General Surgery (Board Review Series) 1st Edition

3

Surgical Nutrition

Gerald A. Cephas

Traves D. Crabtree

1. Assessment of Nutritional Status
2. History and physical examination
3. Weight loss

• is a significant indicator of malnutrition.

1. More than 10% unintentional weight loss

• in a 6 month period is significant.

1. A 5% unintentional weight loss

• in 1 month is also significant.

2. Other suggestive findingsin the history include

• anorexia.
• persistent nausea.
• vomiting.
• diarrhea.
• generalized malaise.

3. Significant physical findingsinclude

• loss of subcutaneous fat.
• muscle wasting.
• edema.
• ascites (late finding).

4. Signs suggestive of specific nutrient deficienciesinclude

• skin rash.
• pallor.
• cheilosis.
• glossitis.

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• gingival lesions.
• hepatomegaly.
• neuropathy.
• dementia.

1. Evaluation of body composition
2. Estimates of ideal body weight (IBW)are:
3. Men:106 lb + 6 lb for each inch over 5 feet (height).
4. Women:100 lb + 5 lb for each inch over 5 feet.

• The IBW also depends on patient age and overall body habitus.

2. Other measures include

• anthropometric measurements, including triceps skin foldor midarm muscle circumference.
• densitometry.

3. The body mass index (BMI)

• is used to characterize the degree of obesity.
• BMI = weight (kg)/total body surface area (m²).

1. Patients with a BMI higher than 40 or over 35 with other comorbid conditions

• are considered candidates for surgical treatment of morbid obesity.

1. Severe obesity

• is associated with a significant increase in overall morbidity and mortality.

1. Laboratory markers of nutritional status
2. Several serum proteins

• are used to evaluate nutritional status (Table 3-1).

1. Severe hypoalbuminemia

• is associated with poor outcome in surgical patients.

1. Serum albumin

• has a long half-life, and as such, it is not a reliable short-term marker for nutritional assessment during nutritional support.

1. Serial measurements of transferrin as well as prealbumin, and retinol-binding protein

• are useful in monitoring the impact of nutritional support.

Table 3-1. Serum Proteins Used as Markers of Nutritional Status

Protein Half-life (days) Albumin 20 Transferrin 8.5 Prealbumin 1.3 Retinol-binding protein 0.4

2. Energy expenditure

• can be measured by the respiratory quotient (RQ).

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1. RQ= carbon dioxide production (VCO₂)/oxygen consumption (VO₂).
2. Indirect calorimetry (metabolic cart)

• allows for gas analysis and subsequent calculation of the RQ.

1. An RQ value

• of 1.0is consistent with predominant glucose utilization.
• of 0.7 and 0.8is consistent with fat and protein utilization, respectively.
• higher than 1.0suggest the presence of lipogenesis or overfeeding.

1. These values are used

• to estimate the adequacy of nutritional support.

3. Measures of immune function

• have also been used to assess nutritional status.
• Skin anergy teststo assess the delayed type hypersensitivity response to antigens (e.g., mumps, tuberculosis, Candida) have been used as such markers.
• Although a poor response may be found in malnourished states, these markers have been relatively unreliable in assessing nutritional status.

1. Nutritional Requirements
2. The basic assessment of patients' nutritional needs includes

• total energy (kcal) requirements.
• total protein requirements.
• the relative distribution of calories between carbohydrates, fats, and protein.

1. Energy requirements
2. The Harris-Benedict equation

• estimates the basal energy expenditure (BEE)or basic energy requirements at rest in kcal/day.

13. Men:66 + (13.7 × weight [kg]) + (5 × height [cm]) – (6.8 × age [years]).
14. Women:655 + (9.6 × weight [kg]) + (1.7 × height [cm]) – (4.7 × age [years]).
15. Most patients at restrequire 25–35 kcal/kg/day.

. Stress significantly increases these values.

• Low stress: 1.2 × BEE.
• Moderate stress: 1.2–1.3 × BEE.
• Severe stress: 1.3–1.5 × BEE.
• Major burn injury: 1.5–2.0 × BEE.

1. Energy requirements are increased by

• fever.

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• infection.
• activity.
• burns.
• head injury.
• trauma.
• renal failure.
• surgery.

1. Energy requirements are decreased by

• sedation.
• paralysis.
• β blockers.

3. Differing amounts of kcal/g are produced by

• carbohydrates, proteins, and lipids.

1. Carbohydrates

• generally provide 4 kcal/g.
• Dextrose provides 3.4 kcal/g.

1. Proteins

• generally provide 4–5 kcal/g, depending on the amino acid composition.

1. Lipids

• generally provide 9 kcal/g.

1. Carbohydrates

• should generally account for 30%–60% of total calories.

1. A minimum of 100–150 g/day

• is necessary to provide the minimum needs of the brain and red blood cells, which prefer glucose as an energy source.

1. Glucose is stored

• as glycogenin the liver (40%) and in muscle (60%).

1. The body stores300–500 g of glycogen.
2. These stores are depleted

• within 48 hoursduring starvation.
• in as little as 12–24 hours in the stressed patient.

1. Proteins
2. Most healthy individualsrequire 0.8–1.0 g protein/kg/day.
3. Stressincreases these requirements:

• Mild stress: 1.0–1.2 g/kg/day.
• Moderate stress: 1.3–1.5 g/kg/day.
• Severe stress: 1.5–2.5 g/kg/day.

3. Patients with renal failure

• may also have a higher protein requirement compared with baseline.

4. Patients with hepatic encephalopathy

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• may require less protein (0.8 g/kg/day) to avoid additional encephalopathy.

5. Nitrogen balance

• is a crude measure of protein consumption.
• is calculated by determining the difference between net nitrogen intake and excretion.
• Positive nitrogen balance
• indicates more protein ingested than excreted (net protein anabolism).
• Negative nitrogen balance
• indicates more protein is excreted than ingested (net protein catabolism).
• Protein excreted in the urine
• can be measured over 12–24 hours:
• protein (g) = nitrogen (g) × 6.25.
• Neutral nitrogen balance
• is the goal, although positive nitrogen balance is frequently present during the recovery phase of illness.

6. Amino acids(Table 3-2)
7. Essential amino acids

• cannot be produced by the body, but nonessentialamino acids can.

1. Amino acid metabolism

• Most amino acids are metabolized by the liver.
• The branched-chain amino acids are metabolized by muscle.

1. Patients require

• at least 20% of their protein intake as essential amino acids.

1. Generally, protein metabolismin muscle

• is regulated by insulin.

Table 3-2. Essential and Nonessential Amino Acids

Essential Semiessential Nonessential Leucine* Glycine Isoleucine* Arginine Valine* Proline Lysine Glutamic acid Tryptophan Aspartic acid Histidine Serine Methionine↔ Cystine† Alanine Phenylalanine↔ Tyrosine† *Branched-chain amino acids. †Cystine and tyrosine are considered semiessential because when methionine and phenylalanine are supplied in adequate amounts, their requirement can be satisfied.

7. Glutamine

• is the most abundant amino acid in the blood.
• It is the principal fuel for enterocytes

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1. and may play an essential role in maintaining mucosal integrity during times of stress.

• Glutamine
• may also be required for lymphocyte and macrophage proliferation.

1. Lipids
2. Lipids should provide

• 25%–40%of total calorie requirements during nutritional supplementation.

2. Fatty acids

• are a major fuel for the heart, liver, and skeletal muscle.

3. Liver oxidation of fatty acidsforms ketone bodies (e.g., β-hydroxybuturate).

• These ketone bodies are used by the heart, skeletal muscle, and the brainspecifically during times of starvation.

4. During the fed state, insulin

• stimulates lipogenesis and fat storage and inhibits lipolysis in adipocytes.

5. Triglycerides
6. Long chain triglycerides

• must be emulsified by bile saltsto form micelles.
• must be hydrolyzed by pancreatic lipasein the proximal small bowel before absorption can occur.

1. Medium chain triglycerides

• are absorbed directly by the enterocytes.
• are transported through the portal venous system to the liver.
• may be readily absorbed despite significant deficiencies in pancreatic function (i.e., severe pancreatitis).

6. During intravenous (IV) nutritional supplementation

• a minimum of 3%–5% of the total calories as fat is necessary to prevent essential fatty acid deficiency.

1. The essential fatty acids

• are linoleicand linolenic acid.
• act as precursors for prostaglandins and eicosanoids.

1. Essential fatty acid deficiencymay result in

• dermatitis.
• ecchymoses.
• alopecia.
• anemia.
• edema.
• thrombocytopenia.
• respiratory distress.

1. The manifestationsof fatty acid deficiency may occur within 4–6 weeks if nutritional support does not include lipids.

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1. Other requirements
2. Vitamins
3. Potential vitamin deficiencies can occur

• in severely malnourished patients.
• in patients receiving chronic nutritional support.

3. Characteristics of several vitaminsas well as implications of deficiency are outlined in Table 3-3.

• Of note, impaired wound healingmay be a direct result of deficiencies in vitamin A, vitamin C, and the mineral zinc.

2. Minerals

• Characteristics of several essential mineralsas well as implications of deficiency are outlined in Table 3-4.

III. Alterations During Stress

1. Carbohydrates
2. The major hormonesthat play an active role in metabolism in the presence of stress or sepsis include

• adrenocorticotropic hormone (ACTH).
• cortisol.
• catecholamines.
• glucagon.

2. Hyperglycemia

• is frequently present during stress secondary to a relatively low insulin level and peripheral insulin resistance.

1. Insulin secretion may be inhibited by

• catecholamines.
• sympathetic nervous system activation.
• somatostatin.

1. Catecholamines and cortisol

• also contribute to a relative resistance of peripheral tissues to the effects of insulin.
• Despite this relative insulin resistance, there is still an overall increase in peripheral glucose utilization.

3. Liver glycogenolysis and gluconeogenesisare stimulated by

• catecholamines.
• cortisol.
• glucagon.

4. The glucoseproduced from these processes is essential for certain tissues, including

• red blood cells.
• white blood cells.

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• the renal medulla.
• neural tissue.
• wound tissue.

Table 3-3. Vitamins and Vitamin Deficiencies

Vitamin RDA Function Characteristics of Deficiency Vitamin A (retinol) 800–1000 µg Active site of rhodopsin (retinal pigmentation), glycoprotein synthesis, soft tissue and bone growth Night blindness, xerophthalmia, keratomalacia,impaired wound healing, hypogonadism Vitamin D (cholecalciferol) 5–7.5 µg Calcium absorption from the gut, calcium homeostasis Rickets (children), osteomalacia (adults) Vitamin E (α-tocopherol) 8–10 mg Antioxidant Hemolytic anemia, ataxia, nystagmus, loss of DTR's, myopathy, edema, infertility Vitamin K 70–140 µg δ-carboxylation of glutamic acid in clotting factors II, VII, IX, X, protein C & S Coagulopathy Vitamin C 60 mg Antioxidant, proline hydroxylation in collagen synthesis and cross-linking Poor wound healing, scurvy, gingivitis Thiamine (B1) 1.2–1.7 mg Decarboxylation of α-keto acids involved in carbohydrate metabolism Wernicke's encephalopathy, peripheral neuropathy (dry beriberi) ± cardiomyopathy and high output heart failure (wet beriberi) Pyridoxine (B6) 2.0–2.2 mg Coenzyme for amino acid deamination, transamination, and carboxylation; involved in synthesis of niacin from tryptophan, DOPA decarboxylase activity, and glucose metabolism Sideroblastic anemia, weakness, cheilosis, glossitis, peripheral neuropathy Cobalamin (B12) 2–4 mg Coenzyme for demethylation involved in purine and pyrimidine synthesis Megaloblastic anemia, peripheral neuropathy Biotin (B2Complex) 100–200 µg Coenzyme for carboxyl transfer in carbohydrates, lipids, and amino acids Dermatitis, mucositis, atrophy of lingual papilla, paresthesia Niacin 13–19 mg Coenzyme for oxidation-reduction reactions and energy metabolism. Active forms: NAD+ and NADP+ Pellagra (dermatitis, diarrhea, dementia) Riboflavin 1.2–1.7 mg Oxidation-reduction reactions, flavoprotein enzymes Dermatitis, glossitis (magenta tongue), mucositis, angular stomatitis Folate – Involved in purine and thymine synthesis for DNA Leukopenia, megaloblastic anemia, glossitis Pantothenic acid 4 mg Involved in synthesis of Coenzyme A; used for acyl transfer in amino acid, carbohydrate, and fat metabolism Heel tenderness, altered mental status, gastro-intestinal complaints RDA = Recommended dietary allowance; DTR's = deep tendon reflexes; NAD+ = nicotinamide adenine dinucleotide (oxidized form); NADP+ = nicotinamide adenine dinucleotide phosphate (oxidized form).

Table 3-4. Minerals and Trace Element Deficiencies

Nutrient RDA Function Characteristics of Deficiency Iron 10–18 mg Component of hemoglobin, myoglobin, and cytochromes Hypochromic anemia Zinc 15 mg Metalloenzymes involved in carbohydrate, protein, and nucleic acid synthesis Impaired wound healing, acrodermatitis enteropathica (bullous skin lesions of the face), hypogonadism Iodine 150 mg Thyroid hormone synthesis Hypothyroidism, goiter Copper 2.0–3.0 mg Metalloenzymes, iron uptake in hemoglobin Menkes' syndrome, anemia, leukopenia Manganese 2.5–5.0 mg Enzyme cofactor in protein and energy metabolism Unknown Fluoride 1.5–4.0 mg Found in bone and tooth apatite Increased caries Chromium 0.05–0.2 mg Insulin cofactor Glucose intolerance, hyperlipidemia Selenium 0.05–0.2 mg Enzyme cofactor in hydrogen peroxide detoxification Keshan disease (cardiomyopathy), anergy Molybdenum 0.15–0.5 mg Bioelement in a number of proteins Unknown RDA = Recommended dietary allowance.

1. Proteins
2. Protein synthesisincreases during stress.

• Net proteolysis and negative nitrogen balance, however, are characteristic of severe stress.

2. Alanine release

• from peripheral tissues increases during stress because it is the major source of amino acid substrate for gluconeogenesis in the liver (Figure 3.1).

3. During severe sepsis, muscle protein loss may occur at 240 g protein/day.

• Interleukin (IL)-1 may play a role in stimulating proteolysis in this setting.

1. Lipids
2. During severe stress, lipolysis is stimulatedby increased

• cortisol.

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• catecholamines.
• glucagon.
• growth hormone.
• ACTH.
• sympathetic activity.

2. This increased lipolysisoccurring during stress is often characterized by an RQ of 0.7.

Figure 3-1. Recycling of metabolites to produce glucose during stress: gluconeogenesis and the Cori cycle. BCAA = branched-chain amino acids; AA = amino acid. (Adapted with permission from Way LW: Current Surgical Diagnosis and Treatment, 10th ed. Stamford, CT, Appleton & Lange, 1996, p 151.)

1. Nutritional Supplementation
2. Nutritional supplementation

• has been shown to improve overall outcome in selected patients.

1. This has benefitedhigh-risk patients who

• are severely malnourished.
• are critically ill.
• have massive burn injury.
• have incurred severe trauma.

1. Other patients who may benefitinclude those in whom an illness or operative procedure may delay oral intake for at least 7–10 days.

• Nutritional support should be initiated early in these settings because it is more effective at preservation of body mass than for repletion.

1. Normally nourished patients

• undergoing surgical procedures where oral intake will be delayed for fewer than 7 days generally do not require nutritional support beyond fluid and electrolyte administration with dextrose.

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1. Enteral nutritional support
2. When a patient requires nutritional support

• the enteral route is indicated in all patients with an intact, functional gastrointestinal (GI) tract.

2. Well-nourished patients with an anticipated inability to eat who may benefit from enteral feedinginclude those with

• severe facial or oropharyngeal trauma.
• swallowing abnormalities.
• oral or upper GI obstruction/dysfunction.

3. Potential benefits include

• prevention of intestinal mucosal atrophy.
• preservation of intrinsic gut immune function.
• inhibition of stress-associated increases in intestinal permeability.

4. Enteral nutritional support may be provided

• via oro-enteric or nasoenteric routes or by direct enteric routes (e.g., gastrostomy or jejunostomy).

1. Small-bore nasoenteric feeding tubes

• may be used for short-term and intermediate-termnutritional support.

1. Nasoduodenal tubes

• are preferred in most patients because of the potential increased risk of aspiration with nasogastric tubes.

1. A gastrostomy or jejunostomy tube

• may be indicated for direct enteral feeding for patients who require long-term nutritional support.

1. Potential complications

• of these routes of nutritional support are outlined in Table 3-5.

5. Relative contraindications to enteral feedinginclude

• mesenteric ischemia.
• bowel obstruction.
• intra-abdominal sepsis.
• necrotizing pancreatitis.
• high-output GI fistula.
• short bowel syndrome (see Chapter 13).

6. The most frequently cited advantageof enteral feeding versus parenteral feeding is the relative decreased infection rate in critically ill patients fed enterally.

• Table 3-6outlines the comparison between enteral and parenteral nutrition.

7. A variety of commercially available formulas are used for enteral feeding.

• They provide varying amounts of calories, carbohydrates, protein, and lipids.

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1. Some specialized formulasare marketed as having an immune-enhancing function because of the addition of certain substrates.

Table 3-5. Complications Associated with Enteral Nutritional Support

Complication Prevention and Management Inadvertent placement of nasoenteric tube into trachea or bronchus Careful attention to proper tube placement Inadvertent intra-abdominal injury during placement of gastrostomy or jejunostomy tube (e.g., liver injury, colon injury, adhesions) Careful surgical technique Aspiration Elevate head of bed ≥ 30°, avoid large gastric residuals (>150 mL), tube placement beyond pylorus, correction of ilius (i.e., electrolyte abnormalities) Obstruction of feeding tube Flush tube frequently with water, avoid insertion of large particles (e.g., pills) Tube rupture or malfunction Handle feeding tube carefully Ulceration of external nares with nasoenteric tube Secure tube appropriately with frequent skin care and monitoring Leakage or irritation around gastrostomy or jejunostomy tube site Appropriate initial tube placement, close wound monitoring, and local wound care techniques Sinusitis or otitis media or parotitis Avoid long-term use of nasoenteric tubes Nausea, vomiting Reduce flow rate, increase time interval Esophageal erosion between intermittent feedings Diarrhea Reduce flow rate, reduce formula concentration, appropriate formula selection Metabolic abnormalities (e.g., hyperglycemia, electrolyte abnormalities, dehydration, overhydration) Monitor blood glucose, electrolytes, and fluid status

1. Glutamine

• may play a role in maintaining intestinal mucosal integrity and immune function.
• levels fall significantly during severe stress and sepsis, therefore repletion may potentially benefit such patients.

2. Argininemay

• improve nitrogen balance.
• improve wound healing.
• stimulate T-cell responsiveness.
• act as a precursor to nitric oxide synthesis.
• reduce overall infectious complications.

3. Omega-3 fatty acidsfound in fish oils

• act as precursors for eicosanoids.
• may also potentially play an immunoregulatory role.

4. Nucleotide supplementationmay improve T lymphocyte function.

• T lymphocytes depend on hepatic synthesis of nucleotides, which is significantly decreased during severe stress and sepsis.

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Table 3-6. Enteral Versus Parenteral Nutritional Support

Enteral Parenteral Advantages Maintains mucosal integrity Decreased infectious complications No IV access required Less expensive Advantages Useful when gut unavailable or nonfunctional Avoids inherent risks of enteral tube placement Disadvantages Risk of aspiration Inherent risks of enteral tube placement Intolerance of GI tract to enteral feeds Disadvantages Increased risk of catheter infection Complications of central venous catheterization (pneumothorax, arterial injury) Rapid metabolic abnormalities (e.g., hyperglycemia, hypoglycemia, dehydration) Very expensive IV = intravenous; GI = gastrointestinal.

1. The potential benefit of decreasing infectious complications

• is suggested by early studies, although the impact of these formulas on improving mortality and overall outcome is still uncertain.

1. These new immune-enhancing formulas contribute to a significant cost increase.
2. Complications of enteral feeding

• are generally related to tube placement and function, although other factors may play a role.

1. Parenteral nutrition
2. Total parenteral nutrition (TPN)

• is indicated in patients who require nutritional support when the GI tract is unavailable or nonfunctional.

2. TPN must be administered

• via a central venous catheter placed in a large central vein (e.g., subclavian vein).

1. The hyperosmolarityof the solutions

• precludes administration through smaller veins.

1. Complications

• associated with central venous catheter placement are a frequent source of morbidity associated with parenteral nutrition.

3. Several metabolic complications

• may occur in association with parenteral nutrition (Table 3-7).

4. Refeeding syndrome

• may develop rapidly in severely malnourished patients started on parenteral nutritional support.

1. This is most frequently associatedwith

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• administration of high-calorie supplements and supplements high in carbohydrates.

Table 3-7. Complications Associated with Parenteral Nutrition

Complication Prevention and Management Complications associated with central venous catheter placement (e.g., pneumothorax, arterial injury, air embolism) Careful attention to catheter placement (see Chapter 2) Catheter-associated infection and sepsis Attentive catheter maintenance care, prompt replacement of catheter (i.e., over guidewire or removal and placement at alternative site) as indicated if infection presents Hyperglycemia Insulin supplementation, decrease rate of infusion, supplement caloric intake with relatively higher percentage of lipids Hypoglycemia (often seen with sudden discontinuation of parenteral nutrition) Glucose administration, slowly wean parenteral therapy over 24 hour period as oral intake increases Electrolyte depletion (e.g., hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia) Monitor serum electrolytes, appropriate IV electrolyte supplementation acutely, supplementation of parenteral solutions with additional electrolytes as needed Electrolyte excess (e.g., hyperkalemia, hyperphosphatemia, hypercalcemia) Immediate discontinuation of current parenteral solution, administration of crystalloid, treatment of specific excess as needed (see Chapter 7) Hyperchloremic metabolic acidosis Decrease chloride supplementation, replace with sodium acetate and potassium acetate salts instead of NaCl and KCl Refeeding syndrome Slowly increase initial rate of administration over 24-hour period, monitor blood glucose and electrolytes, aggressive replacement of PO4- salts as needed for hypophosphatemia Dehydration Monitor fluid status closely, administer crystalloid separate from parenteral solutions as needed Overhydration Concentrate parenteral solutions, provide higher percentage of calories with lipid solutions versus carbohydrates Essential fatty acid deficiency Co-administration of lipid emulsions IV = intravenous.

1. Abrupt administration

• of high energy supplements results in massive cellular utilization of glucose and intracellular phosphatesubstrates.

1. This can result in significant hypophosphatemiawith

• malaise.
• lethargy.
• perioral paresthesias.
• tremors.
• dysarthrias.

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• coma.
• even death.

1. Phosphorus supplementation

• can be used in the treatment and prevention of this syndrome.

5. Co-administration of lipid solutionswith standard parenteral nutrition solutions

• help to prevent essential fatty acid deficiency.
• provide a relatively high density source of calories compared with carbohydrates.

1. Lipid solutions

• provide more calories in a smaller volumethan carbohydrate solutions, which is important in patients at risk for fluid overload.

1. A 10% solution of IV lipids supplies 1.1 kcal/mL.
2. A 20% lipid solution supplies 2 kcal/mL.
3. Vitamin and mineral supplements

• are also available to avoid deficiencies of these nutrients during parenteral nutritional support.

7. Guidelines for placing TPN orders

. Calculate volume requirements

• over 24 hours (see Chapter 7).

1. Determine protein requirements

• as g/kg/day (see II D).

1. Calculate total daily caloric need

• as kcal/kg/day (see II B).

1. Determine percentage of calories

• to be given as protein, carbohydrates, and fat (see II C 1 and II E 1).

1. Add electrolytesand trace elements.
2. Peripheral parenteral nutrition (PPN)

. PPN involves infusion of lower-concentration solutions (carbohydrates, protein, and lipids) into peripheral veins.

1. Indications for PPN are very limited and there are little data demonstrating a benefit from PPN therapy versus other modes of nutritional support.
2. Specialized formulas
3. Specialized formulas

• for patients with renal insufficiency and azotemiaare high in carbohydrates with limited protein.

1. A large percentage of protein

• is administered as essential amino acidsto avoid unnecessary excessive protein administration.

1. This helps to improve nitrogen balance

• and contribute to reduction of blood urea nitrogen levels.

2. Patients with severe liver diseasemay benefit from formulas

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• high in branched-chain amino acids(metabolized by skeletal muscle).
• low in aromatic amino acids and methionine(metabolized by the liver).
• The amino acids metabolized by the liver
• are theoretically thought to contribute to encephalopathy of liver failure.
• Early clinical studies suggest
• these formulas may benefit encephalopathy, but further studies are ongoing to assess their impact on overall outcome.

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Review Test

Directions: Each of the numbered items or incomplete statements in this section is followed by answers or by completions of the statement. Select the ONE lettered answer or completion that is BEST in each case.

1. A 52-year-old, alcoholic man with a 4–5 day history of vomiting and epigastric abdominal pain is admitted to the hospital with a diagnosis of acute pancreatitis. The patient states that he has not eaten a meal in over 1 month and has been binge drinking during that time. He refuses to eat because of persistent vomiting and is started on enteral tube feeds containing medium chain triglycerides. Which of the following statements is appropriate regarding administration of medium chain triglycerides?

(A) They are converted to chylomicrons within the enterocyte.

(B) They require pancreatic lipase for absorption.

(C) They are transported to the liver via lymphatic channels.

(D) They may prevent steatorrhea associated with enteral feeding.

(E) They form micelles in the presence of bile salts.

1–D. Medium chain triglycerides are absorbed directly by enterocytes and transported to the liver via the portal vein. Unlike long chain triglycerides, medium chain triglycerides do not require bile salts or pancreatic lipase for absorption. Once long chain fatty acids are degraded to and absorbed by the enterocyte, they are then reconverted to triacylglycerols to form chylomicrons that are transported through lymphatic channels and then into the bloodstream. Medium chain triglycerides do not undergo this process and therefore are considered useful in patients with pancreatic insufficiency. Malabsorption of long chain triglycerides may also lead to steatorrhea, which may be prevented with the use of medium chain triglycerides.

2. A 66-year-old, 70-kg man undergoes extensive small bowel resection for mesenteric ischemia and receives parenteral nutritional support. He is receiving 5 g/kg/day of carbohydrates, 0.2 g/kg/day of nitrogen, and 0.6 g/kg/day of lipids. Which of the following most closely approximates the number of calories this patient is receiving each day?

(A) 2850

(B) 1800

(C) 2450

(D) 3500

(E) 2100

2–E. Carbohydrates produce ~ 4 kcal/g of substrate while lipids produce ~ 9 kcal/g substrate. Proteins produce ~ 4 kcal/g of substrate as well. Protein content may be frequently expressed as grams of nitrogen: 6.25 g of protein = 1 g of nitrogen. Therefore 0.2 g/kg/day of nitrogen = 1.25 g/kg/day of protein. Using these values, this patient is receiving approximately [(4 kcal/g × 5 g carbohydrates) + (9 kcal/g × 0.6 g lipids) + (4 kcal/g × 1.25 g protein)] × 70 kg = 2128 kcal/day.

3. A 65-year-old man undergoes an emergent sigmoid colectomy with colostomy for a perforated diverticulum. On postoperative day 3 the patient develops persistent fever with a white blood cell count of 24,000. An abdominal computed tomography (CT) scan reveals a large fluid collection in the left lower quadrant. The patient's heart rate is 130, with a blood pressure of 90/60. Which of the following statements is true regarding this patient's metabolic state?

(A) The insulin/glucose ratio is probably high compared to normal.

(B) This patient is probably in positive nitrogen balance.

(C) Glutamine levels are probably increased in this patient.

(D) Alanine levels are probably increased in this patient.

(E) The respiratory quotient (RQ) value in this patient is probably ≥ 1.0.

3–D. Alanine produced by the muscle tissue is a major precursor for gluconeogenesis in the liver and therefore is likely to be elevated in the setting of severe stress where glucagon, cortisol, and catecholamines all play a role in stimulating gluconeogenesis. Frequently in this setting patients become hyperglycemic because of a relative inhibition of insulin secretion as well as a peripheral resistance to the effects of insulin. This would be associated with a relatively low insulin/glucose ratio. In severe stress, there is generally a net proteolysis, resulting in a negative nitrogen balance, while the goal of nutritional therapy and recovery is to produce neutral nitrogen balance. Glutamine levels decrease during stress. In addition, with a relatively prolonged stress (postoperative day 3) there is significant utilization of lipids (lipolysis) resulting in a respiratory quotient (RQ) of ~ 0.7.

4. A 55-year-old man with metastatic carcinoid disease presents to the office complaining of persistent diarrhea for 2–3 weeks. He denies any other symptoms although his wife states that he seems “confused” at times. He states that he has been eating well although his wife states his appetite has been very poor for the past few months. He is currently only taking a topical steroid prescribed by his family physician for a persistent rash. Which of the following is the most appropriate definitive therapy for this patient's condition?

(A) Administer loperamide.

(B) Supplement his diet with vitamins.

(C) Administer somatostatin.

(D) Supplement his diet with zinc.

(E) Administer octreotide.

4–B. This patient's triad of symptoms (dermatitis, diarrhea, and dementia) is characteristic of pellagra associated with niacin deficiency. In humans, despite inadequate intake of niacin, tryptophan can be converted to niacin. However, in patients with carcinoid syndrome, tryptophan may be diverted to synthesis of serotonin, resulting in an increased risk of niacin deficiency. Thus, in this patient, supplementation with vitamins, specifically niacin, may help to relieve his current triad of symptoms. Zinc deficiency is not associated with this triad of symptoms. Although excess serotonin can lead to diarrhea, treatment of serotonin excess with octreotide will not treat the underlying vitamin deficiency, nor will administration of the antidiarrheal agent, loperamide.

5. A 72-year-old man has recently undergone extensive resection of a primary squamous cell carcinoma of the tongue with radical neck dissection. Postoperatively he is found to have extensive esophageal candidiasis with severe diffuse ulceration. His past medical history is significant for a previous sigmoid resection for diverticular disease and he has had intermittent symptoms of nausea and vomiting over the past several months which seem to resolve on their own. Which of the following would be the most appropriate reason for parenteral versus enteral nutritional support?

(A) Severe esophageal ulceration

(B) Extensive oropharyngeal resection

(C) Severe sepsis

(D) Small bowel obstruction secondary to adhesions

(E) Previous abdominal surgery precludes percutaneous placement of gastrostomy tube

5–D. A high-grade small bowel obstruction is a contraindication to the use of enteral nutritional support. Although severe ulceration of the esophagus may be a relative contraindication to placement of a nasoenteric feeding tube, this patient is still an excellent candidate for a gastrostomy tube or a jejunostomy tube for enteral nutritional support. Sepsis is not a contraindication to enteral nutritional support although attention should first be focused on the underlying cause of sepsis before nutritional therapy is initiated. This patient's extensive oropharyngeal resection is not a contraindication to placement of a direct enteral feeding tube such as a gastrostomy tube, which can be placed percutaneously as well as with an open surgical technique in the setting of previous abdominal surgery with significant adhesions.

6.A 68-year-old woman is transferred to a tertiary care hospital after a recent extensive small bowel resection at an outside hospital. She has been diagnosed with short bowel syndrome following the surgery and has received parenteral nutritional support for approximately 3 months. The patient cannot remember exactly what she is taking but she states that she hangs 1 large bag of clear-yellow fluid 3 times a day at home administered through a central venous catheter. She presents with complaints of worsening fatigue and hair loss. Her hematocrit is 34%, white blood cell count 6,000, and platelets 45,000. For managing this patient it would be most appropriate to administer

(A) Niacin

(B) Vitamin C

(C) Zinc

(D) Iron

(E) Lipids

6–E. This patient is suffering from sequelae of essential fatty acid deficiency. Today, this is generally avoided in patients receiving parenteral nutritional therapy by co-administering lipid emulsions with the carbohydrate and amino acid solutions characteristic of parenteral therapy, although inadvertent failure to administer such lipids may result in essential fatty acid deficiency. Characteristics of such a deficiency include fatigue, dermatitis, ecchymoses, alopecia, anemia, edema, thrombocytopenia, and respiratory distress. This patient's signs and symptoms are not characteristic of niacin deficiency (pellagra), vitamin C deficiency (scurvy), or zinc deficiency. Although a coexisting iron deficiency could contribute to the anemia, administering iron would not address the primary deficiency causing the entire myriad of findings.

7. A 37-year-old woman sustains 50% full-thickness burn injury to her torso, neck, and upper extremities. Upon admission appropriate fluid resuscitation and local burn wound care are initiated. She is also intubated and receiving 100% oxygen for significant inhalational injury with significant burns to the face and oropharynx. Which of the following is an appropriate statement regarding nutritional supplementation in this patient?

(A) Parenteral nutritional support should be initiated immediately because of the facial and oropharyngeal burn injuries.

(B) Parenteral nutritional support should be initiated immediately because of the risk of aspiration associated with burn injury-induced gastric ileus.

(C) Enteral nutritional support should be initiated immediately despite the oropharyngeal burns and potential risk of aspiration.

(D) Enteral nutritional support should be initiated within 48–72 hours of the initial injury to allow for adequate volume resuscitation.

(E) Enteral nutritional support should be initiated only if there are no sites available for central venous catheter placement for total parenteral nutrition secondary to burn injury.

7–C. Studies have shown a significant benefit of enteral nutritional therapy in improving overall outcome in patients with severe burn injuries. In addition, this benefit is increased if enteral therapy can be initiated early in the course of therapy for burn injury and even as early as at the time of initial admission. Facial and oropharyngeal burn injury does not preclude the use of enteral nutrition support nor does the risk of aspiration associated with gastric ileus. Generally speaking, although particularly true for burn patients, enteral nutritional support is preferred over parenteral nutritional support when the gastrointestinal tract is functional and available.

8. A 25-year-old man sustains a 45% full-thickness burn injury to his lower extremities and torso. After adequate initial fluid resuscitation and local wound care he is awake and alert. On hospital day 3, his heart rate is 130, blood pressure is 130/80, and respiration rate is 24. He is also noted to have a blood glucose of 300 despite administration of 12 units of regular insulin. His blood urea nitrogen is 45 and his creatinine is 1.8. Which of the following statements is appropriate with regard to this patient's metabolic state?

(A) The major source of glucose for the burn wound is probably via glycogenolysis.

(B) Protein requirements are 1 g/kg/day to avoid excessive azotemia with associated renal insufficiency.

(C) Insulin stimulation of lipolysis plays a critical role in providing glucose for peripheral tissues.

(D) Catecholamines and glucagon play a critical role in stimulating glucose production via hepatic gluconeogenesis.

(E) Cortisol, catecholamines, and glucagon play a critical role in stimulating net protein anabolism in this setting.

8–D. During severe stress such a significant thermal injury, cortisol, glucagon, catecholamines, and sympathetic nervous stimulation all play a role in stimulating glucose production via lipolysis and hepatic gluconeogenesis. To provide substrates for gluconeogenesis, these agents also stimulate net protein catabolism. Glycogen stores within the body are rapidly depleted in the setting of severe injury within 12–24 hours, therefore after this period glycogenolysis is not the major source of glucose production. Patients with burn injuries have a significantly increased requirement for protein intake given the massive proteolysis. This requirement is ~ 1.5–2.5 g protein/kg/day and protein restriction should not be initiated because of the risk of worsening azotemia. Insulin is a major stimulus for lipogenesis.

9. A 65-year-old man undergoes pancreatic débridement for alcohol-induced necrotizing pancreatitis. He is noted to be malnourished on admission to the intensive care unit. He is initially alert but unable to wean from the ventilator postoperatively. He is started on parenteral nutritional therapy with 35 kcal/kg/ day with 60% as carbohydrates, 30% as lipids, and 10% kcal as protein. His prealbumin slowly improves over the next several days and his glucose levels remain relatively stable (130–190). Over a 10-day period the patient fails to wean from the ventilator and becomes more confused and lethargic. He also gradually develops a worsening picture of cardiogenic shock. For definitive management of this patient's underlying problem, which of the following is most appropriate to be administered?

(A) Thiamine

(B) KPO₄^-

(C) Niacin

(D) Insulin

(E) Lipids

9–A. This patient is manifesting symptoms of thiamine deficiency including Wernicke's encephalopathy, and eventual cardiomyopathy (wet beriberi). This may be seen in severely malnourished patients, particularly in alcoholics. Thiamine supplementation in this setting is the most appropriate therapy. The time course is not consistent with acute refeeding syndrome and hypophosphatemia. Additionally, his glucose levels appear to be stable, thus additional insulin would not treat the underlying condition. The clinical manifestations are also not consistent with either a niacin deficiency or an essential fatty acid deficiency.

10. A 65-year-old man underwent resection of the distal 150 cm of his small bowel for severe mesenteric ischemia 3 months ago. He has since recovered and is receiving supplemental enteral nutritional support through a gastrostomy tube in addition to eating small amounts of food each day. He now presents with the complaint of worsening fatigue and malaise over the past several weeks. He has noted an improvement in his appetite and denies any increase in bowel habits. On examination, he appears pale but without muscle wasting or other signs of weight loss. His laboratory results: K⁺× 4.5, Cl^- = 110, blood urea nitrogen = 14, creatinine = 1.2, Mg²⁺ = 2.5, PO₄^- = 5.0, and Ca²⁺ = 8.5. His hematocrit is 25%, white blood cell count is 5,000, platelets are 150,000, and mean red cell volume is 125. Which of the following would be the most appropriate therapy in the definitive management of this patient's current condition?

(A) Vitamin B₁₂ supplementation

(B) Folate supplementation

(C) Iron supplementation

(D) Administration of 2 U packed red blood cells

(E) Essential fatty acid supplementation

10–A. This patient has findings characteristic of megaloblastic anemia caused by inadequate supplementation of vitamin B₁₂ after extensive resection of the distal small bowel. The worsening fatigue and malaise in association with the significant decrease in the hematocrit and a large mean cell volume are characteristic. Vitamin B₁₂ is primarily absorbed in the terminal ileum and resection can result in a B₁₂ deficiency. B₁₂ is currently not available as an enteral supplement so must be provided by intravenous or intramuscular administration in this setting. Although folate may be associated with a megaloblastic anemia, this would not be associated with resection of the terminal ileum. The clinical picture and laboratory data are also not consistent with iron or essential fatty acid deficiency. Administration of packed red blood cells would acutely help with the anemia but it would not address the underlying condition.