Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
The medical and surgical history determine preexisting conditions, metabolic stress, and alterations in organ function that influence nutritional support. Nutritional status is recently having a resurgence of importance as it can be predictive of morbidity and mortality. Assessment begins with the physical exam and evaluates muscle mass, adipose stores, skin integrity, temporal muscle wasting, and clinical signs of micronutrient deficiency or cachexia. Laboratory data should include the basic labs, which include serum sodium (Na), potassium (K), carbon dioxide (CO 2 ), chloride (Cl), blood urea nitrogen (BUN), creatinine, glucose, ionized calcium (Ca), serum phosphate (PO 4 ), magnesium (Mg), and complete blood count (CBC) with differential. Arterial blood gases (ABGs) to assess acid-base status and CO 2 retention, albumin, transferrin, prealbumin, and urinary nitrogen are useful. Glycosylated hemoglobin (HgbA1C), lipid profile, C-reactive protein (CRP), 25-OH vitamin D, trace elements, and liver function tests (LFTs) may also be valuable. The drug profile reveals agents that affect the metabolism of nutrients (insulin, levothyroxine, corticosteroids), alter energy expenditure (β-blockers, propofol), or affect gastrointestinal (GI) function (prokinetic agents, antibiotics). Anthropometric data include height, weight, and waist and hip circumference. Skinfold testing with calipers is useful once edema has resolved, but is rarely used in the fat-free acute care setting. Bioelectrical impedance analysis (BIA) quantifies adipose reserve, intracellular and extracellular water, and third space fluid in stable surgical patients. Dual energy x-ray absorptiometry (DEXA) is effective for tracking bone mineral density that may be compromised with age, hormonal status, drug therapy, and chronic disease. One of the most versatile questions in assessing nutritional status revolves around nutritional history. A simple question, “How have you been eating lately? Have you had any recent weight changes? Can you walk me through a normal day’s diet?” could easily reveal information on the nutritional practices of the individual. The social history explores economic data, social support network, or substance abuse behaviors and may predict the likelihood of adequate home care and treatment compliance for the patient, once discharged.
There are assessments that can be utilized to better understand the nutritional deficits among the critically ill ICU patients. (1) The Nutrition Risk in Critically ill (NUTRIC) score is the first nutritional risk assessment tool developed and validated specifically for ICU patients. The recognition that not all ICU patients will respond the same to nutritional interventions was the main concept behind the NUTRIC score, as most other risk scores and assessment tools consider all critically ill patients to be at high nutrition risk. (2) Another assessment tool of malnutrition in ICU is the Nutrition Risk Score-2002 (NRS). It is based on the concept that nutritional support is indicated in patients who are severely ill with increased nutritional requirements, or who are severely undernourished, or who have certain degrees of severity of disease in combination with certain degrees of undernutrition. Degrees of severity of disease and undernutrition were defined as absent, mild, moderate, or severe from data sets in a selected number of randomized controlled trials (RCTs) and converted to a numeric score. After completion, the screening system was validated against all published RCTs known to us of nutritional support versus spontaneous intake to investigate whether the screening system could distinguish between trials with a positive outcome and trials with no effect on outcome.
Primary malnutrition results when the individual consumes inadequate kilocalories, protein, vitamins, or minerals. It may occur as a result of poor food choices, anorexia, poverty, alcoholism, suboptimal support regimens, or after bariatric surgery. Secondary malnutrition occurs even when adequate food is infused or consumed. It may result from organ dysfunction (hypoalbuminemia with cirrhosis), malabsorption (Crohn’s disease), immobility (muscle wasting), drug therapy (insulin resistance with corticosteroids), or the inflammatory state (Persistent Inflammatory Immunosuppressed Catabolic Syndrome).
The most commonly cited and readily available proteins for nutritional assessment are albumin, transferrin, and prealbumin, which are produced in the liver ( Table 9.1 ). All three constitutive proteins plummet shortly after injury or surgery because the liver reprioritizes the production of acute phase proteins. Then, as the stress response resolves, the liver resumes production of constitutive proteins, as it makes the transition from catabolism to anabolism. Meeting protein and nonprotein caloric needs helps to facilitate this process. As a result of shorter half-lives, prealbumin and transferrin are most useful in the intensive care unit (ICU) and should be limited to patients with creatinine clearance >50 mL/min. Prealbumin travels in the circulation bound to retinol binding protein (RBP) and vitamin A. Levels of prealbumin may be elevated in renal failure despite nutritional compromise resulting from decreased catabolism and excretion of RBP. Transferrin is elevated with iron depletion, independent of the effects of nutrition.
Protein | Synthetic Site | Clinical Significance | Half-Life | Limitations | Interpretation |
---|---|---|---|---|---|
Albumin | Liver | Relates to outcomes; relates to edema | 20–21 days | Best case scenario for hepatic production: 12–25 g/24 hr; dilutional effects; long half-life; used alone, sensitivity poor |
Normal <3.5 g/dL Mild depletion 2.8–3.5 g/dL Moderate 2.2–2.8 g/dL Severe <2.2 g/dL |
Prealbumin | Liver | Indicates nutritional deficits before albumin | 2–4 days | Short half-life | Normal >18 mg/dL Mild depletion 10–18 mg/dL Moderate 5–10 mg/dL Severe <5 mg/dL |
Transferrin | Liver | More sensitive than albumin; relatively useful parameter in liver disease compared with albumin; can calculate from total iron binding capacity (TIBC) | 8–10 days | Poor marker of early repletion; sensitive to changes in body iron | Mild depletion 150–200 mg/dL Moderate 100–150 mg/dL Severe <100 mg/dL |
C-Reactive Protein (CRP) | Liver | Increases abruptly after injury. Early and reliable indicator of disease or injury severity. | 48–72 hr | May be increased with obesity and other chronic inflammatory states | Baseline normal <3 mg/dL Bacterial infection 30–35 mg/dL Viral infection <20 mg/dL Peaks 48–72 h post-trauma up to 35 mg/dL |
Protein need is determined based on patient weight, current stress factors, extraordinary skin losses, and organ function. Although the recommended daily intake (RDI) for protein for healthy individuals is only 0.8 g of protein/kg of body weight, the following guidelines may be used in the surgical patient:
Injury level | Protein requirement |
---|---|
Mild stress/injury | 1.2–1.4 g of protein/kg |
Moderate stress/injury | 1.5–1.7 g of protein/kg |
Severe stress/injury | 1.8–2.5 g of protein/kg |
Total urinary nitrogen (TUN) is the most reliable indicator of nitrogen use and excretion in the patient who is in the surgical intensive care unit (SICU). However, urinary urea nitrogen (UUN) is more readily available in most hospital laboratories. Although TUN and UUN are nearly equal in healthy ambulatory patients with normal renal and hepatic function, critically ill patients have a poor correlation between the two. A 12-hour urine collection compares well with a 24-hour collection (Graves). Optimal nutrition support promotes a +3 to +5 nitrogen balance. Estimate the protein needs of the patient by adding:
Remember that 6.25 g of protein yields 1 g of nitrogen. Insensible losses are increased with burns, decubiti, wound vacuums, and large wounds. UUN is not useful as a guide for nutritional prescription in hepatic failure, renal dysfunction (<50 mL/min creatinine clearance), or recent spinal cord injury.
Limit protein to 0.6–0.8 g/kg in patients with hepatic encephalopathy; if the encephalopathy produces significant clinical consequences, branched chain amino acids can be considered (though no mortality benefit has been found). However, only about 10% of chronic liver disease patients are protein sensitive; thus, other causes of encephalopathy, such as infection, constipation, and electrolyte disturbance, should be explored. Otherwise, give a more typical postsurgical protein load (1.3–1.5 g/kg).
In injured and acutely ill patients with renal failure , withholding protein is now an old recommendation. Giving adequate protein may require more frequent dialysis. Amino acid losses and requirements increase with more intensive hemodialysis (HD) (10–12 g of amino acids removed with each HD, or 5–12 g of amino acids daily with continuous venovenous hemodialysis [CVVHD]).
There are numerous methods for setting kilocalorie targets in the surgical patient: (a) prediction equations, (b) kcal/kg estimations or, (c) indirect calorimetry. One common prediction equation, the Harris Benedict (HBE), was developed in 1919 for use on ambulatory, fasted, healthy people but is of limited usefulness in hospitalized patients.
A number of prediction equations have been developed but most physicians employ a total kcal/kg goal as shown in Table 9.2 .
Patient | Feeding Level (kcal/kg) | Level by Indirect Calorimetry |
---|---|---|
Normal weight patients | 25–30 | REE a × 1.0 |
Underweight patients | 30–35 | REE × 1.2 |
Obese patients | 20–25 b | REE × 0.85 |
Morbidly obese | 10–20 b | REE × 0.75 |
a Basal energy expenditure (BEE) is the number of kilocalories expended at rest, in a fasted state. Resting energy expenditure (REE) is measured in a fed state and is 5%–10% higher than BEE.
b Adjusted weight = [(Actual weight − Ideal weight) × 0.25] + Ideal weight
Indirect calorimetry is a respiratory test that measures the patient’s production of CO 2 and consumption of oxygen for approximately 30 minutes, until steady state is achieved. Results are worked into the modified Weir equation:
Where:
REE = resting energy expenditure (kcal/day)
VO 2 = oxygen consumption (L/min)
VCO 2 = CO 2 exhaled (L/min)
The report indicates the number of kilocalories the patient consumes in 24 hours and the respiratory quotient (RQ). RQ = VCO 2 /VO 2 and provides information on the type of substrate being used. The RQ for the metabolism of fat, protein, and carbohydrate are 0.7, 0.83, and 1.0, respectively. Overfeeding will result in an RQ >1.0 as a result of increased CO 2 production associated with lipogenesis.
The test is useful in the patient on mechanical ventilation (MV) once a patient is relatively stable, with a fractional concentration of oxygen in inspired gas (FiO 2 ) <60% and peak end-expiratory pressure (PEEP) <10. Studies are helpful:
When overfeeding (diabetes mellitus [DM], chronic obstructive pulmonary disease, obesity) is undesirable.
When underfeeding (renal failure, large wounds) is detrimental.
In patients whose physical or clinical factors promote alterations in energy expenditure (spinal cord injury).
When drugs are used that significantly alter energy expenditure (paralytic agents, β-blockers).
In patients who do not respond as expected to calculated regimens.
Always, but especially when a patient is unlikely to meet >70% of nutritional needs by mouth. Patients who have sustained major head injury (Glasgow Coma Scale <8), major torso trauma, major trauma to the pelvis and long bones, or major chest trauma benefit from enteral nutrition. Approximately 85% of patients (even those undergoing GI surgery) tolerate early enteral feeding within 24 hours postoperatively.
Pursue access by blind placement of a nasogastric (NG) tube or a nasoduodenal tube. Place a nasojejunal tube (NJ) blindly, endoscopically, or fluoroscopically. Achieve gastric decompression with concurrent nasojejunal feeds with an endoscopic percutaneous gastrostomy/jejunostomy (PEG/PEJ). Alternatively, place a gastrostomy or feeding jejunostomy intraoperatively.
Polymeric enteral feedings are soy-based, lactose-free products containing intact protein, carbohydrate, and fat. Most offer 1 kcal/mL and 37–62 g of protein per liter. Special modifications of the standard formulas include dietary fiber or “immune-enhancing” agents, such as fish oil, arginine, glutamine, and nucleotides. “Elemental” formulas contain amino acids, di-, tri-, and quatrapeptides, dextrose, and minimal fat. Several concentrated formulas (2 kcal/mL) are available for use in patients with congestive heart failure (CHF), renal failure, and hepatic failure, but have a higher rate of tube-feed–related diarrhea. In general, products that are “disease-specific” or contain nutrients in elemental form are more expensive than standard products.
No. Formulas with reduced carbohydrate and increased fat loads are marketed as being superior in maintaining glycemic control. These products have not shown superior, clinically significant outcome in hospitalized patients in randomized controlled trials. The use of standard high protein formulas in an isocaloric or hypocaloric load, combined with appropriate insulin therapy, is the most effective treatment for hyperglycemia in the stressed patient with type 2 DM. The level of glycemic control associated with enhanced outcome is best achieved with insulin, as opposed to carbohydrate restriction. Furthermore, gastric feedings with high fat formulas in the diabetic patient with gastroparesis may delay gastric emptying and increase risk of aspiration.
No. Specialized, high omega-6 fat formulas have been marketed to reduce CO 2 production in COPD patients who retain CO 2 . In theory, these formulas minimize CO 2 production and facilitate weaning. However, avoiding overfeeding is more important for reducing CO 2 production than providing high fat formula. Gastric feeding with these products increases the risk of aspiration.
Enteral feeding may produce electrolyte abnormalities, hyperglycemia, GI intolerance, pulmonary aspiration, and nasopharyngeal erosions. Surgical complications of enteral access include leaks, tube dislodgement, volvulus, soft tissue infection, and bowel necrosis.
No.
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here