RESEARCH

Research and Practice Innovations

An Overview of Short Bowel Syndrome Management:

Adherence, Adaptation, and Practical
Recommendations
Elizabeth A. Wall, MS, RD, LDN
ARTICLE INFORMATION

ABSTRACT

Article history:

Short bowel syndrome (SBS) refers to the clinical consequences resulting from loss of
small bowel absorptive surface area due to surgical resection or bypass. The syndrome is
characterized by maldigestion, malabsorption, and malnutrition. Survival of patients
with SBS is dependent on adaptation in the remaining bowel and a combination of
pharmacologic and nutrition therapies. Individual plans of care are developed based on
the length and sites of remaining bowel, the degree of intestinal adaptation, and the
patients ability to adhere to the medication and dietary regimens. Antisecretory and
antidiarrheal medications are prescribed to slow intestinal transit times and optimize
uid and nutrient absorption. Based on postsurgical anatomy, enteral feedings, parenteral infusions, complex diet plans, and vitamin and mineral supplementation are used
in various combinations to nourish patients with SBS. In the acute care setting, registered dietitians (RDs) assist with infusion therapy, diet education, and discharge planning. Long-term, as the small intestine adapts, RDs revise the nutrition care plan and
monitor for nutrient deciencies, metabolic bone disease, and anemia. The frequent
monitoring and revision of care plans, plus the appreciable benets from proper
medical nutrition therapy, make this patient population extremely challenging and
rewarding for RDs to manage. This article provides a brief, case study-based overview of
the medical and nutrition management of SBS.

Accepted 30 April 2013

Available online 3 July 2013

Keywords:
Pathophysiology of short bowel syndrome
Medical nutrition therapy
Clinical management of patients with short bowel
syndrome
Copyright 2013 by the Academy of Nutrition
and Dietetics.
2212-2672/$36.00
doi:10.1016/j.jand.2013.05.001

J Acad Nutr Diet. 2013;113:1200-1208.

HORT BOWEL SYNDROME (SBS) REFERS TO THE

clinical consequences resulting from loss of small
bowel absorptive surface area due to surgical resection or bypass. The syndrome is characterized by
maldigestion, malabsorption, and malnutrition. The most
common causes of SBS in adults are small bowel resections
from strangulated bowel, Crohns disease, ischemia, trauma,
or malabsorptive weight loss surgery.1 The metabolic consequences of removing the small intestine are variable and
depend on a number of factors, including the length, condition, and sites of remaining small bowel.2,3 Survival of a patient with SBS is dependent on adaptation in the remaining
bowel and a combination of pharmacologic and nutrition
therapies. This overview covers the pathophysiology of SBS,
medical and nutrition management, and provides practical
advice for clinicians who encounter patients with SBS.

PATHOPHYSIOLOGY
Normal length of the small intestine varies from 300 to 600
cm; approximately half of the upper intestine (jejunum) can
be removed without signicant problems. Patients with <100
cm of small intestine will have severe malabsorption, which
will result in malnutrition if untreated. There are two clinically useful categories of patients with SBS: those with a
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JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS

colon in continuity with the remaining small bowel and those

with a small bowel ostomy. The presence of the ilealcecal
valve and colon, even with as little as 50 cm of small bowel,
markedly improves uid and electrolyte absorption as well as
uptake of short-chain fatty acids and often allows for survival
without articial nutrition support.4 When the small bowel
is <100 cm to an end jejunostomy or ileostomy, parenteral
nutrition (PN) and hydration will likely be needed for
survival.4,5
Consideration of the site of small bowel resection is
important in determining the extent of metabolic consequences. The duodenum and jejunum are the primary sites of
protein, carbohydrate, fat, water-soluble vitamin, and mineral
absorption (particularly calcium, iron, and folate) as well as
the mixing site of pancreatic and biliary secretions. Resection
of the ileum, particularly the terminal ileum, is more detrimental than loss of jejunum because it is the only site for
absorption of intrinsic factor-bound B-12 and bile salts. If
>100 cm of distal ileum is removed, then enterohepatic circulation of bile salts is disrupted resulting in severe fat
malabsorption and steatorrhea.6 The distal ileum is also an
important regulator of gastric emptying and small bowel
transit time.7 Loss leads to rapid gastric emptying and rapid
small bowel transit similar to the dumping syndrome.
2013 by the Academy of Nutrition and Dietetics.

RESEARCH
After surgical resection the remaining small bowel undergoes an adaptation process that involves morphologic and
functional changes.8 The small bowel dilates and the villi
height and crypt depth increase, expanding the absorptive
surface area of the small bowel without change in length.9
The mechanism of adaption is not fully understood. Important factors include hormonal growth factors, nutrients
(particularly complex macronutrients), bile and pancreatic
secretions, and local intestinal hormones such as glucagonlike peptide 2.10 Adaptation begins soon after intestinal
resection and may continue for
2 years.11 Because oral nutrients stimulate intestinal adaptation, it is important to
initiate an oral diet or enteral feedings as soon as possible
after surgery.12

MANAGEMENT OF SBS
The goal of therapy is to maximize small bowel absorption of
uids and nutrients to prevent deciencies and dehydration.12
This is accomplished by controlling the rate at which nutrients and uids move through the intestinal tract with the use
of medications and diet therapy. In some cases infusion
therapy (enteral and/or parenteral) with nutrients and uid
may be required either temporarily after surgery, or lifelong.1

Pharmacotherapy
The common categories of medications used to manage SBS
include antimotility agents, antisecretory agents, and parenteral infusion therapy (intravenous [IV] uids and/or PN).1
Antimotility medications (the most common are loperamide,
diphenoxylate and atropine, codeine, and deodorized tincture
of opium [DTO]) are used to slow peristalsis and improve absorption of uid, electrolytes, and nutrients.13 These medications are usually taken as needed after a loose bowel
movement, but for patients with SBS the dose is given
routinely 30 minutes before meals and at bedtime. Often patients with SBS have to adjust the timing and titrate the dose of
antimotility agents based on meal composition, daily activities,
and degree of bowel adaptation. Patients taking opiate-based
medications to control uid and electrolyte losses (codeine
and DTO) must be closely monitored for side effects, including
impaired mental or physical alertness as well as symptoms of
withdrawal if the medications are abruptly discontinued after
prolonged use.14 Clonidine, an a2-adrenergic agonist, has been
shown to increase intestinal transit time and decrease fecal
weight in patients with SBS.15-17 It can be administered by oral
medication or transdermal patch, which is an effective alternative for patients with reduced small bowel absorption.
Clonidine is commonly used to treat hypertension so blood
pressure should be monitored closely when starting this
medication. Patients with severe coronary heart disease,
chronic renal insufciency, and hemodynamic instability may
not be good candidates for clonidine therapy.14
Hypersecretion of gastrin and gastric acid occurs in patients after extensive small bowel resection.18 Histamine H2
antagonists (ie, H2 blockers) and the more potent proton
pump inhibitors (PPIs) are used in SBS to decrease gastric acid
secretion, diarrheal losses, and risk for peptic ulcer disease
and its complications. The H2 blockers inhibit histamine at
the histamine H2 receptors of gastric parietal cells thus
reducing gastric acid secretion whereas PPIs directly inhibit
hydrogen potassium ATPase pump of parietal cells effectively
September 2013 Volume 113 Number 9

stopping acid secretion.14 Somatostatin analogues inhibit the

release of gastrointestinal hormones and reduce secretion of
intestinal and pancreatic uids, which reduces diarrhea in
patients with SBS.14
In some cases pancreatic enzyme replacement and bile acid
sequestrants may be used to control maldigestion and diarrhea.13 Exogenous pancreatic enzyme mixing with food in the
stomach can increase nutrient absorption in patients with
rapid small bowel transit and poor intestinal mixing of chyme
with pancreatic secretions. Bile acid sequestrants can help
alleviate choleretic diarrhea that occurs when distal ileal
resection disrupts enterohepatic circulation of bile salts.1
Small bowel bacterial overgrowth can occur in conjunction
with SBS and is related to alterations of intestinal anatomy,
motility, and gastric acid suppression.19,20 Bacteria in the
small bowel can deconjugate bile acids, which may worsen
diarrhea and malabsorption.20-22 Treatments for bacterial
overgrowth include antibiotics, probiotics, and bile acid
sequestrants.23 Often broad spectrum antibiotics are cycled
(alternating 1 or 2 weeks of treatment with an antibiotic with
several weeks off antibiotic therapy) to prevent or delay
antibiotic resistance.
Parenteral infusion therapy is often needed immediately
after surgery to maintain uid and electrolyte balance as
bowel function returns.12 IV support can vary from saline or
lactated ringers infusions to full PN support (IV uids that
contain both macro- and micronutrients). The degree of
bowel adaptation will dictate the length of IV therapy. A good
guideline is that patients with SBS with >1.5 L stool output
and <800 mL urine output in 24 hours will have difculty
maintaining hydration and electrolyte balance without some
IV uid support.3

Medical Nutrition Therapy

The macronutrient distribution of diets for SBS will vary
depending upon the sites and length of remaining bowel
(Figure 1). In small clinical studies, patients with end jejunostomies have improved energy absorption and similar stool
losses with moderately high amounts of fats and dietary ber
when compared with diets high in complex carbohydrates
(CHO) alone.24-27 The optimal diet includes generous amounts
of complex CHO and fats with a macronutrient distribution of
approximately (50% CHO, 20% to 30% protein, and 40% fat).28
Foods rich in water-soluble ber can slow both gastric
emptying and intestinal transit time, thicken ostomy efuent,
and promote intestinal adaptation.24,29 It is best to minimize
uid intake with solid food meals; beverages should be sipped
continuously between meals.30,31 Avoidance of foods and
beverages high in simple sugars may alleviate dumping of
hypertonic chyme into the intestine. Patients should eat four
to six small meals a day. Another important goal for patients
with SBS and jejunostomies is to maximize uid uptake by the
small intestine. This is best achieved by utilizing the sodiumglucose cotransport system to pull water across the epithelial
lining.32-35 Liberal use of salt on food and sipping oral rehydration solutions (ORS) between meals (1 to 2 L/day) have
shown to be benecial.3,32
Patients with an intact colon benet from a diet higher in
complex CHO and moderate in fat (50% to 60% CHO, 20% to
30% protein, and 20% to 30% fat) divided into three small
meals plus two to three snacks per day.27,29 The rationale for
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RESEARCH
Small bowel
ostomy

Colonic
continuity

Carbohydrates

50% of total
energy; complex
carbohydrates
including soluble
ber, limit simple
sugars

50%-60% of total
energy; complex
carbohydrates,
including soluble
ber

Proteins

20%-30% of total
energy

20%-30% of total
energy

Fats

40% of total
energy

20%-30% of total
energy

Fluids

ORSb important;
minimize uids
with meals,
sipping of uids
between meals

Minimize uids
with meals,
sipping of uids
between meals

Vitamins

Daily multiple
vitamin with
minerals; monthly
B-12; possibly
vitamins A, Dc,
and E
supplements

Daily multiple
vitamin with
minerals; possibly
B-12 ; possibly
vitamins A, D, and
E supplements

Minerals

Generous use of
sodium chloride
on food; calcium
1,000-1,500 mg
daily; possibly
iron, magnesium,
and zinc
supplements

400-600 mg
calcium with
meals; possibly
iron, magnesium,
and zinc
supplements;
reduced oxalate

Meals

4-6 small meals

3 small meals plus

2-3 snacks

Nutrient

Enteral nutrition (EN) support alone or in combination

with an oral diet has proven to increase absorption of macronutrients in patients with and without colonic continuity.
Joly and colleagues37 demonstrated that continuous nasogastric feedings with a polymeric formula in patients with
SBS signicantly (P<0.001) increased absorption of proteins,
fats, and energy compared with an isocaloric oral diet. This
enhanced nutrient absorption may be related to continuous
infusion of isotonic nutrients, which is better tolerated with
altered gut anatomy when compared with bolus infusion of
feedings or food. The continuous bathing of the gut with
macronutrients may promote release of pancreatic and intestinal enzymes as well as intestinal hormones that enhance
bowel adaptation and overall absorption. EN is less expensive
and presents lower overall risks than PN. In SBS the use of EN
can facilitate reduction in the number of PN infusions each
week and/or complete weaning from PN therapy altogether.
Micronutrient requirements will vary among patients
depending upon the sites of remaining intestine. All patients
with SBS should take a daily multivitamin with minerals by
mouth (preferably chewable or liquid) or IV. Routine monitoring of serum vitamin B-12 and methylmalonic acid (a
marker of vitamin B-12 status) levels is required for any patient with a distal ileum resection or small bowel bacterial
overgrowth; supplementation may be required.21,38-40 Divalent cations, mainly calcium, magnesium, and zinc can be
decient in patients with SBS, and many will require supplementation.1 This may be related to lack of absorptive
surface, rapid transit time, and binding with unabsorbed fat
in the intestinal lumen. Cautious supplementation of magnesium is advisable because oral magnesium preparations
are difcult to absorb and, therefore, have cathartic effects.
Slow-release magnesium chloride, magnesium gluconate, or
magnesium lactate preparations can reduce some of the
gastrointestinal symptoms related to oral magnesium ingestion.13 Practitioners should be cognizant that osteoporosis,
anemia, and fat-soluble vitamin deciencies are common in
patients with SBS and long-term monitoring is necessary.
Individual vitamin and mineral supplements should be prescribed as needed.38 The following case highlights the
importance of comprehensive medical management of patients with SBS and provides an opportunity to discuss
practical clinical applications.

Based on references 24, 47, and 60.

ORSoral rehydration solution.
c
25-hydroxy vitamin D.
b

Figure 1. Medical nutrition therapy for short bowel syndrome.a

emphasizing complex CHO and less fat is twofold. First,

colonic bacteria can metabolize undigested CHO, including
dietary ber, to short-chain fatty acids leading to salvage
absorption and net increase energy, sodium, and water uptake.25,33 Second, steatorrhea from poorly absorbed dietary
fats and increased risk of oxalate absorption in the colon may
result in calcium oxalate kidney stone formation.4,36 A diet
low in fat and oxalate, along with calcium supplementation
at meals, can reduce the risk of kidney stone formation.
Consumption of salty foods and ORS is not as important for
patients with SBS who have an intact colon as long as food
and uid intake is spread throughout the day.24
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PATIENT PROFILE
The patient is a 72-year-old woman with a past medical
history of colon cancer that was treated by partial colectomy
and chemotherapy. Recurrent colon cancer was diagnosed 11
years later requiring a complete colectomy with end ileostomy. Postoperative Day 3, she developed severe abdominal
pain and blood-tinged ostomy efuent; re-exploration surgery demonstrated extensive distal small bowel necrosis. The
necrotic bowel was resected leaving an estimated 105 cm of
proximal small bowel to an end jejunostomy. The patients
recovery was uneventful; she was discharged from the hospital on a regular diet.
During the rst month after discharge from the hospital,
the patient had multiple admissions for dehydration and
weight loss. During one such hospitalization, a double-lumen
peripherally inserted central catheter (PICC) was placed and
PN initiated. Soon after the start of therapy, she developed an
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RESEARCH
upper extremity deep vein thrombosis originating at the PICC
insertion site; anticoagulation therapy was started. During
the same hospitalization, she developed fevers due to a
catheter-related blood infection, hypotension, hypokalemia,
and increased liver function tests. On Hospital Day 17, the
patient was transferred to a tertiary care hospital for management of SBS.

TERTIARY CARE CENTER COURSE

The PICC was pulled and the patient was given a central line
holiday while antibiotic therapy was completed. Peripheral
PN (1 L 50-g dextrose and 20-g amino acids without lipid
emulsion due to an egg allergy) was initiated along with
antisecretory (ie, PPI) and antimotility (ie, DTO) medications.
Her diet was changed to six small meals with sipping of ORS
between meals. On Hospital Day 9, a tunneled central catheter was placed and the PN formulation was increased to 50 g
dextrose, 80 g amino acids, infusing over 10 hours each night
(490 kcal/day). After intensive diet and infusion therapy education, the patient was discharged to home with the same
PN formula, diet, and medications.

AT HOME
At home, the patients oral intake increased with subsequent
increase in jejunostomy output, necessitating adjustment of
the PN volume to 1.5 L infused over 12 hours and titration of
the DTO dose to 1 mL four times a day. Six months after
discharge PN, she had stable serum chemistry values,
adequate hydration, and she was slowly losing weight; the
PN infusion was changed to every other day and the anticoagulation therapy was discontinued. Subsequent serum
chemistry results suggested negative uid balance, and the
patient complained of extreme thirst and fatigue. A 24-hour
urine collection during an off day from PN resulted in only
400 mL urine. The PN volume was increased to 2.4L over 12
hours every other day, and the patient was instructed to
strictly adhere to the diet and ORS therapy. The patient had
improved hydration on noninfusion days and the repeat 24hour urine collection yielded 850 mL.
The patient remains on every-other-day IV infusions for
uid, vitamins, minerals, and electrolytes; her weight has
stabilized at 86 kg (body mass index 30.7). Four years after
discharge on PN her insurance provider mandated a switched
to noneamino acid-containing IV uid (Table). She continues
to strictly adhere to the diet regimen, but has ceased using
ORS because she no longer appreciates hydration benets
from the therapy. Repeat chemistry data, including normal
vitamin levels and triene to tetraene ratio (an indication of
adequate absorption of essential fatty acids), plus stable body
mass index, suggest adequate hydration and nutrient uptake
with the current management.

DISCUSSION
Historically, loss of a signicant portion of the intestine was
physically devastating and often a death sentence. During the
past 50 years, with the advent of PN and a better understanding of small bowel physiology, most patients with SBS
recover and live without signicant reduction in quality of
life.41-44 The case of the patient provided is an excellent
example of the metabolic consequences of massive small
bowel resection and the complications of infusion therapy.
September 2013 Volume 113 Number 9

Per the Nutrition Care Process, this patient had altered

gastrointestinal function due to extensive intestinal resection
as evidenced by inability to maintain hydration on an oral
diet. Through aggressive medical management, strict dietary
adherence, and appreciable bowel adaptation, she has
reduced her dependence on IV support and ORS by approximately 80%. The dietary key to her success was the transition
from eating two large meals a day and drinking large volumes
of sugar-containing beverages to separating food and uid
ingestion, eating four small meals daily, limiting simple sugar
intake, and sipping ORS daily. Through trial and error, the
patient has rened her schedule for antisecretory and antimotility medications to maximize uid and electrolyte absorption. With remnant bowel length of only 105 cm, it is
unlikely she will ever completely wean from infusion therapy, but with the conversion to every-other-day IV infusion
therapy she reports improved quality of life.
Like many patients receiving home PN, this patient has
had complications related to infusion therapy, including a
thrombosis around a PICC, catheter-related blood infections,
and liver function abnormalities. The incidence of catheterrelated complications has been minimized by using single
lumen, tunneled catheters to minimize the diameter of the
catheter and reduce the risk of clot formation; limiting access
for bacterial introduction with a single lumen; and by reeducation in aseptic technique. Her liver function has
returned to normal with the reduction of PN support and
fewer central line infections (a frequent cause of abnormal
liver tests). She will require lifelong monitoring of overall
health and nutrition parameters, vitamin levels, and trace
mineral levels, as well as bone and vital organ health. Every
6 months the patient returns to clinic for monitoring. She has
dual-energy x-ray absorptiometry scans every 2 years to
assess her risk of metabolic bone disease (postmenopausal
and SBS-related). Her overall prognosis is excellent given her
signicant small bowel adaptation, the low rate of central line
complications, and reduced dependence on IV support.

PRACTICE APPLICATIONS
Management of patients with SBS requires a thorough understanding of intestinal physiology, knowledge of pharmaconutrition therapy (ie, the use of nutrients for therapeutic
benet), close attention to detail, and patience. Each SBS
patient presents with unique nutrient requirements based on
the length, site, and health of their remaining intestine.
When caring for a patient with SBS, a registered dietitian
(RD) must know the exact intestinal anatomy so that a plan of
care is developed to optimize bowel function and nourish the
patient. If the operative report is unavailable or there is
question as to the length or health of the remaining bowel, an
upper gastrointestinal with small bowel follow-through
barium study provides vital information on the length and
condition of intestine remaining as well as transit time.45 In
addition, RDs must have accurate intake and output data to
assess uid balance; awareness of all prescribed medications
and supplements; knowledge of IV access, including catheter
tip location; weight history; and laboratory data.
Before hospital discharge, there are many details RDs
must ensure are in place for patients with SBS (Figure 2).
First, the patient must understand the proper diet and oral
hydration guidelines as well as the dosage and timing of
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RESEARCH
Table. Data for a 72-year-old female patient from hospital admission to 4 y after massive small bowel resection
Transfer to
tertiary
care center

Patient data
Body mass index

35.3

Time After Discharge

3 wk
35.0

5.5 mo

6 mo

6.5 mo

7.5 mo

32.5

32.5

31.5

30.7

4y
30.7

Laboratory dataa
Glucose (65-110 mg/dL)b

169

148

115

122

100

119

89

Sodium (136-144 mEq/L)

138

137

138

144

140

140

141

Potassium (3.6-5.1 mEq/L)

3.3

4.4

4.2

4.2

4.2

3.8

4.2

Chloride (101-111 mEq/L)

95

103

105

102

103

105

105

Bicarbonate (22-32 mEq/L)

35

26

26

29

33

30

29

Blood urea nitrogen (7-19 mg/dL)c

22

37

28

22

26

22

21

Creatinine (0.50-1.5 mg/dL)

1.0

0.8

1.0

1.3

1.2

1.0

0.96

7.7

9.3

8.9

9.5

9.2

8.7

9.5

Phosphorus (2.4-4.7 mg/dL)

3.8

3.9

4.0

3.8

4.2

3.6

3.5

Magnesium (1.8-2.5 mg/dL)g

1.9

2.2

2.2

2.1

2.2

2.2

2.3

Total protein (g/dL)h

6.0

7.8

7.9

7.6

6.7

7.6

2.9

3.3

4.5

4.0

3.9

4.0

1.6

0.95

0.9

1.29

0.97

0.8

Calcium (8.6-10.6 mg/dL)e

Albumin (g/dL)

Total bilirubin (0-1.3 mg/dL)j

Alkaline phosphatase (38-126 IU/L)

239

204

320

24-h urine volume (mL)k

Measured energy expenditure (kcal/d)
Respiratory quotient

217
400

850

163

95

1,794
0.69

Medications
Warfarin (mg)
Proton pump inhibitor (mg/d)
Deoderized tincture of opium (mL/day)

40

40

40

40

40

40

30

1.2

4
l

1l

Oral multivitamin

Vitamin D-3 (IU/d)

1,000

Calcium carbonate (mg/d)

500

Oral rehydration solution (L/d)

Parenteral nutrition volume (L/d)

Parenteral nutrition energy (kcal/d)
Parenteral nutrition amino acids (g/d)

1.5

1.5

490

490

490

80

60

60

2.4

410

60m

410

60m

2.4
410

60m

2.4m
170m
0

Ranges shown in parentheses are reference ranges.

To convert mg/dL glucose to mmol/L multiply, mg/dL by 0.0555. To convert mmol/L glucose to mg/dL, multiply mmol/L by 18.01. Glucose of 65 mg/dL3.61 mmol/L.
c
To convert mg/dL blood urea nitrogen to mmol/L, multiply mg/dL by 0.357. To convert mmol/L blood urea nitrogen to mg/dL, multiply mmol/L by 2.80. Blood urea nitrogen of 7 mg/
dL2.50 mmol/L.
d
To convert mg/dL creatinine to mmol/L, multiply mg/dL by 88.4. To convert mmol/L creatinine to mg/dL, multiply mmol/L by 0.01. Creatinine of 0.5 mg/dL44.2 mmol/L.
e
To convert mg/dL calcium to mmol/L, multiply mg/dL by 0.25. To convert mmol/L calcium to mg/dL, multiply mmol/L by 4. Calcium of 8.6 mg/dL2.15 mmol/L.
f
To convert mg/dL phosphorous to mmol/L, multiply mg/dL by 0.323. To convert mmol/L phosphorous to mg/dL, multiply mmol/L by 3.09. Phosphorous of 2.4 mg/dL0.78 mmol/L.
g
To convert mg/dL magnesium to mmol/L multiply mg/dL by 0.411. To convert mmol/L magnesium to mg/dL, multiply mmol/L by 2.43. Magnesium of 1.8 mg/dL.74 mmol/L.
h
To convert g/dL total protein to g/L multiply g/dL by 10. To convert g/L total protein to g/dL, multiply g/L by 0.1. Total protein of 6.0 g/dL60 g/L.
i
To convert g/dL albumin to g/L multiply g/dL by 10. To convert g/L albumin to g/dL, multiply g/L by 0.1. Albumin of 2.9 g/dL29 g/L.
j
To convert mg/dL total bilirubin to mmol/L multiply mg/dL by 17.1. To convert mmol/L total bilirubin to mg/dL, multiply mmol/L by .058. Total bilirubin of 1.6 mg/dL27.37 mmol/L.
k
24-h urine volume collected on a day without parenteral nutrition infusion.
l
Off parenteral nutrition day.
m
Every other day.
b

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September 2013 Volume 113 Number 9

RESEARCH
Checklist item

Acute care setting

Home care setting

Diet education

Educate and reinforce as diet is advanced

in the hospital

Reinforce and adjust diet as bowel adapts

Laboratory data

Daily chemistry panel including magnesium

and blood count
Twice weekly liver function tests
Baseline vitamin and trace mineral
levels (A, E, Db, folate, B-12, iron, zinc,
copper, and selenium) before discharge

Weekly comprehensive metabolic panel,

including magnesium until stable, then monthly
Annually vitamin and trace mineral levels

Weights and I/Oc

data

Daily weight
Daily I/O data

Weekly weight
Once weekly I/O data until stable, then monthly
(more frequently if change in medical
management or status)

Medications

Antimotility agent
PPId or H2 blockere
Multivitamin and mineral supplements

Antimotility agent
PPI or H2 blocker
Multivitamin and mineral supplements
Possibly pancreatic enzyme replacement or bile
acid sequestrant

Nutrition support

If on enteral nutrition, then know the

type of tube and enteral formula
If parenteral nutrition know the type of
catheter, the position of the catheter
tip, and the formula
Note any additional intravenous uids

Talk to the patient and/or caregiver

Communicate with the home care company any
changes in enteral or parenteral formulas
Obtain report from home nurse

Monitoring frequency

Daily

Weekly until stable, then reduce frequency

as appropriate

Other

Know the exact post-operative intestinal

anatomy
Communicate long-term plan with the
primary care physician prior to discharge

Monitor for bowel adaptation and make

alterations in MNTf as possible
Screen for bone disease and anemia

Based on references 46 and 59.

25-hydroxy vitamin D.
c
I/Ointake and output. Includes oral, enteral, and parenteral intake plus urine, stool, and drain output.
d
PPIproton pump inhibitor.
e
H2histamine 2 antagonist.
f
MNTmedical nutrition therapy.
b

Figure 2. Checklist for registered dietitian management of patients with short bowel syndrome.a
antimotility and acid-blocking medications.46 In addition,
the patient should be aware that the dosage of the medications may change once he or she is home and eating
more food. Emphasis should be placed on proper eating
techniques; for example, eating slowly, resting after eating,
minimal uid intake with the meal, and sipping of uids
between meals.47 If an ORS is required, recipes to prepare
the solution or information on where to purchase ORS
must be given to the patient. The RD may have to reinforce
this information repeatedly before and after discharge.
Adults in particular have difculty changing their eating
habits and may nd it challenging to adhere to the new
guidelines until they begin to see reduction in stool output
and improved overall sense of well-being. Also, the patient
September 2013 Volume 113 Number 9

must have prescriptions for antisecretory therapy (either

PPI or H2 blocker) and vitamin and mineral supplements, if
needed. For those discharged on PN, the patient and family
require education on catheter care and aseptic technique
for infusion therapy before discharge.48,49 Patient monitoring of oral intake, stool and urine output, as well as
weight in the early period after hospital discharge will
facilitate decisions regarding medication adjustments and
possibly weaning of EN or PN support. The patient and
family may require education on proper techniques for
measuring body uid output at home.48 Nursing support in
the home can help to reinforce the concepts of SBS management and provide RDs essential insight to the home
environment.
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RESEARCH
After hospital discharge, patients with SBS are best served
by frequent follow-up appointments with all members of the
nutrition support team, in particular the managing physician
and RD. The primary goals of these appointments are to
assess adherence to the prescribed therapies; monitor uid,
electrolyte, hydration, and nutritional status; reinforce the
principles of nutrition therapy; and adjust the therapies as
necessary.50 Periodic weights and blood chemistry levels
(including liver function tests) will help to determine the
extent of bowel adaptation, liver-related complications of PN,
and the possibility of weaning from EN or PN.48 If a patient
develops PN-related liver disease, the workup should assess
for small bowel bacterial overgrowth, blood infection, and reevaluate IV fat emulsion deliveryall of which can alter liver
function.51 Treatment may include a reduction in the amount
and frequency of IV fat emulsion infusions (<1 g/kg/day as
infrequently as once a week) with periodic monitoring for
essential fatty acid deciency.52
Baseline vitamin (eg, folate; B-12; and vitamins A, D, E);
mineral (eg, iron, calcium, and magnesium); and trace mineral
(eg, zinc, copper, and selenium and chromium and manganese
for PN patients) levels and dual-energy x-ray absorptiometry
scan are required for comparison purposes in long-term follow
up.53 The standard parenteral multivitamin and trace mineral
additives may not meet a patients exact requirements and can
cause deciency or toxicity states over time.54 For example,
daily trace mineral infusions of 0.3 mg manganese over time can
lead to deposits in the brain,55 and chronic standard multivitamin dosing of 200 IU vitamin D can cause insufciency or
deciency states.56 Further complicating the issue of monitoring micronutrient levels of patients dependent on PN are the
ongoing product shortages. These shortages have led to omission or rationing of certain nutrients that can cause lifethreatening deciency states.50,57,58 These levels should be
checked no less than every 6 to 12 months, or more frequently if
abnormal levels are identied.58,59 With time, as a patient stabilizes and thrives at home, the length of time between clinic
visits can be extended. For patients with stable, chronic SBS the
minimum follow-up should occur every 6 to 12 months. As with
the patient prole provided, bowel adaptation can occur slowly.
It can take more than 2 years before adaptation has fully
occurred to change the treatment plan and wean articial
nutrition support.11

CONCLUSIONS
Management of SBS is complex and requires a concert of
medical, nutrition, and pharmaceutical therapies to optimize
uid and nutrient absorption for survival. Each patients
unique care plan depends on the amount and site of
remaining intestine and the patients ability to adhere to the
medical and nutrition therapies. Some patients will be able to
survive with antisecretory and anti-motility agents along
with strict diet adherence alone, whereas other patients will
require lifelong infusion therapy. In either case, patients with
SBS must have close follow-up with a specialized medical
team to monitor for nutrient deciencies and potential
complications of SBS. The most common long-term complications include metabolic bone disease, PN-related liver disease, nephrolithiasis, anemia, central line infection, central
access problems (thrombosis and superior vena cava syndrome due to vein stenosis), and vitamin and trace mineral
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JOURNAL OF THE ACADEMY OF NUTRITION AND DIETETICS

deciencies.6,27,38 Patients with SBS are medically complex

and require long-term monitoring and revisions of the care
plan. The substantial benet of medical nutrition therapy is
what makes these patients both challenging and extremely
rewarding for RDs to manage.

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AUTHOR INFORMATION
E. A. Wall is a nutrition support dietitian, The University of Chicago Medicine, Chicago, IL.
Address correspondence to: Elizabeth A. Wall, MS, RD, LDN, The University of Chicago Medicine, 5841 S. Maryland Ave, MC 4080, Chicago,
IL 60637. E-mail: elizabeth.wall@uchospitals.edu

STATEMENT OF POTENTIAL CONFLICT OF INTEREST

No potential conict of interest was reported by the author.

ACKNOWLEDGEMENTS
The author thanks Patricia Sheean, PhD, RD, for the invitation to write this article and for her guidance with respect to the content. The author
also thanks Carol E. Semrad, MD, for her expert review of this articles content as well as Linda Trumbore, MS, RD, and Scott Lozano, PharmD, for
providing editorial assistance.

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September 2013 Volume 113 Number 9