CHAPTER 16 Caroline Tonozzi VCA Aurora Animal Hospital, Aurora, Illinois Tell me what you eat, and I will tell you what you are. (Jean Anthelme Brillat‐Savarin, 18th century) Starvation is the lack of food. “Simple starvation” occurs when a previously healthy animal has not eaten for a 72‐hour period. The body will respond by decreasing the metabolic rate to conserve energy and to maintain body mass. Glucose is produced from glycogen and fat stores in this situation and used to make energy. Once the animal resumes eating, these compensatory metabolic changes are rapidly reversed, and the animal returns to normal. Illness and injury can cause a catabolic state that results in a reduced prognosis for recovery. Anorexia, nausea, pain, discomfort or the physical inability to eat will also lead to starvation. This form is called “stressed starvation” and occurs when a patient has been either anorexic for ≥3 days due to a severe illness or malnourished at the time of presentation for an illness. Increased release of stress hormones (cortisol, glucagon, catecholamines) and inflammatory cytokines shifts energy production away from glucose and fat to lean muscle proteolysis (Figure 16.1) [1]. Marked proteolysis exceeds protein synthesis, with energy consumed during the process. Muscle wasting will occur while fat deposits are spared, causing a negative nitrogen and energy balance [2]. Delayed wound healing, altered immune function, gastrointestinal (GI) dysfunction, and weakened skeletal and respiratory muscle strength contribute to a worse overall prognosis for recovery. Many of the effects of protein‐calorie malnutrition on the immune response are listed in Table 16.1. Figure 16.1 Mechanism of “stress” starvation compared to “simple” starvation. Green arrows: simple starvation. Red arrows: stress starvation. Table 16.1 Effects of protein‐calorie malnutrition on immunity. Adapted from: Saker KE. Nutrition and immune function. Vet Clin North Am. 2006;36;1199–224 [41]. GI, gastrointestinal; IG, immunoglobulin; IL, interleukin; TNF, tumor necrosis factor. The small bowel is a primary component of the immune system due to the abundant amount of lymphoid tissue present and the protective mucosal barrier function. The GI mucosal cells extract the majority of their nutrients from the enteral side of the bowel rather than from the capillaries. Certain nutrients, specifically glutamine, arginine, nucleotides, omega‐3 fatty acids, and dietary fiber, are required for growth and normal function of the mucosal epithelial cells and lymphoid tissue [3,4]. IgA is secreted into the GI lumen to prevent adherence of microbes to the mucosa. During states of starvation in critically ill animals, the enterocytes become malnourished and are unused, rapidly causing villus atrophy. Transit time within the bowel is increased with decreased absorptive capacity and increased bacterial proliferation within the lumen. The mucosal barrier becomes damaged, causing an increase in GI mucosal permeability. Various factors have been found to promote the translocation of luminal pathogens. These factors include luminal bacterial overgrowth, impaired host defense mechanisms, protein‐calorie malnutrition, trauma, critical illness, and interruption of the luminal nutritional stream [5]. The subsequent bacteremia may contribute to the “two‐hit” theory of critical illness, with the second physiological injury potentially arising from the bowel [6]. A deficiency of a specific nutrient can cause specific life‐threatening problems. Thiamine deficiency in the cat can lead to dementia, seizures, and coma. Carnitine deficiency in the Boxer can cause cardiomyopathy. Taurine deficiency in the cat can cause blindness or dilated cardiomyopathy. Vitamin A deficiency can cause blindness. A list of common nutrient components, their functions, and possible consequences of deficiency is provided in Table 16.2. Table 16.2 Important nutrients to be supplemented in diets for critical small animal patients [40,42,43]. ATP, adenosine triphosphate; GH, growth hormone; GI, gastrointestinal; IC, intracellular. When illness limits the intake of adequate nutrients, a prolonged recovery time is anticipated. Protein‐calorie malnutrition will impair immune function and result in a greater risk of infection. However, providing nutritional support early in the course of hospitalization has been shown to improve outcome of both human and veterinary ICU patients [7,8]. A positive correlation has been found between the type of nutritional support provided, the amount of energy produced, and the outcome from critical illness [9,10]. The goals of nutritional support are to meet nutritional requirements, reverse metabolic consequences of malnutrition (such as muscle loss), and improve recovery time [2]. A nutritional plan is prepared for the small animal patient on the first day of hospitalization. The plan should address the following four questions: Information derived from diagnostic and monitoring procedures will be incorporated into the patient nutritional assessment. The data collection begins with a thorough history and physical examination, followed by cage‐side point of care (POC) laboratory testing, clinicopathological testing, and diagnostic imaging. The goal is to create a nutritional plan that answers the four questions above. The World Small Animal Veterinary Association has produced a Global Nutrition Toolkit containing guidelines and forms to assist the veterinary team in creating an optimal nutritional plan for small animal patients (http://www.wsava.org/nutrition‐toolkit). Monitoring procedures will assess the response to feeding, with the goal of minimizing complications and maximizing outcome. The history begins with the species and signalment (age, sex, breed). There are different nutritional requirements for the dog compared to the cat (Table 16.3). Young growing animals, gestating or lactating females, and geriatric animals will have differing caloric and nutritional needs. Breed‐related nutritional concerns such as predisposition for carnitine deficiency in Boxers, Doberman Pinschers, Great Danes, Irish Wolfhounds and other giant breeds and primary hyperlipidemia in Miniature Schnauzers and Shetland Sheepdogs can become important. Table 16.3 Nutritional requirements for adult cats and dogs [40]. *% dry matter basis. Past medical history and exposure to medications or toxins will guide the nutritional plan. Renal disease, liver disease, diabetes mellitus, pancreatitis, protein‐losing disease, and hypothyroidism are but a few of the chronic or recurrent disease states that can warrant a nutritional plan that might require alterations and supplementation. The diet history is necessary and should include the type and brand of food, amount fed, frequency of feeding, and length of time fed the current diet. Cats are carnivores and require many of their nutrients from meat‐based diets (see Table 16.2). Weight gain or loss and the period of time for the weight change are recorded as well as any food allergies. Current history should include when the patient last had a normal appetite, and the progression of change in appetite and food intake through to presentation. Any signs of GI dysfunction, such as bloating, excessive borborygmus, flatulence or eructation, salivating, nausea, regurgitation, vomiting, diarrhea or constipation, should be recorded. Any problems with food prehension, chewing or swallowing could become important. The physical examination begins with the temperature, pulse rate and intensity, respiratory rate and effort, and body and muscle condition scores. Hyperthermia suggests an increased demand for calories (increased metabolic rate). Hypothermia implies a slower metabolic rate that may be due to poor perfusion and shock, especially in the cat. Correction of the hypothermia is necessary before initiating the nutritional plan. Tachycardia (dogs), poor or absent peripheral pulses, pale mucous membrane color, and prolonged capillary refill time are physical peripheral perfusion parameters that indicate shock. Rapid or labored breathing requires active contraction of the respiratory muscles and an important expenditure of energy. Dehydration can be determined by tenting of the skin, dry mucous membranes and corneas, and eyes sunken within the orbit. Resuscitation and initial stabilization of circulatory and respiratory distress are required prior to initiating the nutritional plan (Figure 16.2). Figure 16.2 An algorithm to help determine when and how to initiate a nutritional plan. A complete physical examination is required, with particular attention given to the body weight, body condition score (BCS) (Figure 16.3) and muscle condition score (MCS) (Figure 16.4). A BCS <4/9 is low and >5/9 is high, each potentially prompting an adjustment in total calories to be fed and percentage distribution of protein, fats, and carbohydrates. Hepatomegaly and icterus are signs compatible with hepatic lipidosis in the cat and warrant early nutrition as a key component of therapy. Figure 16.3 Body condition score for dogs. A similar system may be used for cats. Used with permission from Nestlé Purina Pet Care. Figure 16.4 Muscle condition score for the dog and cat. Global Nutrition Committee Toolkit provided courtesy of the World Small Animal Veterinary Association. These guidelines were first published in J Small Anim Pract. 2011;52(7):385–96, published by John Wiley and Sons Ltd, and are published here with permission. The physical examination findings are used to select the feeding tube most appropriate for the patient. Problems within the oral cavity, altered mentation, and profound weakness are but a few of the viable reasons to initiate tube feedings. Nasogastric or nasoesophageal tubes may be an ideal choice for short‐term ( <5 days) enteral feeding. An esophagostomy or gastrostomy tube might be the better choice if resolution of an oral problem is going to take >5 days. Evidence of gastric paresis or ileus (bloated abdomen, reduced or absent bowel sounds, regurgitation) might direct placement of a tube with the distal end within the stomach to allow gastric decompression. Should it be necessary to bypass the stomach and upper duodenum, a jejunostomy tube is selected. A list of enteral feeding tube sites with tube size, indication, advantages, and potential complication is provided in Table 16.4. The finding of nausea or retching on abdominal palpation or diarrhea found on rectal examination will become important when prescribing the method of enteral feeding (Figure 16.5). The use of antiemetics and motility modifiers may be warranted, as well. Table 16.4 Common small animal enteral feeding tube location, size, indication, advantages, and disadvantages. Figure 16.5 Decision‐making schematic for the initiation of enteral feeding in a critically ill small animal with anorexia. The minimum database is obtained by POC testing and consists of the packed cell volume (PCV), total protein (TP), blood glucose, blood urea nitrogen (BUN), electrolyte panel (sodium (Na+), potassium (K+), chloride (Cl‐), ionized calcium (Ca++) and magnesium (Mg++)), blood gas, coagulation profile, platelet estimate, and urinalysis. The PCV and TP are evaluated together for an indication of dehydration or acute blood loss, requiring volume support prior to initiating any form of nutritional support. Anemia warrants an assessment of the need for iron supplementation. Low TP could warrant a higher percentage of calories from protein in the diet. Hyperglycemia might merit a lower percentage of carbohydrates in the diet and the administration of insulin while hypoglycemia could justify a higher percentage of carbohydrates. Examination of the serum for lipemia can direct a lower percentage of fat in the diet calculations where icterus, especially in the cat, can direct diagnostics for hepatic lipidosis. A high BUN can suggest renal disease, directing further testing and possibly altering the selection of diet to reduce the percentage of protein. A low BUN can bring concern for liver failure and hepatoencephalopathy, potentially warranting a lower percentage of dietary protein with an emphasis on branched chain amino acids. Prolongation of clotting times should trigger an assessment to determine the need for calcium and vitamin K supplementation. Significant electrolyte disorders should be corrected during the initial stabilization period and prior to implementation of the nutritional plan. Acid–base disorders should be stabilized prior to feeding when possible and monitored closely since metabolic acidosis can occur during parenteral feeding. The urinalysis should provide evidence of the kidneys’ ability to concentrate urine (specific gravity), proteinuria, glycosuria, and crystal formation, each a potential marker for dietary adjustments. A complete blood count (CBC) and serum biochemical profile should be submitted, with blood ammonia and thyroid panel. The presence of neutropenia or lymphopenia could indicate depression of immune function and warrant supplementation of specific nutrients, vitamins or minerals (see Tables 16.1 and 16.2). Hypoalbuminemia, as a component of low TP associated with infection or inflammation, warrants support of the immune system and supplementation of protein from the diet. The baseline serum phosphorus is very important in assessing the potential for refeeding syndrome, with hypophosphatemia requiring careful monitoring and supplementation (see Nutritional disorders, later in this chapter). High blood ammonia can justify lowering the protein in the diet. Low levels of thyroid hormone or high cholesterol might support a lower percentage of fat in the diet and potential adjustment of required calories. Imaging begins with plain thoracic and abdominal radiographs to assess organ size, position, and structure. An assessment of the entire length of the GI tract is important for evidence of obstruction, megaesophagus, stricture, gastric distension, ileus, fluid‐filled bowel, abdominal mass or peritoneal fluid. An assessment of the size of the caudal vena cava can provide an indication of intravascular volume and direct fluid stabilization prior to nutritional support. Special attention should be given to any evidence of aspiration pneumonia, which could contribute to the decision concerning the type of feeding tube (see Table 16.4) and the need for gastric decompression and antiemetics. A radiograph should be taken centering over the distal (internal) end of the feeding tube after placement to confirm the location and to discover any curling or kinking of the tube that needs correction prior to feeding. Endoscopy can be used to place gastrostomy tubes and direct placement of a feeding tube through the pylorus into the upper duodenum. Advanced imaging with ultrasound, computed tomography or nuclear magnetic resonance imaging may be necessary to diagnose the underlying problem. Indirect calorimetry is a technique that provides accurate estimates of energy expenditure from measures of carbon dioxide production and oxygen consumption during rest and steady‐state exercise. There are open and closed circuit methods. The technology has advanced to fully portable, electronic equipment that provides continual and instantaneous breath‐by‐breath values of pulmonary gas exchange. Open‐flow indirect calorimetry has been described in the dog and found to provide accurate data regarding oxygen consumption, carbon dioxide production, and resting energy expenditure [11]. While the calculation for the resting energy requirement (RER) is only an estimation, the measured resting energy expenditure in dogs provides a more accurate determination [11]. Indirect calorimetry is carried out on an individual basis. Disadvantages of indirect calorimetry include the lack of equipment availability, cost of equipment, time required for testing, and expense. Routine assessment of parameters related to nutrition should occur at least a twice daily (Table 16.5). Physical assessment should include body weight, BCS, perfusion and hydration status, and food consumption or delivery. While the body weight may fluctuate daily based on the fluid status and the underlying disease, a gain or loss in body weight of >1 kg in a 24‐hour period should be investigated. The amount of fluids given by IV or oral route is assessed to determine the impact this could have. A change in BCS during hospital stay would indicate a severe metabolic challenge and support the patient’s need for nutritional intervention. Alterations in mentation or level of consciousness should prompt further investigation for glucose alterations, serious electrolyte disorders, thiamine deficiency, refeeding syndrome or hepatoencephalopathy associated with protein in the diet or swallowing and digesting blood. The catheter site used for infusion of peripheral parenteral nutrition (PPN) or central parenteral nutrition (CPN) is evaluated for heat, redness, irritation or pain. Table 16.5 Parameters used to assess the impact of the nutritional plan in the critically ill dog and cat. BCS, body condition score; CPN, central parenteral nutrition; GRV, gastric residual volume; HE, hepatic encephalopathy; MCS, muscle condition score; PPN, peripheral parenteral nutrition. Monitoring the gastric residual volume (GRV) can be helpful in assessing tolerance to enteral feeding. A nasogastric or gastrostomy tube is used to aspirate gastric contents (fluid and air). Gastric residual volume is the volume of fluid aspirated from the stomach after a given period of time and before a new feeding [12,13]. High GRV has been correlated with a higher incidence of vomiting or regurgitation, leading to aspiration pneumonia and cessation of feeding in humans [14]. However, an increased GRV in the canine patient had no significant correlation with the occurrence of vomiting or aspiration pneumonia [15]. A high GRV can be an indication of enteral feeding intolerance (see Nutritional disorders, later in this chapter), requiring an adjustment in the amount, concentration or frequency of feeding. Every patient in the ICU deserves a nutritional plan formulated to meet his or her individual needs. Evaluating the history, physical examination, laboratory results, and diagnostic imaging results provides the initial nutritional assessment of the patient. Specific factors considered include current body weight, recent change in body weight, BCS, MCS, activity level, level of consciousness, condition of GI tract, blood glucose, presence of lipemia, and, of course, the underlying disease process. Oxygenation, ventilation, perfusion, bleeding, and hydration are key patient parameters requiring rapid stabilization prior to initiating any type of feeding regimen. Oxygen supplementation and intravenous fluid therapy (see Chapter 2) are common therapeutic interventions incorporated into the initial resuscitation plan. Serious electrolyte abnormalities, including disorders of Na+, K+, Ca++, and PO4‐, must be addressed (see Chapter 6). Hypoglycemia <60 mg/dL (3.33 mmol/L) is treated with IV dextrose (0.5 g/kg) and high blood ammonia reduced with oral lactulose or lactulose enemas prior to feeding. Hyperglycemia due to a diabetic crisis must be managed (see Chapter 5) prior to complicating glucose management with enteral or parenteral feeding. Evaluation of the GI tract will determine the need for gastric decompression or antiemetic, GI protectants, and motility modifying drugs. Common GI drugs used in the ICU, their mechanism of action, and dose are listed in Tables 15.6, 15.7, and 15.8, in Chapter 15. Short‐term intravenous amino acid solutions and trickle‐flow gastric feeding of glucose‐electrolyte oral solutions may provide a method of support and testing of gastric tolerance while determining the ability of the GI tract to tolerate feeding. There are only two routes for providing nutrition in the critically ill patient: enteral and parenteral. Providing nutrition through a functional digestive system is the preferred route of feeding. Maintenance of normal gut flora depends on normal GI motility and nourishment of the enterocytes. This form of feeding is less expensive, stimulates the immune system, decreases hospitalization days, and minimizes the metabolic consequences of refeeding [16–20]. Oral voluntary feeding is ideal but rarely results in consistent intake of adequate quantities of the desired nutrients in critically ill small animals. Oral forced feeding is not recommended and can lead to food aversion, excessive salivation, and stress to the animal. Appetite stimulants, such as cyproheptadine (cats only: 0.1–0.5 mg/kg PO q 8–12 h) and mirtazapine (3.75 mg/cat PO q 3 days; 0.55 mg/kg PO q 24 h, maximum dose 30 mg per day), can be given but do not result in consistent intake of nutrition, making them unreliable for critical patients. Tube feeding provides a convenient and consistent method for delivering a desired quantity and concentration of diet to the GI tract. Choosing the ideal feeding tube depends on the desired diameter and length of the tube, ease of placement, comfort level to the patient, cost of placement, and the estimated length of time the tube will be in place. Table 16.4 lists common sizes, indications, advantages, and disadvantages for nasogastric (NG), nasoesophageal (NE), esophagostomy (E), gastrostomy (G), jejunostomy (J), nasoduodenal (ND), and nasojejunal (NJ) tubes. Feeding tube placement should be confirmed by radiography, endoscopy or at the time of surgery. Complications include tube dislodgment, misplacement, inadvertent tube removal by patient, local infection or inflammation, or clogged tubes from medications or food. For surgically placed G or J tubes, early dislodgment may cause further complications such as peritonitis or fasciitis. Should the patient vomit a tube, there is a possibility that the animal can bite and swallow the tube segment, creating a gastric foreign body. When the tube is no longer needed, it is removed and confirmation that the entire tube has been removed is made (measure removed tube length against identical unused tube). Any stoma present is cleaned and allowed to heal by second intention. Nasal and J tubes must be small in diameter to pass through the nose or into the bowel, limiting the diet to liquid formulations. Diluted blended canned diets can be placed through the larger diameter E and G tubes. Enteral tube feeding can occur by one of two methods: bolus feeding (liquid or blended diets) and trickle‐flow feeding (liquid). Figure 16.5 provides a schematic for determining which methods might be most appropriate for the individual patient. Bolus feeding is chosen when the GI tract is assessed as having normal motility and function. Bloat, poor motility, vomiting or frequent bouts of diarrhea are signs of GI sensitivity justifying the selection of trickle‐flow feeding methods. Box 16.1 outlines the method for bolus feeding a patient an enteral diet. Box 16.2 outlines the method for trickle‐flow (continuous rate of infusion) feeding. Nursing care for feeding tubes is found in Table 20.6.
Nutritional status
Introduction
Component
Effect
Hypoalbuminemic malnutrition
associated with infection or inflammation; modulated by hormones and cytokines (IL‐1, TNF‐alpha)
Depletes visceral protein (albumin) stores; depressed cell‐mediated immunity
Humoral immunity
Decline in production of IG, secretory antibodies, complement
Neutropenia
Capacity of neutrophils to kill phagocytosed bacteria decreased; decreased cytokine secretion
Immune components
Complement, interferon production, opsonization, plasma lysosome production, acute‐phase reactants
Depressed production and/or function
Thyroid, lymphoid tissues
Atrophy, decreased peripheral T‐lymphocytes, impaired response of lymphocytes to mitogens; depressed response to contact sensitivity, inflammatory reactions, and vaccines
Anatomical barriers
Disrupted, atrophy of skin and GI mucosa
Nutrient
decreased
Functions
Clinical consequences
Notes
Water
(most important nutrient)
Water is necessary for cellular life, chemical and metabolic reactions, transport of nutrients and other substances, cushion joints and brain tissues, body temperature regulation, and elimination of wastes
Dehydration; poor skin turgor, dull, dry corneas, mucous membranes, oliguria, eventually death
Severe deficit causes poor perfusion
Arginine
(essential amino acid for dog and cat)
Entry into urea cycle with high blood ammonia; stimulates release of GH, insulin, glucagon; substrate for nitric oxide production; promotes collagen deposition in wounds; stimulates T‐cell function and growth of lymphocytes
Dementia, seizures, altered consciousness; poor wound healing, poor immune response
Cats lack intestinal pyrroline‐5‐carboxylate synthase to make precursor ornithine; enriched diets enhance immune function and wound healing; better results if combined with omega‐3 fatty acids; energy and protein requirements must be met for good result of supplementation
Glutamine
(essential amino acid in catabolic state)
Synthesis pathway attenuated in critical illness; low levels signal skeletal muscle protein catabolism; provides fuel for rapidly dividing enterocytes, endothelial cells, renal tubular cells and lymphocytes; essential nucleotide precursor
Muscle wasting, gastrointestinal signs with poor healing, immune system dysfunction infection; supplement could cause azotemia in renal failure, high ammonia in liver failure
Decreased IC concentration in critical illness; unstable in solution; immune enhancing when added to standard diets; enhances GI tolerance in shock; ideal in early management of critical surgical patients
Carnitine
Key component of lipid metabolism and energy production
Myocardial disease in some dogs; possible hepatic lipidosis cats
Taurine
Required to synthesize bile acids to absorb dietary fats; regulates calcium flux; neurotransmission; antioxidant; stabilizes cells membranes; may have role in bioelectrical potentials, myocardium, retinas
Reproductive failure, developmental abnormalities, retinal degeneration, dilated cardiomyopathy
Cats cannot synthesize and have ongoing loss in feces and urine
Thiamine (vitamin B1)
Helps convert carbohydrates to glucose for energy production; needed to form ATP by all cells, especially brain
Deficit causes GI (vomiting, salivation), and neurological signs (ventroflexion of head and neck, vocalization, dementia, seizures, abnormal gait, stupor)
Cats very susceptible; diets deficient or thiaminase in some GI bacteria and in some raw fish common causes; water‐soluble vitamin
Vitamin A
Hormone‐like growth factor for epithelial and other cells; necessary for light absorption in retina; important for immune function, gene transcription and protein formation
Blindness, impaired immunity
Cats must ingest preformed vitamin A; lack dioxygenase enzymes in the intestinal mucosa to split the beta‐carotene molecule to vitamin A aldehyde
Arachidonic acid
(essential omega‐6 fatty acid)
Maintains cells wall integrity
Poor hair coat quality, poor tissue integrity
Cats cannot produce from linoleic acid; animal source fats required for cats
Niacin
(vitamin B3)
Helps convert carbohydrates to glucose for energy; helps use fats and proteins; affects nervous system, skin, eyes, hair coat
Diarrhea, flaky skin, poor response to stress
Cats cannot convert tryptophan to niacin; high meat diet required; high doses can cause “flushing”; water‐soluble vitamin
Zinc
Role in protein and nucleic acid metabolism
Depressed wound healing, increased protein catabolism, depressed immune function
Omega‐3 fatty acids
Source of energy in dogs and cats; incorporated into cell membranes, maintain membrane fluidity, permeability, receptor functions; precursors to eicosanoids (omega‐3 derived less metabolically active than omega‐6 derived eicosanoids); antiinflammatory – inhibit production of inflammatory mediators; positive effect immune barrier of skin
Must be incorporated in cell membranes to be metabolically active;
supplementation could increase vitamin E requirements
Diagnosis
History and physical examination
Nutrient
Adult cats
Adult dogs
Type (source)
Carnivore (meat)
Omnivore (meat and plant)
Essential amino acids
Arginine, histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine, and taurine
Arginine, methionine, histidine, phenylalanine, isoleucine, threonine, leucine, tryptophan, lysine, and valine
Protein %*
30–45%
15–30%
Fats %*
10–30%
10–20%
Carbohydrates %*
<50%
50%
Tube location
Indications
Advantages
Disadvantages
Notes
Nasogastric
Size: 5–12 Fr
<7 days; aspiration of gastric fluid, air;
deposit food in stomach
Only mild sedation required; inexpensive; no incisions; monitor gastric fluid/air; gastric decompression; easy removal
Irritation to nose (epistaxis, rhinitis); can cause irritation to gastric mucosa; dacryocystitis; can stimulate vomiting; aspiration pneumonia; small diameter tubes; liquid diet required
Ideal for early trickle‐flow feeding; excellent for severely emaciated animals; radiograph confirms placement
Nasoesophageal
Size: 5–12 Fr
<7 days; feeding small volumes, liquid diet
Only sedation required; inexpensive; no surgical incisions; unlikely to stimulate vomiting or irritate gastric mucosa
Irritation to nose (epistaxis, rhinitis); can cause irritation to gastric mucosa; dacryocystitis; can stimulate vomiting; aspiration pneumonia; small diameter tubes; liquid diet required; not ideal if increased intracranial pressure
Ideal for early trickle‐flow feeding; excellent for severely emaciated animals
Esophagostomy
Size:
12–22 Fr
>5 days; functioning esophagus; oral and pharyngeal disease (bypasses mouth and pharynx)
Short surgical procedure; remains for weeks to months if needed; easy removal; can feed canned food mixed with water or liquid diet
Requires anesthesia w/tracheal intubation; incisions in skin and esophagus; possible infection at stoma site
Excellent for cats with hepatic lipidosis; possible placement of tube through esophagus into mediastinum
Gastrostomy
Size:
18–24 Fr
balloon or mushroom tipped
>14 days;
oral, pharyngeal or esophageal disorders, permanent supplemental feeding, altered level of consciousness
Remains for weeks to months if needed; leaves head and neck free; can feed canned food mixed with water or liquid diet; easy removal after 14 days
Requires surgery or endoscopy for placement; incision through gastric and abdominal body wall required; possibility of peritonitis, abscess, fasciitis; stoma must form prior to removal of tube
Jejunostomy
Size:
5–12 Fr
>7 days; bypass mouth, esophagus, stomach and duodenum (pyloric obstruction, pancreatitis, gastric motility disorders, biliary disease)
Feed liquid diet by constant rate of infusion
Requires laparotomy for placement; stoma formation required prior to removal; possibility of peritonitis or abdominal abscess; requires liquid diet
Primarily used for in‐hospital feeding of critical patients; requires monomeric diet
Nasoduodenal or nasojejunal
Size:
5–12 Fr
<7 days;
bypass mouth, esophagus, stomach and duodenum (pyloric obstruction, pancreatitis, gastric motility disorders, biliary disease)
Feed liquid diet by constant rate infusion; no surgery required
Requires endoscopy or fluoroscopy for placement; not ideal if increased intracranial pressure; required liquid diet
Primarily used for in‐hospital feeding of critical patients; requires monomeric diet 
Point of care laboratory testing
Clinicopathological testing
Diagnostic imaging
Advanced testing
Monitoring methods
Monitored parameter
Impact
Notes
Body weight
Should remain constant or slightly increase after stabilization
Is a function of fluid input (IV and oral fluids), third body fluid spacing, fluid losses (urine, vomit, diarrhea, gastric aspiration, evaporation from panting)
BCS, MCS
Should only improve over time
A decline suggests an inadequate nutritional plan
Physical perfusion parameters (heart rate, body temperature, mucous membrane color, pulse intensity, capillary refill time)
Poor perfusion implies an intravascular volume deficit if cardiac function is adequate
Will have significant effect on fluid balance and body weight
Physical hydration parameters (skin turgor, mucous membrane and corneal moisture, eye position in bony socket)
Dehydration implies inadequate fluid balance; peripheral edema, chemosis or rapid, labored breathing can indicate overhydration
Both can affect body weight. An abnormality in hydration requires immediate adjustment of quantities of IV and oral fluids administered
Feeding tube productivity
Air and fluid aspirated should be quantified
Can serve as an estimate of GRV, guiding enteral diet volume and concentration
Neurological exam
Onset of dementia, depressed mentation, stupor, coma or seizures warrants rapid assessment of the nutritional plan
Glucose, electrolyte, and thiamine concentrations are assessed and stabilized. Concern for HE in a patient with liver disease warrants treatment with lactulose by enema and orally. An alteration in the dietary protein may be required
Catheter sites for CPN, PPN
Examined for heat, redness, swelling, pain, exudate
Any evidence of inflammation warrants removal of catheter and replacement in a different location
Blood glucose
(2× daily)
Alterations warrant evaluation of carbohydrate source and quantity in diet and assessment for glucose disorders
Serum electrolytes
(2× daily)
Na+, K+, Ca++, Mg++, and PO4‐ are evaluated for alterations
Total body deficits can be present in spite of normal serum levels. Abnormalities could suggest refeeding syndrome and require stabilization
Formulating the nutritional plan
Patient preparation
Feeding methods
Enteral feeding methods
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