Dr. Mazzaferro has a special interest in the nutritional support of the critically ill patient. Her PhD research involved evaluation of carbohydrate and protein metabolism in critically ill dogs.
Nutritional Assessment of the Critical Patient
Many patients present to you with some degree of acute or chronic malnutrition. It is important to identify risk factors for malnutrition when formulating a nutritional plan for each individual patient. In some cases, chronic malnourishment may be obvious on physical examination, historical information from the owner, and diagnostic bloodwork. A body condition score should be performed at the time of presentation to you. Patients that are chronically malnourished may have muscle wasting, cachexia, poor haircoat quality, nonhealing wounds and decubital ulcers on physical examination. Often, although it may take some questioning, the owners of the patient will reveal a loss or decrease in appetite. It is sometimes useful to ask "At what weight was he or she the heaviest?" to provide some information regarding acute or chronic weight loss. In some cases, the only presenting complaint is vomiting or diarrhea, both risk factors for malassimilation of nutrients and malnutrition. Diagnostic bloodwork abnormalities that have been associated with malnutrition include hypoalbuminemia, leukopenia and suppressed immune system function, and coagulation abnormalities.
The goals of nutritional support are to provide the patient with adequate nutrition such that protein catabolism and negative nitrogen balance are corrected and/or prevented.
Ideally, you want to prevent further catabolism of lean muscle mass and provide adequate nutrient substrates for healing and recovery. Nutrient supplementation must be carefully monitored; however, as severe complications can ensue with very critical patients, leading to increased patient morbidity and mortality.
Wherever possible, you should replenish dehydration estimates and correct acid-base and electrolyte disturbances before starting any form of enteral nutrition. The adage "If the gut works, use it" should carefully be considered in all patients. Enterocytes within the gut lumen undergo atrophy within 24–48 hours of anorexia. The lack of trophic stimuli of nutrients within the gut lumen causes severe villous atrophy. The atrophied villi become poorly functional or nonfunctional for nutrient absorption. Additionally, the lack of trophic nutrients within the GI lumen causes a decrease in secretory IgA, and an increased risk of infection. Bacterial translocation can also occur, leading to an increased risk of sepsis. Early enteral nutritional supplementation has been positively correlated with improved patient outcome in canine patients with severe parvoviral enteritis.
Calculation of Energy Requirements
Nutritional supplementation is meant to provide all substrates necessary for protein, carbohydrate and fat synthesis and metabolism in critical illness. Adequate energy, glucose and protein production should occur, sparing the body's stores for healing purposes. In the past, it was traditionally thought that all patients with an illness or injury should have their resting energy requirements (RER) multiplied by an arbitrary "illness, infection, injury" factor to determine their daily caloric requirements. More recent studies, however, have demonstrated that the majority of critically ill dogs actually are hypometabolic in response to injury. The random multiplication by an arbitrary illness factor could potentially provide oversupplementation that can be detrimental to the patient's metabolic and acid-base status. By definition, the resting energy expenditure (REE) or resting energy requirement (RER) is the amount of energy or calories that an animal requires for rest in a post-prandial (nondigestive) state in a thermoneutral environment. In human medicine, bedside calorimetry carts help provide assessment of a patient's caloric needs on a regular basis. In veterinary medicine, however, the use of calorimetry analyses has largely been limited to research studies, and is not available for use in all patients. Resting energy requirements have often been calculated by the formula:
[(30 x BW kg) + 70] = Kcal/day
This formula largely holds true for patient ranging from 3–40 kg in body weight. Approximately 1/3 of a patient's caloric requirements as determined by the above formula should be fed on Day 1 of supplementation. The caloric requirements can be gradually increased over a period of 2–3 days, until 100% of the RER is provided.
Deleterious consequences of overfeeding early in nutritional supplementation after prolonged starvation can lead to severe metabolic derangements associated with refeeding syndrome.
Refeeding syndrome can occur within several hours of refeeding in some patients following prolonged illness and starvation. Severe electrolyte depletion often occurs in prolonged starvation. Upon refeeding, the pancreas releases insulin in response to the high carbohydrate load. Insulin requires potassium as a cofactor to import glucose into the cell for metabolism. Serum potassium declines due to a transcellular shift of potassium into the cell. Clinical signs associated with hypokalemia include cervical ventroflexion, muscle weakness, and respiratory muscle fatigue and distress. Treatment for this condition is potassium supplementation. If a patient has refractory hypokalemia in the face of higher and higher supplementation, consider replacing magnesium as well as potassium. Magnesium is an essential ion necessary as a cofactor for many enzyme systems in the body, including the Na-K-ATPase pump. Magnesium also becomes rapidly depleted in critical illness and starvation. Magnesium supplementation can be administered as a constant rate infusion at 0.75 mEq/kg/day.
With prolonged starvation, energy stores become depleted. When the body receives a carbohydrate load after a prolonged fast, it responds by producing large quantities of energy substrates in the form of ATP and ADP. Phosphorus stores can become depleted, leading to the severe hypophosphatemia associated with refeeding syndrome. Hypophosphatemia can result in severe muscle weakness, respiratory failure and acute red blood cell lysis. Phosphorus supplementation can be in the form of potassium phosphate. Hyperglycemia secondary to peripheral insulin resistance can occur when feeding enteral formulations high in carbohydrates. Hyperglycemia and metabolism can increase the respiratory work to drive off excess CO2. In some human studies, prolonged refractory hyperglycemia increased risk of morbidity and mortality. It may be beneficial to maintain normoglycemia by using small amounts of regular insulin in the early stages of refeeding. In most cases, however, refeeding syndrome and its associated electrolyte abnormalities can be avoided by supplementing just 1/3 of the caloric requirements on the first day of supplementation, then gradually increasing the calories provided over a period of 72 hours. Blood glucose, bicarbonate and electrolytes including potassium, magnesium and phosphorus should evaluated on a regular (at least daily) basis during the early stages of refeeding.
Placement and Maintenance of Various Types of Feeding Tubes
Nasoesophageal and Nasogastric Feeding Tubes
Nasoesophageal and nasogastric tubes are among the easiest and least expensive forms of feeding tubes available for use by veterinary practitioners. Three to 5-Fr Argyle infant feeding tubes are ideal, are soft and pliable, and are well tolerated after placement by most patients. A nasoesophageal feeding tube should be placed in patients with expected or known short-term anorexia that are not vomiting, and have no problems with esophageal motility or strictures, and have no maxillofacial trauma. Alternatively, a nasogastric tube can be placed for both enteral nutrition and for gastric decompression in cases of gastric atony, as seen with severe parvoviral enteritis and pancreatitis or severe ileus. Liquid diets can easily be fed through the tube as a bolus infusion or as a constant rate infusion, as tolerated by the patient. Potential complications of nasogastric or nasoesophageal feeding include aspiration pneumonitis, vomiting, diarrhea, and tube obstruction due to their small diameter.
Esophagostomy tubes are an excellent method of feeding patients with severe head or facial trauma, oral oropharyngeal masses, and anorexia. Esophagostomy tubes are easy to place and are well-tolerated by most patients. Client compliance is very positive, and there is a minimal risk of complication compared with percutaneous gastrostomy feeding tubes. Contraindications of an esophageal feeding tube include esophageal motility disorders or strictures, protracted vomiting, or a history of esophageal reflux or esophagitis. Depending on the type of tube placed, minimal equipment is necessary. Typically tube sizes range from 8–16 French, depending on the size of the patient. Always check tube placement with a lateral thoracic radiograph. Unlike PEG tubes, the E-tube can be used immediately, with fluid or a blenderized diet. The author's preference is to feed Eukanuba Maximum Calorie diet, warmed to room temperature or slightly warmer.
Intraoperatively, jejunostomy tubes can be placed in any patient with a history of vomiting or proximal gastrointestinal obstruction, resection, or pancreatitis that will need continued nutritional support in the immediate post-operative period. A jejunostomy tube (5–8-French polyvinylchloride feeding tube) can be placed into the proximal to mid-jejunum, or alternatively can be placed through a gastrostomy tube and used until the patient is ready for gastric feedings. Any liquid diet can be placed through the jejunostomy tube either as a constant rate infusion or as bolus feedings, as tolerated by the patient. J-tubes are relative easy to place, although have the risk of peritonitis if they come loose. Other potential complications include orad migration of the tube into the stomach, tube clogging, and diarrhea.