commercially available diets usually contain nonenergy nutrients properly balanced to the caloric density of the product. Thus, all of the animals nutrient needs will be met if its energy needs are met.

About the Author

Dr. Thatcher is Head of the Department of Large Animal Clinical Science, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, Virginia, and is a Diplomate of the American College of Veterinary Nutrition.

SERUM ALBUMIN I BIOCHEMICAL PROFILES I ENERGY REQUIREMENTS

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