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, calcium, magnesium, and

zinc are common to this patient population.

Given the prevalence of these deficiencies, S.P. should be prescribed a daily

multivitamin and mineral supplement. If it is determined that S.P. has significant fat

malabsorption, a water-miscible fat-soluble vitamin formulation can be considered.

There is an increased incidence of osteoporosis in patients with Crohn’s disease

(with or without corticosteroid use), and therefore, S.P. should be assessed to ensure

that her calcium and vitamin D intake is normal. Recommended daily oral calcium

requirements are from 800 to 1,500 mg/day, but increase from 1,500 to 2,000 mg/day

when replacement is needed for a deficiency. S.P. should be consuming a daily

amount of 400 international units of vitamin D orally; however, if serum 25-

hydroxyvitamin D levels are subtherapeutic, greater amounts will be required and

also doses based on the specific disease progression and functionality of S.P.’s GI

tract.

Medications such as methotrexate (a folate antagonist) and sulfasalazine (which

blocks folate absorption) can be used to treat inflammatory bowel disease and,

therefore, increase folate requirements for patients. Daily folate supplementation at a

dose of 1 mg orally can be beneficial to S.P. if she is prescribed either of these

medications.

Patients with surgical resection of the stomach or terminal ileum are at risk of

developing vitamin B12 deficiency given the locations of intrinsic factor production

and site of absorption, respectively. Given that S.P. has had no surgical intervention

to date, it is wise to monitor her vitamin B12 status and look for signs of deficiency

(i.e., megaloblastic anemia) before instituting aggressive supplementation.

Magnesium deficiency can be a concern in patients with increased intestinal

losses, as is the case with many individuals who have inflammatory bowel disease.

When considering enteral magnesium supplementation, the change in pH along the GI

tract, GI transit time, and fat content of a meal can all affect magnesium absorption.

Large doses of enteral magnesium can result in diarrhea; therefore, administering

smaller doses throughout the day can lead to improved tolerance and therapeutic

efficacy. Choosing a magnesium supplement that can deliver 150 mg of elemental

magnesium and dosing it 4 times a day is the recommended oral replacement regimen

for patients.

Inflammatory bowel disease patients can experience excessive stool losses

resulting in a zinc deficiency. S.P. should receive an oral zinc supplement that

delivers 50 mg of elemental zinc daily.

Maintenance Fluids

CASE 35-1, QUESTION 5: Determine the daily fluid requirements for S.P. while she receives specialized

nutritionalsupport.

When determining the fluid needs of a patient, the clinician should consider the

following steps: (a) correction of fluid imbalances, (b) maintenance fluid

requirements, and (c) replacement of ongoing fluid losses.

The extended periods of diarrhea, vomiting, or both that occur with inflammatory

bowel disease may lead to dehydration. Dehydration results in a loss of body weight,

decreased urine output, dry mouth, and progressive thirst. Hypotension, tachycardia,

and poor skin turgor are all clinical signs of dehydration. Apathy, stupor, coma, and

death will follow if fluid replacement is not undertaken. Fluid deficits should be

estimated from the clinical appearance of the patient, recent weight loss, and serum

sodium and blood urea nitrogen concentrations, and replaced by giving half the

estimated deficit intravenously over the course of 8 hours. After 8 hours, a new

assessment of fluid status should be made, and half of the new estimated deficit

should be replaced during the next 8 hours. This process should be repeated until

normal hydration is achieved (see Chapter 10, Fluid and Electrolyte Disorders).

Maintenance fluid is that volume of daily fluid intake that replaces the insensible

losses and at the same time allows excretion of the daily production of excess solute

load in a volume of urine that is of an osmolarity similar to plasma. Maintenance

fluid needs can be estimated using several methods. The simplest method uses 30 to

35 mL/kg/day as the basis. Another method is to provide 1,500 mL for the first 20 kg

of body weight plus an additional 20 mL/kg for actual weight beyond the initial 20

kg.

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Both methods provide estimates of fluid needs for basic maintenance. S.P.’s fluid

needs are estimated as follows:

If S.P. experiences vomiting, nasogastric tube output, diarrhea, or other significant

fluid losses, additional fluid must be provided. Some losses are measurable and can

be directly replaced milliliter for milliliter on a regular basis. Others, however, are

not measurable and can only be estimated. The electrolyte composition of the lost

fluid is an important consideration for the clinician and dictates the ultimate choice of

the replacement fluid.

Evaluating Specialized Nutritional Support

Effectiveness

CASE 35-1, QUESTION 6: What parameters should be examined to determine the effectiveness of S.P.’s

nutritionalsupport regimen?

Implementing a successful nutritional support regimen begins with proper

nutritional assessment of the patient. Nutritional goals that identify macronutrient,

micronutrient, and fluid requirements are then established. Follow-up support and

monitoring of the patient once nutritional support has been instituted is important to

maintain the integrity and efficacy of the therapy.

To minimize the risk of refeeding syndrome in S.P. (a metabolic and electrolyte

disturbance that occurs as a result of supplying nutrition to patients who are severely

malnourished), all electrolyte abnormalities must be corrected before any nutrition is

initiated. Because S.P.’s electrolytes are within normal ranges, no adjustments are

necessary. Nutrition should then be implemented slowly, and vitamins administered

routinely. Electrolytes, including phosphorus, potassium, magnesium, and glucose,

should be monitored at least daily during the first week. Although electrolyte and

mineral abnormalities may not be avoided, careful recognition of and close

monitoring for refeeding syndrome will prevent serious complications.

33,34

Although it can sometimes be difficult to obtain a reliable weight for a patient,

weight can be an important parameter to help assess not only fluid balance but also

the long-term appropriateness of caloric intake. Most patients should gain or lose no

more than 1 kg/week when receiving nutritional support (assuming normal fluid

status). However, clinicians must be aware of the impact that fluids have on the

weight of a patient. Large intake or loss of fluids can influence weight measurements

and mask the trends of body mass. Having S.P. record of daily weights, in addition to

fluid intake and output, and monitoring trends can serve as one, but not the only, key

in determining the effectiveness of her regimen.

Nitrogen balance is another parameter that can help determine the degree of

catabolism and protein requirements in a patient. Nitrogen balance is the difference

between nitrogen intake and nitrogen excretion. It is estimated by the nitrogen intake

along with collecting a 24-hour urine urea nitrogen sample from the patient. Positive

nitrogen balance is a reasonable goal during nutritional support therapy for recovery

of a patient, but may also require increasing caloric loads on a periodic basis. If a

nitrogen balance study is ordered for S.P., increasing protein intake should be

considered if results indicate a negative nitrogen balance; however, a negative

nitrogen balance may be unavoidable during high-stress states, regardless of the

amount of nutrients provided.

Finally, prealbumin levels for S.P. should also be monitored once a week as a

marker for short-term gross adequacy of calorie and protein intake. A lack of

prealbumin increase is an indicator of poor patient outcomes. With adequate feeding,

prealbumin can increase more than 4 mg/dL/week. It should be noted that in the case

of S.P. who is suffering from Crohn’s disease and may likely be receiving either oral

or parenteral corticosteroids as treatment, administration of corticosteroids can

falsely elevate prealbumin levels, making S.P. appear to be at a lower nutritional

risk.

CASE 35-1, QUESTION 7: Members of the medical team are anxious to have S.P. gain weight and are

concerned by her malnourished appearance. Therefore, there is a desire to increase the calories provided to

S.P. What potential complications could result from overfeeding S.P.?

Overfeeding should be avoided in all patients because of a plethora of potential

complications, especially those with respiratory concerns.

35 Although restoration and

maintenance of body cell mass is the goal of nutritional support therapy, a gradual

and conservative approach yields fewer metabolic abnormalities. Supplying an

abundance of calories to a patient in need of nutritional support increases the

metabolic rate, which in turn places greater demands for cardiopulmonary effort and

oxygenation. Overfeeding with carbohydrates is particularly detrimental because of

the amount of carbon dioxide produced relative to the amount of oxygen consumed.

This results in carbon dioxide retention that may lead to acid–base disturbances.

Hyperglycemia is also a common metabolic abnormality secondary to excessive

carbohydrate administration that can lead to osmotic diuresis and immune

dysfunction.

KEY REFERENCES AND WEBSITES

A full list of references for this chapter can be found at

http://thepoint.lww.com/AT11e. Below are the key references and websites for this

chapter, with the corresponding reference number in this chapter found in parentheses

after the reference.

Key References

ASPEN Board of Directors and the Clinical Guidelines Task Force. Guidelines for the use of parenteral and

enteral nutrition in adult and pediatric patients [published correction appears in J Parenter Enteral Nutr.

2002;26:144]. J Parenter Enteral Nutr. 2002;26(1 Suppl):1SA. (16)

Brooks MJ, Melnik G. The refeeding syndrome: an approach to understanding its complications and preventing its

occurrence. Pharmacotherapy. 1995;15:713. (34)

McClave SA et al. Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral

Nutrition (A.S.P.E.N.). J Parenter Enteral Nutr. 2016;40(2)159–211. (32)

Mueller C et al. A.S.P.E.N. Clinical guidelines: nutrition screening, assessment, and intervention in adults. J

Parenter Enteral Nutr. 2011;35:16. (1)

Key Websites

American Society for Parenteral and Enteral Nutrition. http://www.nutritioncare.org.

USDA Food and Nutrition Information Center. http://fnic.nal.usda.gov.

COMPLETE REFERENCES CHAPTER 35 BASICS OF

NUTRITION AND PATIENT ASSESSMENT

Mueller C et al. A.S.P.E.N. clinical guidelines: nutrition screening, assessment, and intervention in adults. J

Parenter Enteral Nutr. 2011;35:16.

Ames SR. The joule—unit of energy. J Am Diet Assoc. 1970;57:415.

Dahlqvist A, Semenza G. Disaccharidases of small-intestinal mucosa. J Pediatr Gastroenterol Nutr. 1985;4:857.

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat,

Fatty Acids, Cholesterol, Protein, and Amino Acids (Macronutrients). Washington, DC: National Academy

Press; 2005.

Cahill GF, Jr. Starvation in man. N EnglJ Med. 1970;282:668.

Posner BM et al. Diet and heart disease risk factors in adult American men and women: the Framingham

Offspring-Spouse nutrition studies. Int J Epidemiol. 1993;22:1014.

Carroll HJ, Oh MS. Water, Electrolyte, and Acid-Base Metabolism: Diagnosis and Management. Philadelphia, PA:

JB Lippincott; 1989.

Grant JP. Nutritional assessment in clinical practice. Nutr Clin Pract. 1986;1:3.

Jensen GL, Hsiao PY. Nutrition screening and assessment. In: Mueller CM, ed. The A.S.P.E.N. Adult Nutrition

Support Core Curriculum. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition;

2012:155.

McWhirter JP, Pennington CR. Incidence and recognition of malnutrition in hospital. BMJ. 1994;308:945.

Leiter LA, Marliss EB. Survival during fasting may depend on fat as well as protein stores. JAMA.

1982;248:2306.

Keys A et al. The Biology of Human Starvation. Minneapolis, MN: University of Minnesota Press; 1950.

Robinson G et al. Impact of nutritionalstatus on DRG length of stay. JPEN J Parenter Enteral Nutr. 1987;11:49.

Reilly JJ, Jr et al. Economic impact of malnutrition: a model system for hospitalized patients. JPEN J Parenter

Enteral Nutr. 1988;12:371.

Detsky AS et al. The rational clinical examination. Is this patient malnourished? JAMA. 1994;271:54.

Brantley SL, Mills ME. Overview of enteral nutrition. In: Mueller CM, ed. The A.S.P.E.N. Adult Nutrition

Support Core Curriculum. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition;

2012:170.

Russell MK et al. Standards for specialized nutrition support: adult hospitalized patients. Nutr Clin Pract.

2002;17:384.

[No authors listed]. Definitions of terms used in A.S.P.E.N. guidelines and standards. A.S.P.E.N. Board of

Directors. Nutr Clin Pract. 1995;10:1.

Lipman TO. Grains or veins: is enteral nutrition really better than parenteral nutrition? A look at the evidence.

JPEN J Parenter Enteral Nutr. 1998;22:167.

Braunschweig CL et al. Enteral compared with parenteral nutrition: a meta-analysis. Am J Clin Nutr.

2001;74:534.

Beier-Holgersen R, Boesby S. Influence of postoperative enteral nutrition on postsurgical infections. Gut.

1996;39:833.

Hernandez G et al. Gut mucosal atrophy after a short enteral fasting period in critically ill patients. J Crit Care.

1999;14:73.

Kudsk KA et al. Enteral versus parenteral feeding. Effects on septic morbidity after blunt and penetrating

abdominal trauma. Ann Surg. 1992;215:503.

Moore FA et al. Early enteral feeding, compared with parenteral, reduces postoperative septic complications: the

results of a meta-analysis. Ann Surg. 1992;216:172.

Charney P. Nutrition assessment in the 1990s: where are we now? Nutr Clin Pract. 1995;10:131.

McDowell MA et al. Anthropometric reference data for children and adults: United States, 2003–2006. In:

National Health Statistics Reports: No. 10. Hyattsville, MD: National Center for Health Statistics; 2008.

http://www.cdc.gov/nchs/data/nhsr/nhsr010.pdm. Accessed March 9, 2016.

Gabay C, Kushner I. Acute-phase proteins and other systemic responses to inflammation [published correction

appears in N EnglJ Med. 1999;340:1376]. N EnglJ Med. 1999;340:448.

Vanek VW The use of serum albumin as a prognostic or nutritional marker and the pros and cons of IV albumin

therapy. Nutr Clin Pract. 1998;13:110.

Detsky AS et al. What is subjective global assessment of nutritional status? JPEN J Parenter Enteral Nutr.

1987;11:8.

Garrel DR et al. Should we still use the Harris and Benedict equations? Nutr Clin Pract. 1996;11:99.

Wooley JA, Frankenfield D. Energy. In: Mueller CM, ed. The A.S.P.E.N. Adult Nutrition Support Core

Curriculum. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition; 2012:22.

McClave SA et al. Society of Critical Care Medicine (SCCM) and American Society for Parenteral and Enteral

Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr. 2016;40(2):159–211.

Solomon SM, Kirby DF. The refeeding syndrome: a review. JPEN J Parenter Enteral Nutr. 1990;14:90.

Brooks MJ, Melnik G. The refeeding syndrome: an approach to understanding its complications and preventing its

occurrence. Pharmacotherapy. 1995;15:713.

Kumpf VJ, Gervasio J. Complications of parenteral nutrition. In: Mueller CM, ed. The A.S.P.E.N. Adult Nutrition

Support Core Curriculum. 2nd ed. Silver Spring, MD: American Society for Parenteral and Enteral Nutrition;

2012:284.

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Body mass index (BMI) should be measured at each patient encounter

and patients should be assessed for overweight and obesity and the risk

for related comorbid conditions.

Case 36-1 (Questions 1, 3)

An understanding of body composition is essential when evaluating the

health status of a patient with regard to body fat.

Case 36-1 (Question 1)

The medication lists of patients with increased body weight should be

evaluated for drugs associated with weight gain and alternative agents

that are weight neutral or associated with weight loss should be

considered.

Case 36-1 (Question 1)

Obesity is a chronic disease and therapeutic interventions must be long

term.

Case 36-1 (Questions 2, 7)

An appropriate weight loss goal is 5% to 10% of baseline body weight in

6 months.

Case 36-1 (Question 4)

Management and treatment of overweight and obesity should include a

combination of diet and increased physical activity along with behavioral

modifications.

Case 36-1 (Questions 4, 5)

Medication to treat obesity should be considered for patients with a body

mass index greater than 30 kg/m

2 without risk factors or greater than 27

kg/m

2 with an obesity-related risk factor such as hypertension,

dyslipidemia, sleep apnea, cardiovascular disease, and type 2 diabetes

Case 36-1 (Questions 6, 7, 9)

Short-term weight loss drugs are unlikely to be clinically useful and

should not be recommended.

Case 36-1 (Question 6)

Medication for chronic weight management includes orlistat,

phentermine/topiramate, lorcaserin, naltrexone/bupropion, and liraglutide.

Case 36-1 (Question 7)

The use of dietary supplements for weight loss is not supported by

clinical literature and should be avoided due to safety concerns and lack

of regulation.

Case 36-1 (Question 8)

Bariatric surgery may be considered for patients with a BMI >40 or

BMI >35 with obesity-related comorbid conditions.

Case 36-1 (Question 10)

Alteration of gastrointestinal tract and stomach size after bariatric

surgery can alter drug pharmacokinetics and place patients at risk for

adverse events associated with some medications.

Case 36-1 (Question 10)

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p. 757

Obesity is a chronic disease that is characterized by excess body fat accumulation

which may impair health.

1,2 The prevalence of obesity has become an epidemic.

More than two-thirds of the US adult population is overweight with more than onethird considered obese.

3 And more than one-third of the worldwide population is

overweight.

4

It is recognized by the World Health Organization (WHO) and US

Federal Government as a growing problem that is burdening our healthcare

organizations and economy. Analyses estimate the total annual US economic costs

associated with obesity are in excess of $215 billion.



organizations and economy. Analyses estimate the total annual US economic costs

associated with obesity are in excess of $215 billion.

5

DEFINITIONS

Overweight and obesity are defined by body mass index (BMI), a measure of weight

in relation to height. BMI is calculated as weight (in kg) divided by height (in meters)

squared. Normal weight is defined as BMI of 18.5 to less than 25 kg/m2

; overweight

is defined as BMI greater than or equal to 25 to less than 30 kg/m2

; and obesity is

defined as BMI greater than or equal to 30 kg/m2

(Table 36-1).

6,7 Obesity is further

divided into class I (BMI 30–35 kg/m2

), class II (BMI 35–40 kg/m2

), and class III

(BMI 40 kg/m2

). Class III obesity is also referred to as extreme or severe obesity

and was formerly known as morbid obesity. Obesity is a chronic metabolic disorder

that is determined by multiple biologic and environmental factors, an obesogenic

lifestyle, and a genetic predisposition. The increase in the prevalence of obesity and

negative health outcomes are major public health problems throughout the world.

1,8

Body mass index (BMI) is widely accepted as the standard to classify weight.

However, a major limitation of BMI is that it does not consider body composition.

According to BMI, a person may be classified as “overweight” if their muscle mass

is great enough to significantly contribute to total weight. On the other hand, a patient

may be considered “normal weight” while having excess fat accumulation and

decreased muscle mass. The use of BMI to assess body fat and risk of morbidity and

mortality is particularly problematic in certain ethnic groups because BMI does not

account for differences in distribution of body fat. For example, research suggests

that in the Asian population, BMI underestimates body fat.

9

Fat distribution in the abdominal region has been linked to many of the metabolic

consequences of obesity.

10 Measurement of waist circumference (WC) is used to

assess for increased abdominal fat accumulation and to determine health risk. Waist

circumference measurements greater than 102 cm (40 inches) in men and 88 cm (35

inches) in women are associated with increased risk of metabolic diseases.

10

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