i. understanding the disease and pathophysiology...ii. understanding the nutrition therapy 13. what...

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Katie Davis KNH 411 Mrs. Matuszak Case Study 11 – Inflammatory Bowell Disease: Crohn’s Disease Matt Sims was diagnosed with Crohn’s Disease 2 ½ years ago. He is now admitted with an acute exacerbation of that disease. I. Understanding the Disease and Pathophysiology 1. What is inflammatory bowel disease? What does current medical literature indicate regarding its etiology? Inflammatory bowel disease (IBD) is an autoimmune, chronic inflammatory condition of the gastrointestinal tract; IBD is actually the term designating a syndrome consisting of two diagnosis: ulcerative colitis (UC) and Crohn’s disease (Nelms, Sucher, Lacey, & Roth, p. 377). At this time, the complete etiology for both Crohn’s disease and UC is unknown, but current literature indicates that there are multiple factors that may trigger this abnormal inflammatory response such as environmental factors like smoking, infectious agents, intestinal flora, and physiological changes in the small intestine. Additionally, there is a strong link of IBD to genetics. Research has shown that 5% to 15% of patients with IBD have a family history of IBD. Also, the incidence of IBD in identical twins is 44% and in fraternal twins is 3.8%. These genetic associations are for both innate immune responses and acquired immune responses (Nelms, p. 415- 417). 2. Mr. Sims was initially diagnosed with ulcerative colitis and then diagnosed with Crohn’s. How could this happen? What are the similarities and differences between Crohn’s disease and ulcerative colitis? There are a few reasons why Mr. Sims was initially diagnosed with UC. First, because the onset of UC is typically in a person’s twenties and thirties, whereas Crohn’s peak onset it teens to twenties, which was not the case for Mr. Sims. Also, some of the diagnostic test results for GI tract disorders can be indicators of either Crohn’s disease or UC such as calprotectin and lactoferrin (fecal markers of inflammation), unclear

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Page 1: I. Understanding the Disease and Pathophysiology...II. Understanding the Nutrition Therapy 13. What are the potential nutritional consequences of Crohn’s disease? The biggest nutritional

Katie Davis

KNH 411

Mrs. Matuszak

Case Study 11 – Inflammatory Bowell Disease: Crohn’s Disease

Matt Sims was diagnosed with Crohn’s Disease 2 ½ years ago. He is now admitted

with an acute exacerbation of that disease.

I. Understanding the Disease and Pathophysiology

1. What is inflammatory bowel disease? What does current medical literature

indicate regarding its etiology?

Inflammatory bowel disease (IBD) is an autoimmune, chronic inflammatory condition

of the gastrointestinal tract; IBD is actually the term designating a syndrome consisting

of two diagnosis: ulcerative colitis (UC) and Crohn’s disease (Nelms, Sucher, Lacey, &

Roth, p. 377). At this time, the complete etiology for both Crohn’s disease and UC is

unknown, but current literature indicates that there are multiple factors that may

trigger this abnormal inflammatory response such as environmental factors like

smoking, infectious agents, intestinal flora, and physiological changes in the small

intestine. Additionally, there is a strong link of IBD to genetics. Research has shown

that 5% to 15% of patients with IBD have a family history of IBD. Also, the incidence of

IBD in identical twins is 44% and in fraternal twins is 3.8%. These genetic associations

are for both innate immune responses and acquired immune responses (Nelms, p. 415-

417).

2. Mr. Sims was initially diagnosed with ulcerative colitis and then diagnosed with

Crohn’s. How could this happen? What are the similarities and differences between

Crohn’s disease and ulcerative colitis?

There are a few reasons why Mr. Sims was initially diagnosed with UC. First, because

the onset of UC is typically in a person’s twenties and thirties, whereas Crohn’s peak

onset it teens to twenties, which was not the case for Mr. Sims. Also, some of the

diagnostic test results for GI tract disorders can be indicators of either Crohn’s disease

or UC such as calprotectin and lactoferrin (fecal markers of inflammation), unclear

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results from a wireless capsule, endoscopy, or colonoscopy or mucosal biopsy (Nelms,

p. 416-419).

Ulcerative Colitis Similarities Crohn’s Disease Etiology: -association with ex-smokers -Abnormal immune

response resulting in

inflammatory damage of

GI mucosa

-genetic susceptibility

-association with

cigarette smoking

Epidemiology: -peak onset 20 to 30 years

and secondary peak in

middle age

-Both sexes affected

equally

-peak onset in teens and

20 years

Pathology: -GI tract is unable to

distinguish foreign from self-

antigens

-chronic inflammation of

colonic mucosa and

submucosa

-atrophy and possible

dysplasia limited to the colon

-can involve only rectum or

entire colon

-Localized

inflammation in bowel

mucosa progressing

through bowel wall

-Localized in terminal

ileum and colon but can

involve any part of GI

tract

Signs and

symptoms:

-Rectal pain

-Constipation and rectal

spasm

-Arthritis

-Dermatological changes

-Ocular manifestations

-Blood/mucus in stool

-Fever

-Weight loss

-Abdominal pain

-Diarrhea

-Cramping

-Delayed growth in

teens

-Malnutrition

-Anorexia

Complications: -Severe bleeding

-Toxic colitis

-Toxic megacolon

-Strictures

-Perforation

-Intolerance to

immunosuppression

-Colonic strictures

-Dysplasia

-Carcinoma

-Malabsorption

-Malnutrition

-Abdominal fistulas and

abscesses

-Intestinal obstruction

-Bacteria overgrowth

-Gallstones

-Kidney stones

-Urinary tract infections

-Thromboembolic

complications

-Perianal disease

-Neoplasia

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Diagnosis: -Abdominal ultrasound

-MRI

-CT

-Antiglycan antibodies

(ASCA/ANCA)

-Calprotectin (Cal),

lactoferrin (Lf), and

polymorphonuclear

neutrophil elastase

(PMN-e)

-Clinical presentation—

CDAI score

Prognosis: -Chronic, repeated

exacerbations and

remissions, 30% patients

require surgery, localized UC

have best prognosis, normal

life expectancy

-Rarely cured,

intermittent

exacerbations, 70%

patients require surgery

(Nelms, p. 416-419)

3. A CT scan indicated bowel obstruction and the Crohn’s disease was classified as

severe-fulminant disease. CDAI score of 400. What does a CDAI score of 400

indicate? What does a classification of severe-fulminant disease indicate?

CDAI stands for Crohn’s Disease Activity Index, which is a way of describing the stage

of a patient’s Crohn’s disease. A score over 150 indicates that a patient is experiencing a

flare-up of the disease and a score over 300 indicates that a patient is experiencing

severe exacerbation of the disease. A score of 400 indicates that the patient is in the

Moderate-Severe stage of the disease. The Severe-Fulminant stage of the disease (CDAI

greater than 450) indicates that a person has persisting symptoms despite steroids or

biologic agents or a person has high fever, persistent vomiting, evidence of intestinal

obstruction, rebound tenderness, cachexia, or evidence of an abscess (Nelms, p. 418-419)

4. What did you find in Mr. Sims’ history and physical that is consistent with his

diagnosis of Crohn’s? Explain.

Mr. Sims’ physical indicated that he experienced increased abdominal pain and

diarrhea when he began school. This is consistent with typical diagnosis of Crohn’s

because typical acute symptoms of Crohn’s disease are diarrhea and abdominal pain

that worsen with increased motility due to decreased success of digestion and

absorption. Also, his history indicates that the initial diagnostic workup indicated acute

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disease within the last 5-7 cm of his jejunum and first 5 cm of ileum. This is more

typical of Crohn’s disease because Crohn’s disease can involve any portion of the GI

tract (Nelms, p. 416-418). The rectum is always involved in the case of UC and not

necessarily involved in the case of Crohn’s disease (Mahan, Excott-Stump, & Raymond,

p. 628)

5. Crohn’s patients often have extraintestinal symptoms of the disease. What are

some examples of these symptoms? Is there evidence of these in his history and

physical?

Some extraintestinal symptoms of Crohn’s disease include osteopenia and osteoporosis,

dermatitis, rheumatological conditions such as ankylosing spondylitis, ocular

symptoms, and hepatobiliary complications (Nelms, p. 418). There appears to be no

evidence of these extraintestinal symptoms in patient history and physical.

6. Mr. Sims has been treated previously with corticosteroids and mesalamine. His

physician had planned to start Humira prior to this admission. Explain the

mechanism for each of these medications in the treatment of Crohn’s.

Corticosteroids affect immune cells by activating receptors that induce or suppress the

transcription of certain steroid-responsive target genes that are important in the

inflammatory process, which can suppress the production of a variety of

proinflammatory proteins (Yang & Lichtenstein , p. 804). Mesalamine reduces intestinal

cell transcription of inflammatory mediators to reduce the inflammation and immune

responses associated with the disease (Karagozian & Burakoff, p. 896). Finally, Humira

reduces inflammation by binding to and blocking TFN (tumor necrosis factor), which is

a protein that is produced in excess in the body of a Crohn’s disease patient and causes

inflammation (“Crohn’s Disease: How HUMIRA Works”).

7. Which laboratory values are consistent with an exacerbation of his Crohn’s

disease? Identify and explain these values.

Typically, severe exacerbations of Crohn’s disease patients commonly show low

albumin levels and elevated WBC (Nelms, p. 418). Mr. Sims’ WBC levels are in the

normal range (4.8-11.8 x 103/mm3), but are on the higher end of the spectrum (11.1 x

103/mm3). His albumin levels (3.2 g/dL) are consistent with exacerbation of his Crohn’s

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disease because they are well below the normal range (3.5-5 g/dL). Decreased albumin

is an indicator of chronic inflammation (Nelms, p. 55). WBC are part of the body’s

natural immune system; therefore, levels may be elevated due to the fact that the

immune system in not being suppressed in patients with Crohn’s disease.

8. Mr. Sims is currently on several vitamin and mineral supplements. Explain why

he may be at risk for vitamin and mineral deficiencies.

Many of the vitamins and minerals such as vitamin A, zinc, iron, and B vitamins that

are involved in cellular differentiation are essential for WBC production. Because

WBCs are being produced at a much higher rate in a person with exacerbated Crohn’s

disease to cause inflammation, Mr. Sims may be at risk for some vitamin and mineral

deficiencies if he did not consume supplements (Nelms, p. 55). Also, it is important to

consider that he is at risk for iron deficiency due to blood loss and malnutrition,

magnesium and zinc deficiencies due to high-volume diarrhea, calcium and vitamin D

deficiencies due to long-term steroid use, and folate deficiencies due to his current

medications (Nelms, p. 420). He is at risk for deficiencies in vitamin B12 and iron

because loss of portions of the ileum means that he has less of the receptor sites on the

ileum that allow for vitamin B12 (Nelms, p. 421). Additionally, the lack of vegetables in

his diet puts him at risk for vitamin and mineral deficiencies as well.

9. Is Mr. Sims a likely candidate for short bowel syndrome? Define short bowel

syndrome, and provide a rationale for your answer.

Short bowel syndrome (SBS) is defined as “inadequate absorptive capacity resulting

from reduced length or decreased functional bowel after resection.” Loss of 70% to 75%

of small bowel results in SBS. SBS can also be defined as “the inability to maintain

nutrition and hydration needs with normal fluid and food intake” (Mahan, p. 637).

Another definition of SBS is “intestinal failure that results from surgical resection,

congenital defect or disease-associated loss of absorption and is characterized by the

inability to maintain protein, energy, fluid, and electrolyte, or micronutrient balances

when on a conventionally accepted, normal diet” (Nelms, p. 424). Although Mr. Sims

has not had and surgical resection of his bowels, he does have Crohn’s disease-

associated loss of the last 5-7 cm of jejunum and first 5 cm of ileum that inhibit proper

absorption of nutrients from his diet to meet his nutritional needs. He also has some of

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the classic symptoms of SBS such as malabsorption and micronutrients and

macronutrients and frequent diarrhea.

10. What type of adaptation can the small intestine make after resection?

Patients are weaned off nutrition support and slowly take on whole nutrients in order

to facilitate the adaptation process and restore bowel movements and regular functions

(Mahan, p. 638).

11. For what classic symptoms of short bowel syndrome should Mr. Sims’ health care

team monitor?

Mr. Sims’ health team should monitor his malabsorption and micronutrients and

macronutrients and frequent diarrhea in order to prevent nutrient deficiencies.

12. Mr. Sims is being evaluated for participation in a clinical trial using high-dose

immunosuppression and autologous peripheral blood stem cell transplantation

(autoPBSCT). How might this treatment help Mr. Sims?

Participation in this clinical trial may achieve medication-free remission after 1 year that

continues long-term for Mr. Sims (Hassleblatt, p. 726)

II. Understanding the Nutrition Therapy

13. What are the potential nutritional consequences of Crohn’s disease?

The biggest nutritional concern that can result from Crohn’s disease is the loss of

absorptive ability of the GIT from inflammation and/or surgery that will result in

malnutrition and nutrient deficiencies.

14. Mr. Sims underwent resection of 200 cm of jejunum and proximal ileum with

placement of jejunostomy. The ileocecal valve was preserved. Mr. Sims did not have

an ileostomy, and his entire colon remains intact. How long is the small intestine,

and how significant is this resection?

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The duodenum is approximately 50 cm long, the jejunum is 200 to 300 cm long, and the

ileum is 300 to 400 cm. In total, the small intestine is approximately 550 cm to 750 cm

(5.5-7.5 m) long (Mahan, p. 9). Mr. Sims lost approximately 36% to 27% of his small

intestine. Because the small intestine is very adaptive having the ability to change

functions efficiently, more than 50% of it has to be removed in order to loose significant

functional capabilities (Nelms, p. 377-378). Therefore, this is not an extremely

significant resection because the small intestine is able to adapt so well.

15. What nutrients are normally digested and absorbed in the portion of the small

intestine that has been resected?

The jejunum normally digests and absorbs lipids, monosaccharides, amino acids, small

peptides, Thiamin, riboflavin, niacin, pantothenate, biotin, folate, vitamin B6, vitamin C,

vitamin A, vitamin D, vitamin E, vitamin K, calcium, phosphorus, magnesium, iron,

zinc, chromium, manganese, and molybdenum. The proximal ileum digests and

absorbs vitamin C, folate, vitamin B12, vitamin D, vitamin K, and magnesium (Nelms, p.

384).

III. Nutrition Assessment

16. Evaluate Mr. Sims’ % UBW and BMI.

BMI:

(140 lbs) / (2.2) = 62.64 kg

(69 in) x (0.0254) = 1.75 m

(62.64 kg) / (1.75 m)2 = 20.45 kg/m2

Mr. Sims is a normal weight.

% UBW:

( (167 lbs - 140 lbs) / (167 lbs) ) x 100 = 16.1% change over the last six months

Mr. Sims is at nutritional risk for health complications because he had an

unexplained weight change of more than 10% from UBW in the last six

months (Nelms, p. 47). He also claims to be even lighter than 140 lbs.

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17. Calculate Mr. Sims’ energy requirements. 17 need an activity factor and a stress factor-

1.2 and 1.3 would be appropriate

Mifflin-St. Jeor resting energy expenditure equation is to be used.

(10 x 62.64 kg) + (6.25 x 175.26 cm) – (5 x 36 yrs) + 5 = 1546.78 kcal

18. What would you estimate Mr. Sims’ protein requirements to be?

The estimation of Mr. Sims’ protein requirements will be based on the fact that there is a

presence of lean body mass wasting and biochemical parameters measuring protein

status of low prealbumin and albumin (1.5 to 1.75 g protein per kg weight of adult)

(Nelms, p. 421).

(62.64 kg) x (1.75) = 109.62 g protein

19. Identify any significant and/or abnormal laboratory measurements from both his

hematology and his chemistry labs.

Significant or abnormal laboratory measurements:

Low total protein

Low albumin

Low prealbumin

Low hemoglobin

Low hematocrit

Low transferrin

Low ferritin

High ZPP

Low vitamin D

Low vitamin A

Low ascorbic acid

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IV. Nutrition Diagnosis

20. Select two nutritional problems and complete the PES statement for each.

1. Patient has inadequate oral intake (NI-2.1) related to Crohn’s disease-related

malabsorption of nutrients in resected and diseased portions of the small

intestine as evidenced by unexplained weight loss of greater than 10% UBW over

a six month period.

2. Patient is experiencing malnutrition (NI-5.2) related to Crohn’s disease-related

diarrhea and abdominal pain as well as jejunum and ileum resection as

evidenced by abnormal laboratory results.

(“IDNT Reference Manual”, p. 205-206)

V. Nutrition Intervention

21. The surgeon notes Mr. Sims probably will not resume eating by mouth for at

least 7-10 days. What information would the nutrition support team evaluate in

deciding the route for nutrition support?

Because there is no single dietary regimen to follow for Crohn’s disease, the nutrition

support team need to investigate foods that work specifically with Mr. Sims’ body to

reduce symptoms and flares so that he is able to successfully reach his goals (Mahan, p.

631).

22. The members of the nutrition support team note his serum phosphorus and

serum magnesium are at the low end of the normal range. Why might that be of

concern?

Low serum magnesium is also referred to as hypomagnesemia and may result in

tremor, muscle twitching, cardiac arrhythmias, and paralysis. Also low serum

potassium is also referred to as hypokalemia and is also associated with cardiac

abnormalities. Both of these conditions indicate a shift in a patient’s primary energy

source from ketones to glucose. This is of concern because of the serious health risks

associated with the conditions and the fact that the use of ketones as a primary energy

source is an indication of starvation or inadequate absorption of oral intake (Nelms, p.

92-93).

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23. What is refeeding syndrome? Is Mr. Sims at risk for this syndrome? How can it

be prevented?

Refeeding syndrome is a condition where a starved patient experiences metabolic

alterations that occur during nutritional repletion. Patients who present malnutrition,

have a history of long-term inadequate oral intake, or have minimal intake over a

period of several days are at risk for refeeding syndrome; therefore, Mr. Sims is at risk

because he fits into all three categories. A slow introduction of feedings to avoid

overfeeding is important in order to prevent refeeding syndrome (Nelms, p. 93).

24. Mr. Sims was placed on parenteral nutrition support immediately

postoperatively, and a nutrition support consult was ordered. Initially, he was

prescribed to receive 200 g dextrose/L, 42.5 g amino acids/L, and 30 g lipid/L. His

parenteral nutrition was initiated at 50 cc/hr with a goal rate of 85 cc/hr. Do you agree

with the team’s decision to initiate parenteral nutrition? Will this meet his estimated

nutritional needs? Explain. Calculate: pro (g); CHO (g); lipid (g); and total kcal from

his PN.

I think that initiation of parenteral nutrition was appropriate in order to provide Mr.

Sims with the nutrients his body needs before he is transitioned to an oral diet.

(200 g dextrose/L) x (1L/1000ml) = 0.2 g dextrose/ml or 0.2 g dextrose/cc

(42.5 g AA/L) x (1L/1000ml) = 0.0425 g AA/ml or 0.0425 g AA/cc

(30 g lipid/L) x (1L/1000ml) = 0.03 g lipid/ml or 0.03 g AA/cc

(0.2 g dextrose/cc) x (85 cc/hr) = 17 g/hr x 24 hr = (408 g dextrose per day) x (3.4 kcal/g) =

1632 kcal from CHO

(0.0425 g AA/cc) x (85 cc/hr) = 3.61 g/hr x 24 hr = (86.7 g AA per day) x (4 kcal/g) =

346.8 kcal from protein

(0.03 g lipid/cc) x (85 cc/hr) = 2.55 g/hr x 24 hr = (61.2 g lipid per day) x (10 kcal/g) =

550.8 kcal from lipid

2529.6 kcal total from PN. This will meet and exceed his energy needs estimated by

both Mifflin-St. Jeor resting energy expenditure equation and indirect calorimetry.

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25. For each of the PES statements you have written, establish an ideal goal (based on

the signs and symptoms) and an appropriate intervention (based on the etiology). 25

MVI provided in PN solution - would need oral supplement when able to tolerate po

1. Goal: Maximize energy and protein intake to facilitate rehabilitation (orally or

parenteral) in order to rebuild muscle mass, protein stores, and allow weight to

eventually reach UBW of 167 lbs.

Intervention: Patient will be transitioned to an oral diet that includes include

small, frequent meals with high protein content and that are nutrient dense into

his daily diet to maximize energy and protein and include 15 minutes of

moderate physical activity each day.

2. Goal: Return all lab values related to malnutrition to the normal range.

Intervention: Patient will receive a multivitamin that meets the RDA or AI for all

nutrients daily.

VI. Nutrition Monitoring and Evaluation

26. Indirect calorimetry revealed the following information:

Measure Mr. Sims’ data

Oxygen consumption (mL/min) 295

CO2 production (mL/min) 261

RQ 0.88

RMR 2022

What does this information tell you about Mr. Sims?

The oxygen consumption values and CO2 production values are in the normal range,

which indicates his energy requirements are being met and he is not being overfed

(Mahan, p. 891). The RQ value of 0.88 indicates the fact that Mr. Sims diet is a mix

between carbohydrates and protein (Mahan, p. 23). His RMR indicates that he needs

roughly 700 kcal more each day than we calculated using Mifflin-St. Jeor resting energy

expenditure equation and that we need to increase his energy intake more than

originally thought.

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27. Would you make any changes to his prescribed nutrition support? What should

be monitored to ensure adequacy of his nutrition support? Explain.

The only change I would make to Mr. Sims’ nutrition support is to add the vitamins and

minerals that he may have trouble absorbing due to the recesction of portions of his

small intestine to improve and prevent future malnutrition or vitamin and mineral

deficiencies. Also, I would include the introduction of an oral diet as part of his

nutrition support. His chemistry and hematology should be monitored regularly in

order to track changes to his nutrition status based on the prescribed nutrition support.

28. What should the nutrition support team monitor daily? What should be

monitored weekly? Explain your answers. 28 state specific labs

Chemistry and hematology should be monitored daily in order for the nutrition support

team to make changes to Mr. Sims’ nutrition support as needed and make sure he is

reaching his goals. Also, his weight should be measured weekly to mark his progress

towards his goal body weight.

29. Mr. Sims’ serum glucose increased to 145 mg/dL. Why do you think this level is

now abnormal? What should be done about it? 29 metabolic stress, may need insulin in PN

bag

This level may be high because his PN consists of 65% dextrose (CHO). Dextrose

should be reduced to 50% to 60 % dextrose in order for this value to return to a more

normal level.

30. Evaluate the following 24-hour urine data: 24-hour urinary nitrogen for 12/20: 18.4

grams. By using the daily input/output record for 12/20 that records the amount of

PN received, calculate Mr. Sims’ nitrogen balance on postoperative day 4. How

would you interpret this information? Should you be concerned? Are there

problems with the accuracy of nitrogen balance studies? 30 use formula and calculate

Urinary nitrogen balance is used primarily to accurately follow the protein catabolic

response during disease and response to nutritional support. There are inaccuracies in

nitrogen balance studies because they account for all sources of nitrogen, not just those

of nutrition support (Mahan, p. 1082). It is also important to remember that positive

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nitrogen balance may not necessarily mean that protein catabolism has decreased

(Mahan, p. 198).

Nitrogen balance is a measure of the daily intake of the daily intake of nitrogen minus

the daily excretion

Nitrogen balance=nitrogen intake-nitrogen losses

Nitrogen intake=protein intake (g/day)=4g

Uun is determined from a 24 hour urine collection

4g is a fudge factor

Positive NB indicates an anabolic state

86.7/8.24-18.4-4

31. On post-op day 10, Mr. Sims’ team notes he has had bowel sounds for the

previous 48 hours and had his first bowel movement. The nutrition support tem

recommends consideration of an oral diet. What should Mr. Sims be allowed to try

first? What would you monitor for tolerance? If successful, when can the parenteral

nutrition be weaned?

First, Mr. Sims should be allowed to try liquids and slowly progress to a low-residue

diet with four to six small feedings each day, if tolerable. Foods that may not be

completely digested in the GIT should be avoided for the first 6-8 weeks after surgery.

He will need to be educated on how to eat slowly, chew thoroughly, and drink

sufficient liquids. After 8 weeks successfully into the oral diet, he should be back to a

normal diet and PN can be weaned (Nelms, p. 424).

32. What would be the primary nutrition concerns as Mr. Sims prepares for

rehabilitation after his discharge? Be sure to address his need for supplementation

of any vitamins and minerals. Identify two nutritional outcomes with specific

measures for evaluation. 32 state specific labs and timetable for weight change

Mr. Sims needs to be sure to maintain adequate vitamin and mineral intake through

fruits and vegetables as well as a daily a multivitamin that meets the RDA or AI for all

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nutrients. This will be monitored through follow-up appointments to assess his blood

chemistry and hematology. In addition to this, he needs to be sure to consume 2600

kcal each day (amount he “consumed” through his PN) in order to return to his UBW.

This will also be monitored through follow-up appointments to assess the progression

of his weight gain.

References

American Dietetic Association. (2009). International Dietetics& Nutrition Terminology

(IDNT) Reference Manual: Standardized Language for the Nutrition Care Process,

Second Edition. Chicago, IL: American Dietetic Association.

Crohn’s Disease: How HUMIRA Works (2013). Humira. Retrieved from

http://www.humira.com/crohns/how-humira-works.aspx

Hassleblatt, P., Drognitz, K., Fotthoff, K., Bertz, H., Kruis, W., Schmidt, C., Stallmach,

A., Schmitt-Graeff, A., Finke, J., Kreisel, W. (2012). Remission of refractory

Crohn’s disease by high-dose cyclophosphamide and autologous peripheral

blood stem cell transplantation. Alimentary Pharmacology and Therapeutics. 36. 726.

Karagozian, R., Burakoff, R. (2007). The role of mesalamine in the treatment of

ulcerative colitis. Therapeutics and Clinical Risk Management. 3(5). 896.

Mahan, L.K., Escott-Stump, S., and Raymond, J.L. (2012). Krause’s Food & The Nutrition

Care Process, Thirteenth Edition. St. Louis, MO: Elsevier Saunders.

Nelms, M., Sucher, K. P., Lacey, K., and Roth, S. L. (2011). Nutrition Therapy &

Pathophysiology, Second Edition. Belmont, CA: Brooks/Cole Cengage Learning.

Yang, Y., Lichtenstein, G. R. (2002). Corticosteroids in Crohn’s disease. The American

Journal of Gastroenterology. 97(4). 804.