Nutrition, Malnutrition, and Probiotics


  • 1.

    What is meant by nutritional status?

    Nutritional status reflects how well nutrient intake contributes to body composition and function in the face of the existing metabolic needs. The four major body compartments are water, protein, mineral, and fat. The first three compose the lean body mass (LBM); functional capacity resides in a portion of the LBM called the body-cell mass. Registered dietitians or registered dietitian nutritionists concentrate their efforts on preservation or restoration of this vital component.

  • 2.

    Define malnutrition.

    Malnutrition refers to states of overnutrition (obesity) or undernutrition relative to body requirements, resulting in dysfunction.

  • 3.

    How do different types of malnutrition affect function and outcome?

    • Marasmus is protein-calorie undernutrition associated with significant physical wasting of energy stores (adipose tissue and somatic muscle protein) but preservation of visceral and serum proteins. Patients are not edematous and may have mild immune dysfunction.

    • Hypoalbuminemic malnutrition occurs with stressed metabolism and is common in hospitalized patients. They may have adequate energy stores and body weight, but have expanded extracellular space, depleted intracellular mass, edema, altered serum protein levels, and immune dysfunction.

    • A similar state of relative protein deficiency occurs in classic kwashiorkor, in which caloric provision is adequate but quantity and quality of protein are not.

  • 4.

    How is a simple nutritional assessment performed?

    Simple bedside assessment may be as valuable for predicting nutrition-associated outcomes as sophisticated composition and function tests. Two popular methods, the Subjective Global Assessment (SGA) and the Mini Nutritional Assessment are simple-to-use validated nutritional assessment tools. Each incorporates basic questions about weight history, intake, gastrointestinal (GI) symptoms, disease state, functional level, and a physical examination to classify patients as well-nourished, mildly to moderately malnourished, or severely malnourished ( Figure 58-1 ).

    Figure 58-1, Mini nutritional assessment.

    A weight history, estimate of recent intake, brief physical examination, consideration of disease stress and medications, and assessments of functional status and wound healing allow a good estimate of nutritional status. They predict the risk for malnutrition-associated complications as well as or better than laboratory data. Poor intake for longer than 1 to 2 weeks, a weight loss of more than 10%, or a weight less than 80% of desirable warrants closer nutritional assessment and follow-up.

  • 5.

    Serum proteins are a marker of overall nutritional health. Which plasma proteins will have the most sensitive turnover rate?

    • Ferritin: 30 hours

    • Retinol binding protein: 2 days

    • Prealbumin: 2 to 3 days

    • Transferrin: 8 days

    • Albumin: 18 days

  • 6.

    What simple blood tests offer an instant nutritional assessment?


  • 7.

    List desirable weights for men and women.

    Body mass index (BMI) is calculated from a person’s weight and height, and is a reliable indicator of body fatness. It is used to determine categories of disease risk based on weight status.

Calculation of BMI

BMI is calculated the same way for both adults and children. The calculation is based on the following formulas ( Table 58-1 ):

Table 58-1
Calculation of BMI
Measurement Units Formula and Calculation
Kilograms and meters (or centimeters) Formula: weight (kg) ÷ [height (m)] 2
With the metric system, the formula for BMI is weight in kilograms divided by height in meters squared. Because height is commonly measured in centimeters, divide height in centimeters by 100 to obtain height in meters.
Example: Weight = 68 kg, Height = 165 cm (1.65 m)
Calculation: 68 ÷ (1.65) 2 = 24.98
Pounds and inches Formula: weight (lb) ÷ [height (in)] 2 × 703
Calculate BMI by dividing weight in pounds (lb) by height in inches (in) squared and multiplying by a conversion factor of 703.
Example: Weight = 150 lb, Height = 5′5′′ (65′′)Calculation: [150 ÷ (65) 2 ] × 703 = 24.96
BMI, Body mass index.

The standard weight status categories associated with BMI ranges for adults are shown in Table 58-2 .

Table 58-2
BMI Ranges for Adults
Centers for Disease Control and Prevention. How is BMI calculated and interpreted? Accessed September 22, 2014, from http://www.cdc.gov/healthyweight/assessing/bmi/adult_bmi/index.html#Interpreted .
BMI Weight Status
Below 18.5 Underweight
18.5-24.9 Normal
25.0-29.9 Overweight
30.0 and above Obese
BMI, Body mass index.

BMI can be easily determined by using a BMI calculator ( http://www.cdc.gov/healthyweight/assessing/bmi ) or by referring to a BMI chart ( Figure 58-2 ).

Figure 58-2, Body mass index chart.

Basal energy expenditure in calories can be derived from the Harris Benedict equation:


  • Stress: Factor

  • Mild stress: (× 1 to 1.3)

  • Moderate stress: (× 1.3 to 1.4)

  • Severe stress: (× 1.5)

See Table 58-3 .

  • 8.

    Describe the types of commonly prescribed oral diets.

    The clear liquid diet supplies fluid and calories in a form that requires minimal digestion, stimulation, and elimination by the GI tract. It provides approximately 600 calories and 150 g carbohydrate but inadequate protein, vitamins, and minerals. Clear liquids are hyperosmolar; diluting the beverages and eating slower may minimize GI symptoms. If clear liquids are needed for longer than 3 days, a dietitian can assist with supplementation.

    The full liquid diet is used often in progressing from clear liquids to solid foods. It also may be used in patients with chewing problems, gastric stasis, or partial ileus. Typically, the diet provides more than 2000 calories and 70 g protein. It may be adequate in all nutrients (except fiber), especially if a high-protein supplement is added. Patients with lactose intolerance need special substitutions. Progression to solid foods should be accomplished with modifications or supplementation, as needed.

  • 9.

    What is a hidden source of calories in the intensive care unit?

    Watch out for significant amounts of lipid calories from propofol, a sedative in 10% lipid emulsion (1.1 kcal/mL).

  • 10.

    Summarize the typical findings in deficiency or excess of various micronutrients.

    See Table 58-4 .

    Table 58-4
    Vitamin and Mineral Deficiencies and Toxicities
    Micronutrient Deficiency Toxicity
    Vitamin A Follicular hyperkeratosis, night blindness, corneal drying, keratomalacia Dermatitis, xerosis, hair loss, joint pain, hyperostosis, edema, hypercalcemia, hepatomegaly, pseudotumor
    Vitamin D Rickets, osteomalacia, hypophosphatemia, muscle weakness Fatigue, headache, hypercalcemia, bone decalcification
    Vitamin E Hemolytic anemia, myopathy, ataxia, ophthalmoplegia, retinopathy, areflexia Rare: possible interference with vitamin K, arachidonic acid metabolism, headache, myopathy
    Vitamin K Bruisability, prolonged prothrombin time Rapid intravenous infusion: possible flushing, cardiovascular collapse
    Vitamin C Scurvy: poor wound healing, perifollicular hemorrhage, gingivitis, dental defects, anemia, joint pain Diarrhea; possible hyperoxaluria, uricosuria; interference with glucose, occult blood tests; dry mouth, dental erosion
    Vitamin B 1 (thiamine) Dry beriberi (polyneuropathy): anorexia, low temperature
    Wet beriberi (high-output congestive heart failure): lactic acidosis
    Wernicke-Korsakoff syndrome: ataxia, nystagmus, memory loss, confabulation, ophthalmoplegia
    Large-dose intravenous: anorexia, ataxia, ileus, headache, irritability
    Vitamin B 2 (riboflavin) Seborrheic dermatitis, stomatitis, cheilosis, geographic tongue, burning eyes, anemia None
    Vitamin B 3 (niacin) Anorexia, lethargy, burning sensations, glossitis, headache, stupor, seizures
    Pellagra: diarrhea, pigmented dermatitis, dementia
    Hyperglycemia, hyperuricemia, GI symptoms, peptic ulcer, flushing, liver dysfunction
    Vitamin B 6 (pyridoxine) Peripheral neuritis, seborrhea, glossitis, stomatitis, anemia, CNS/EEG changes, seizures Metabolic dependency, sensory neuropathy
    Vitamin B 12 Glossitis, paresthesias, CNS changes, megaloblastic anemia, depression, diarrhea None
    Folic acid Glossitis, intestinal mucosal dysfunction, megaloblastic anemia Antagonizes antiepileptic drugs, decreases zinc absorption
    Biotin Scaly dermatitis, hair loss, papillae atrophy, myalgia, paresthesias, hypercholesterolemia None
    Pantothenic acid Malaise, GI symptoms, cramps, paresthesias Diarrhea
    Calcium Paresthesias, tetany, seizures, osteopenia, arrhythmia Hypercalciuria, GI symptoms, lethargy
    Phosphorus Hemolysis, muscle weakness, ophthalmoplegia, osteomalacia Diarrhea
    Magnesium Paresthesias, tetany, seizures, arrhythmia Diarrhea, muscle weakness, arrhythmia
    Iron Fatigue, dyspnea, glossitis, anemia, koilonychia Iron overload (hepatic, cardiac), possible oxidation damage
    Iodine Goiter, hypothyroidism Goiter, hypo/hyperthyroidism
    Zinc Lethargy, anorexia, loss of taste/smell, rash, hypogonadism, poor wound healing, immunosuppression Impaired copper, iron metabolism, reduced HDL, immunosuppression
    Copper Anemia, neutropenia, lethargy, depigmentation, connective tissue weakness GI symptoms, hepatic damage
    Chromium Glucose intolerance, neuropathy, hyperlipidemia None
    Selenium Keshan’s cardiomyopathy, muscle weakness GI symptoms
    Manganese Possible weight loss, dermatitis, hair disturbances Inhalation injury only
    Molybdenum Possible headache, vomiting, CNS changes Interferes with copper metabolism, possible gout
    Fluorine Increased dental caries Teeth mottling, possible bone integrity/fluorosis
    CNS, Central nervous system; EEG, electroencephalography; GI, gastrointestinal; HDL, high-density lipoproteins.

  • 11.

    What are the nutritional concerns in patients with short bowel syndrome?

    Loss of bowel surface puts the patient at great risk for dehydration and malnutrition. The small bowel averages 600 cm in length and absorbs approximately 10 L/day of ingested and secreted fluids. A patient may tolerate substantial loss of small bowel, although preservation of less than 2 feet with an intact colon and ileocecal valve or less than 5 feet in the absence of the colon and ileocecal valve may make survival impossible when just the enteral route of nutrition is used. In addition, the loss of the distal ileum precludes absorption of bile acids and vitamin B 12 . Remaining bowel, especially ileum, may adapt its absorptive ability over several years, but underlying disease may hamper this process.

  • 12.

    Describe the management of nutritional problems in patients with short bowel syndrome.

    Therapy in the acute postsurgical phase is aimed at intravenous fluid and electrolyte restoration. Parenteral nutrition may be required while the remaining gut function is assessed and adaptation takes place. Attempts at oral feeding should include frequent, small meals with initial limitations in fluid and fat consumption. Osmolar sugars (e.g., sorbitol), lactose, and high-oxalate foods are best avoided. In patients with small bowel–colon continuity, increased use of complex carbohydrates may allow the salvage of a few hundred calories from colonic production and absorption of short-chain fatty acids (SCFAs). Antimotility drugs and gastric acid suppression should be used if stool output remains high. Oral rehydration with glucose- and sodium-containing fluids (e.g., sports drinks) may help prevent dehydration. Pancreatic enzymes, bile acid–binding resins (if bile acids are irritating the colon), and octreotide injections may play a role in selected cases. If oral diets fail, the use of elemental feedings may enhance absorption and nutritional state. Studies of gut rehabilitation with growth hormone and glutamine, as well as intestinal or combined intestinal-liver transplantation, are available at selected centers.

  • 13.

    Describe the approach to nutritional support in patients with acute pancreatitis.

    Pancreatitis can resemble other cases of stressed metabolism. If severe pancreatitis precludes the resumption of food intake beyond 4 to 5 days, consideration should be given to nutrition support. The route of feeding remains controversial; neither bowel and pancreatic rest nor nutritional support has been shown conclusively to alter the clinical course beyond improvement of the nutritional state. Several recent randomized trials suggest that distal (jejunal) enteral feeding may be tolerated as well as bowel rest and total parenteral nutrition (TPN), with fewer complications ( Figure 58-3 ). The enteral route may be tried in the absence of GI dysfunction (e.g., ileus). Energy expenditure is variable, but most likely only 20% to 30% above basal. Use partial parenteral nutrition or TPN if the enteral approach fails. Experiments suggest that parenteral nutrition, including intravenous fat, elicits little significant pancreatic secretion; however, all patients with pancreatitis should be monitored to exclude severe hypertriglyceridemia.

    Figure 58-3, Nutrition for pancreatitis.

  • 14.

    What adverse GI effects may be encountered in a patient using herbal supplements?

    It is estimated that one third to one half of the U.S. population uses herbal products in supplementary form and that 60% to 75% do not inform health care providers. Because herbal products are not regulated and their composition is not standardized, toxicity data are less clear than with regulated pharmaceuticals. However, popular products that may cause adverse GI effects include saw palmetto, Ginkgo biloba (nonspecific GI upset), garlic (nausea, diarrhea), ginseng (nausea, diarrhea), aloe (diarrhea, abdominal pain), and guar gum (obstruction). In addition, hepatotoxicity (ranging from asymptomatic enzyme elevation to fulminant necrosis) has been documented with germander, chaparral, senna, Atractylis, and Callilepis. Hepatotoxicity associated with the use of valerian, mistletoe, skullcap, and various Chinese herbal mixtures has been noted but awaits a cause-and-effect confirmation. The pyrrolizidine alkaloids in Crotalaria, Senecio, Heliotropium, and comfrey have long been implicated in cases of venoocclusive liver disease.

  • 15.

    How is obesity defined, and how common is it among U.S. residents?

    BMI has become the standard of measurement for obesity.


    A BMI higher than 30 kg/m 2 is defined as obese ( Table 58-5 ).

    Table 58-5
    BMI Data for Adults
    BMI Category BMI, kg/m 2
    Normal 18.5 to 24.9
    Overweight 25 to 29.9
    Obesity 30 to 39.9
    Extreme 40 +
    Adults 1998-1994 1995 1999-2000 2000 2008 2010
    Obese 22.9% 15.9% 30.5% 20% 26.6% 37%
    Overweight 55.9% 35.5% 64.5% 36.7% 36.6% 30%
    Extremely Obese 2.9% 4.7%
    BMI, Body mass index.

    Although the number of adults has doubled since 1980, the number of obese adults has quadrupled; approximately 72 million adults in the United States are obese. According to the National Health and Nutrition Examination Survey from 2007 to 2010, among Americans age 20 and older, 154.7 million are overweight or obese: http://apps.nccd.cdc.gov/brfss/ (Accessed September 22, 2014).

  • 16.

    In 2007, what U.S. state had an obesity rate of less than 20%?

    Colorado. However, the 2011 data shows that no state has an obesity rate less than 20% as Colorado’s has risen to 20.7%. Open the link showing the percentage of each state’s population that is obese: http://www.cdc.gov/obesity/data/adult.html (Accessed September 22, 2014).

  • 17.

    Does obesity carry a significant risk for death?

    Yes. In the United States, 300,000 persons die annually from obesity-related diseases:

    Cardiomyopathy Degenerative joint disease (DJD)
    Coronary artery disease Immobility
    Dyslipidemia Depression
    Hypertension Low self-esteem
    Diabetes Malignancy
    Infertility Dyspnea
    Fatty liver Obstructive sleep apnea
    Deep vein thrombosis Obesity hypoventilation
    Gallstones Chronic fatigue
    Pulmonary embolus Venous stasis
    Urinary stress incontinence Gastroesophageal reflux disease (GERD)

  • 18.

    What are the medical therapies for obesity?

    Dietary restriction of calories, while maintaining adequate protein, fluid electrolyte, mineral, and vitamin intake, is the key. A sensible weight reduction program targets gradual weight reduction by behavior modification, including dietary and activity changes. Numerous fad diets claim success, but key to the weight loss is patient commitment and total lifestyle modification. The U.S. Preventive Services Task Force 2012 recommendations include screening all adults for obesity. Clinicians should offer or refer patients with a BMI of 30 kg/m 2 or higher to intensive, multicomponent behavioral interventions.

    Intensive, multicomponent behavioral interventions for obese adults include the following components:

    • Behavioral management activities, such as setting weight-loss goals

    • Improving diet or nutrition and increasing physical activity

    • Addressing barriers to change

    • Self-monitoring

    • Strategizing how to maintain lifestyle changes

    For a summary of the evidence systematically reviewed in making this recommendation, the full recommendation statement, and supporting documents, please go to http://www.uspreventiveservicestaskforce.org/ (Accessed September 22, 2014).

  • 19.

    What are the surgical options for obesity?

    Bariatric surgery dates to the 1950s when intestinal bypass was first performed. The total weight lost correlates with the total length of bowel bypassed. Gastric bypass (GBP) is the most common weight loss surgery performed in the United States (see Chapter 77 ). The laparoscopic adjustable gastric banding procedure is the most common bariatric surgery in Australia and Europe. A recent systematic review concluded that weight loss outcomes strongly favored Roux-en-Y GBP over laparoscopic adjustable gastric banding.

  • 20.

    What are the National Institutes of Health consensus criteria thought to be viable indications for bariatric surgery?

    • Failure of a major weight-loss program plus excessive obesity BMI of more than 40 kg/m 2

    • or

    • Failure of a major weight-loss program plus BMI of more than 35 kg/m 2

    • and

    • Obesity-related comorbidities *

      * Hypertension, type 2 diabetes mellitus, DJD and disc disease, GERD, sleep apnea, obesity hypoventilation, severe venous stasis, abdominal wall hernias, and pseudotumor cerebri

  • 21.

    What is the operative mortality of GBP surgery?

    Operative mortality ranges from 0.3% to 1.6%, and perioperative complications occur in 10% of patients:

Table 58-3
Quick Formulas for Calculation of Protein and Caloric Requirements
Illness Severity Protein, G/Kg/Day Calories, Kcal/Kg/Day
Minimal 0.8 20 to 25
Moderate 1 to 1.5 25 to 30
Severe 1.5 to 2.5 30 to 35

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