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Nutrition Management of Infants With Surgical Short Bowel Syndrome and Intestinal Failure
Conrad R. Cole and Samuel A. Kocoshis
Nutr Clin Pract published online 12 June 2013
DOI: 10.1177/0884533613491787

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491787
research-article2013
NCPXXX10.1177/0884533613491787Nutrition in Clinical PracticeCole and Kocoshis

Invited Review
Nutrition in Clinical Practice
Volume XX Number X
Nutrition Management of Infants With Surgical Short Month 2013 1­–8
© 2013 American Society
Bowel Syndrome and Intestinal Failure for Parenteral and Enteral Nutrition
DOI: 10.1177/0884533613491787
ncp.sagepub.com
hosted at
online.sagepub.com
Conrad R. Cole, MD, MPH, MSc1, and Samuel A. Kocoshis, MD1

Abstract
Appropriate nutrition recommendations are important for the successful management of the infant with an injured gastrointestinal tract
postsurgery who is at risk for intestinal failure. Management strategies that can be used to augment successful adaptation and prevent
liver disease are summarized in this review. These include appropriate postoperative fluid and electrolyte management, modification of
parenteral nutrition to minimize intestinal failure–associated liver disease, early and aggressive enteral feeding advancement, the use of
hormonal and trophic agents, prevention of central line–associated bloodstream infections using ethanol lock, appropriate treatment, and
prevention of pathologic small bowel bacterial overgrowth. (Nutr Clin Pract. XXXX;xx:xx-xx)

Keywords
Pediatrics; nutrition; enteral nutrition; parenteral nutrition; gastroenterology; short bowel syndrome

Nutrition therapy following significant gut injury from surgery
or as a result of a congenital disorder or dysmotility is usually
complex and requires close attention to detail. The ultimate
goal of management is enteral autonomy. Depending on the
type of injury, recovery and adaptation of the gut can be fast
(over a couple of days) or quite prolonged (years).1 If the
patient is dependent on parenteral nutrition (PN) for >4 weeks,
that patient’s intestinal dysfunction is operationally defined as
intestinal failure.2 The goal of this review is to provide an
update on the acute and long-term nutrition management of the
infant with significant surgical resection of the intestines who
is at risk for intestinal failure.
In infants, intestinal failure is usually a complication arising
from significant injury to the gastrointestinal (GI) tract. The
resultant functional intestinal mass may fall below the mini-
mum required to maintain adequate nutrition and fluid balance
needed for normal growth and development.3,4 The duration of
PN and the need for intestinal rehabilitation make the manage-
ment of these children challenging. The outcome of these chil-
dren is significantly improved if they are managed by a
multidisciplinary team that allows for fully integrated care of
inpatients and outpatients with intestinal failure by fostering
coordination of surgical, medical, and nutrition management.5
Necrotizing enterocolitis (NEC) is still the most common
indication for surgery that leads to short bowel syndrome
(SBS) and subsequently intestinal failure.6,7 Gastroschisis
and its accompanying motility disorder are now identified
as the second most common cause of intestinal failure.7,8
Although infants with gastroschisis might not have under-
gone bowel resection, they can develop some degree of
intolerance to enteral nutrition (EN) and so are dependent
on PN for a variable time after repair or closure of the
abdominal wall defect. Absolute remnant intestinal length
following resection is not the best predictor of weaning
from PN despite early reports suggesting otherwise.9 The
quality of the remnant bowel is now considered significant,
as is the use of proven strategies to augment adaptation and
prevent complications associated with prolonged PN. The
healthcare costs for infants with intestinal failure are very
high and estimated to average $505,000 in the first year and
about $300,000 in subsequent years.10 The difference in cost
between the first year and subsequent years is attributed to
the length of initial hospitalization and frequent repeat
hospitalizations.
The factors that determine how well an infant does after the
initial surgery include (1) age at the time of the surgery, (2) site
and amount of bowel resected, (3) function (absorption and
motility) of the remnant bowel, (4) adaptive capacity of the
remnant bowel, (5) injury to the bowel (due to infections, bac-
terial overgrowth, ischemia, stricture), and (6) whether compli-
cations associated with chronic PN (liver disease, recurrent
line infections, and loss of vascular access) occur.
From 1Division of Gastroenterology, Hepatology and Nutrition,
Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio.
Financial disclosures: Conrad R. Cole is supported by National Institutes
of Health grant 1R21DK088027-01A1.
Corresponding Author:
Conrad R. Cole, MD, MPH, MSc, Division of Gastroenterology,
Hepatology and Nutrition, Cincinnati Children’s Hospital Medical
Center, 3333 Burnet Ave, MLC 2010, Cincinnati, OH 45229, USA.
Email: conrad.cole@cchmc.org.

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2 Nutrition in Clinical Practice XX(X)
Initial Phase of Management
In the immediate postoperative phase, fluid and electrolyte
management as well as nutrition care is dependent on the use
of PN. Postoperatively, there is usually ileus, which can last
from 48 hours to up to a week depending on the degree of
injury and the primary disease. This period can be associated
with high gastric output followed by increased jejunostomy/
ileostomy output or profuse diarrhea. During this phase, if the
fluid and electrolyte resuscitation is not appropriately man-
aged, the patient can become dehydrated and experience elec-
trolyte abnormalities. Fluid resuscitation involves the use of
maintenance volumes based on the weight of the patient and
fluid replacement based on fluid losses. Fluid replacement is
usually 1 mL for every mL of fluid loss initially. Replacement
fluid is determined by the volume lost from ostomies, fistulas,
or drainage tubes (gastric, jejunum, ileum, or colon).
Transient gastric acid hypersecretion and hypergastrinemia
have been reported in these patients in response to the injury
and resection.11 This is more significant in patients with more
than two-thirds of their estimated bowel resected. These
patients should be managed in the immediate postoperative
period with intravenous (IV) proton pump inhibitors or H2
blockers.12 Gastric acid hypersecretion leads to further malab-
sorption because the acidic environment inactivates pancreatic
enzymes and precipitates bile acid. This further damages the
epithelium of the proximal small bowel and stimulates motil-
ity. The use of acid-reducing medication should be temporally
around the postoperative period and in the immediate period
around starting enteral feeds as the hypergastrinemia is tran-
sient. However, this therapy can be continued in patients with
significant gastroesophageal reflux.
Modification of PN
Patients receiving prolonged PN due to intestinal failure are at
increased risk for developing PN-associated cholestasis
(PNAC). This is defined as a direct bilirubin level >2 mg/dL
along with elevated transaminases and γ-glutamyl transferase
after at least 2 weeks of PN in an infant who does not have a
primary liver disease.13 The specific cause of PNAC is
unknown, but most researchers and clinicians hypothesize that
PNAC is as a result of a combination of factors, including the
composition of the PN, central line–associated bloodstream
infections (CLA-BSIs), and lack of enteral feeds. In patients
with surgical SBS and other forms of intestinal failure, PNAC
is referred to as intestinal failure–associated liver disease
(IFALD).
Although excesses in any of the macronutrients (glucose,
protein, and lipid) have been found noxious to the liver, the
single parenteral nutrient most closely associated with cho-
lestasis and subsequent end-stage liver disease is lipid. The
type and amount of lipid administered in patients with intesti-
nal failure have been identified as factors associated with
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severe IFALD.14,15 Patients who received soy-based lipid infu-
sions >1 g/kg body weight for long periods are at increased risk
for developing IFALD.14,16 Published reports of the use of a
fish oil–based investigational lipid emulsion to treat IFALD
have lent credence to this theory. Confounding these findings
is the fact that with the use of fish oil–based lipids, the investi-
gators also markedly decreased lipids to 1 g/kg/d compared
with the 3-g/kg/d dose of soy-based lipid emulsion in the con-
trol historic group of patients.15,17 This has led to the use of a
lipid minimization strategy among intestinal rehabilitation pro-
grams in North America. One center has shown in a prospec-
tive study that lipid minimization with 1 g/kg/d twice a week is
associated with decreased PNAC and reversal of cholestasis.18
Although in this study, essential fatty acid deficiency was doc-
umented, there was no difference in the growths (weights and
lengths) between the patients who had lipid minimization com-
pared with the control group. To prevent essential fatty acid
deficiency, patients should receive an average of >0.5 g/kg/d of
lipid, and serum evaluation of essential fatty acids should be
done periodically. Our practice is to limit the lipid dose to 1 g/
kg/d in infants likely to develop IFALD and those with PNAC
who are going to continue receiving long-term PN.
The attention regarding the potential impact of the type of
lipid was stimulated by the investigational use of fish oil–based
lipid solutions in North America.15,17 The constituents of the
major IV lipid infusions are summarized in Table 1. These dif-
ferences might account for the different rates of developing
liver disease in patients receiving long-term PN. Fish oil–based
lipid solutions are available only at specific institutions in
North America under an investigational new drug evaluation
with approval from institutional review boards and are
restricted to children with IFALD. These products have being
approved for use in Europe. There is a need to evaluate the
safety and long-term effects of lipid minimization and use of
lipid alternatives on patients with regard to long-term growth,
neurodevelopment, and hepatic fibrosis.
With the use of lipid minimization, excessive glucose infu-
sions rates (GIRs) are being used in these children, which can
lead to hepatic steatosis. The American Society for Parenteral
and Enteral Nutrition (A.S.P.E.N.); the European Society for
Pediatric Gastroenterology, Hepatology, and Nutrition; and the
American Academy of Pediatrics guidelines for infants and
young children recommend limiting the GIR at 12–14 mg/kg/
min.19,20 It is important that these guidelines are followed if at
all possible. However, it may be impossible to stay within
these guidelines for GIRs to account for calories lost from lipid
minimization. Patients needing higher GIRs should be moni-
tored for hyperglycemia and liver disease periodically.
Enteral Nutrition
The most important strategy for stimulating intestinal rehabili-
tation is EN. In neonates, continuous enteral tube feeding,
beginning with breast milk or an amino acid–based formula,
Cole and Kocoshis 3

Table 1.  Comparison of the Constituents of Major IV Fat Emulsions.

Soy-, MCT-, Olive Oil–, Fish

Fatty Acid Soy-Based IV Fat Emulsiona Fish Oil–Based IV Fat Emulsionb Oil–Based IV Fat Emulsionc
α-Tocopherol, mg/L 38 150–296 200
Phytosterols, mg/L 348 0 47.6
Linoleic, g/100 mL 5 0.1–0.7 2.9
α-Linolenic, g/100 mL 0.9 <0.2 0.3
EPA, g/100 mL 0 1.28–2.82 0.3
DHA, g/100 mL 0 1.44–3.09 0.05
Oleic, g/100 mL 2.6 0.6–1.3 2.8
Palmitic, g/100 mL 1 0.25–1 0.9
Stearic, g/100 mL 0.35 0.05–0.2 0.3
Arachidonic, g/100 mL 0 0.1–0.4 0.05

DHA, docosahexaenoic acid; EPA, eicosapentaenoic acid; IV, intravenous; MCT, medium-chain triglyceride.
a
Intralipid (Baxter Healthcare Corporation, Deerfield, IL).
b
Omegaven (Fresenius Kabi, Bad Homburg, Germany).
c
SMOF lipid (Fresenius Kabi).

should be added as soon as postoperative ileus resolves.21,22
When breast milk is not available, one of the amino acid for-
mulas should be used as they have been shown to be effective
in decreasing the duration of PN.21,23 Although long-chain tri-
glycerides (LCTs) are a major trophic factor for intestinal
adaptation in SBS, they are not well absorbed in the small
intestines and require micelle formation.13,24 A combination of
medium-chain triglycerides (MCTs) and LCTs (ratio of MCTs
to LCTs of 30%:70%) has been shown to be the optimal com-
bination of fat source for absorption in patients with significant
intestinal resection, with or without colon in continuity.25
Feeds should be gradually increased in volume and supple-
mented by small oral meals. Continuous enteral feeds are bet-
ter tolerated compared with intermittent bolus feeds.26 This
permits the continuous saturation of carrier proteins.27,28 As the
volume of enteral feeds is increased, PN should be decreased
isocalorically (calorie for calorie, not volume for volume).
Enteral feeding is important for protecting against cholestatic
liver disease.29
Bolus oral feedings in small quantities, 3–4 times a day
(equal or less than the volume tolerated continuously per hour),
and the timely introduction of solid feeds at the same develop-
mental age as healthy infants will allow the child to swallow
and chew appropriately. Feeding therapy is usually required as
these infants are likely to have some degree of oral aversion
due to delayed introduction of oral feeds as a result of prema-
turity, prolonged intubation, and cardiovascular instability.
These patients tend to have a relative lactase deficiency and
tolerate complex carbohydrates rather than simple sugars.
Advancement of enteral feeds is based on several factors,
including stool output, vomiting, and irritability. An increase in
stool output that is >50% is usually a contraindication to
increasing enteral feeds. If stool output is between 30 and 40
mL/kg body weight, then the increase should be accomplished
cautiously. An output >40 mL/kg body weight is a relative
contraindication to increasing enteral feeds.30 Patients without
a colon tolerate diets that are high in fat (30%–40% of caloric
intake) better, whereas those with intact colons experience ste-
atorrhea, magnesium, and calcium loss with high-fat intake.
With calcium loss, oxalate absorption is enhanced in the colon
and kidneys, which can lead to the formation of oxalate renal
stones.31,32 Hence, it is necessary to restrict oxalate intake in
SBS patients with a colon to decrease the risk of oxalate renal
stones. Oral calcium supplements can also reduce the forma-
tion of oxalate stones.
Cycling of PN is the next step as enteral feeds are tolerated.
When EN constitutes 20% or more of total nutrition intake, the
duration of PN should be reduced if the child’s serum glucose
level can be adequately maintained by continuous enteral infu-
sion.33 As soon as sufficient stability is reached, the child
should be discharged home under continued outpatient care
with a team experienced in intestinal rehabilitation.
The main long-term problems comprise bacterial over-
growth, fluid and electrolyte abnormalities, nutrition deficien-
cies, PN-related liver disease, and central venous line
complications such as sepsis and thrombosis.34 Aggressive
laboratory monitoring of patients while they receive PN and
during the transition to full EN, as shown in Table 2, is required
to prevent nutrition deficiencies and electrolyte disturbances.
After successfully weaning off PN, these patients need to con-
tinue to have frequent laboratory monitoring to prevent the
development of essential micronutrient deficiencies.
Hormonal and Trophic Agents
Growth hormone (GH) administration studies in animal mod-
els showed enhanced mucosal hyperplasia and increased water,
sodium, and amino acid absorption.35-37 Pediatric and adult
studies initially produced contradictory results regarding the
impact of GH on tolerance of EN.35,38-40 In a double-blind

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4 Nutrition in Clinical Practice XX(X)

Table 2.  Laboratory Monitoring for Patients Receiving Parenteral Nutrition (PN).

With Every Weekly Until

Laboratory Test Initial Change in PN Stable Long Term/Home Indications Chargea

PN profile (renal, calcium, Yes Yes Yes, then per MD Per MD discretion $$$
phosphate, magnesium, liver discretion
panel, total protein, serum
albumin, triglyceride, bile
acid, prealbumin, random
glucose)
Complete blood count with Yes Yes Yes, then per MD Monthly/as indicated Monitor anemia $
differential discretion
Urine electrolytes Yes Weekly until Monthly Dehydration, poor weight/ $$
stable length gain
Urine-specific gravity Yes Weekly until As indicated Dehydration; after $
stable, then at decrease in intravenous
MD discretion volume administered;
input/output not
monitored
Prothrombin time/international If indicated, first level Liver disease/cholestasis/ $
normalized ratio should occur after 1 mo gastrointestinal bleed
on PN and then every
2–4 wk
25-OH vitamin D First level should occur Patient with low serum $$
after 3 mo on PN and 25-OH levels on therapy
then every 6 mo
If indicated, every 3 mo
Red blood cell folate Every 6 mo $
Iron/total iron-binding capacity/ Every 3 mo Anemia with microcytosis $$
ferritin If indicated, every 1 mo and patient on enteral or
parenteral iron
Ceruloplasmin and copper If indicated, after 30 days Cholestasis, persistent $
of PN, then every 2 mo anemia
Zinc and selenium If indicated, first level Patients with chronic $
should occur after 6 mo diarrhea, high ostomy
on PN or if high ostomy output
output, after 30 days,
and then every 3–6 mo
Vitamins A, E, and K First level should occur Cholestasis $$
after 6 mo on PN and
then every 6 mo
α-Fetoprotein Every 12 mo Liver cirrhosis or chronic $
liver disease
Chromium If indicated Glycemic control difficult $
despite glucose
infusions rate <15
Triene/tetraene ratio If indicated Total fat intake (enteral $$
and parenteral fat) <0.5
g/kg for <5 d
D-lactate If indicated Encephalopathy or anion- $$
gap metabolic acidosis
Manganese If indicated, every 3 mo Patient is cholestatic $
Urine methylmalonic acid If indicated, first level at a Ileal resection, macrocytic $$
year, then every 12 mo anemia
Serum B12 If indicated, first level at a Ileal resection, macrocytic $$
year, then every 12 mo anemia
a
$, <$100; $$, $100–200; $$$, >$200. Based on current charges.

randomized controlled trial involving 41 adult patients with with standard therapy.41 The benefits associated with this ther-
SBS, GH (0.1 mg/kg/d for 4 weeks) reduced PN volume by apy lasted almost 4 months following completion of the ther-
approximately 2 L/wk in addition to the reduction achieved apy. Increase in body weight, lean body mass, and fat-free

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Cole and Kocoshis 5
mass was also documented using a lower dose of GH (0.5 IU/
kg/d or 0.024 mg/kg/d).42 Based on these data, GH therapy is
approved by the U.S. Food and Drug Administration (FDA) for
the treatment of PN-dependent SBS only in adult patients.
Glucagon-like peptide 2 (GLP-2) is produced by the intesti-
nal mucosal L cells in the ileum and proximal colon and
pancreatic A cells. Postprandial serum GLP-2 is decreased in
patients with extensive small bowel resection,43 and the
level best correlates with residual small intestinal length.44
Exogenous GLP-2 has a significant trophic effect on the intes-
tine and appears to stimulate enterocyte proliferation while
reducing rates of enterocyte apoptosis.45 GLP-2 appears to act
via the highly localized expression of GLP-2 receptor in the
intestinal epithelium.46 Teduglutide, a novel recombinant ana-
logue of the human GLP-2, differs from GLP-2 in the substitu-
tion of alanine by glycine at the second position at the
N-terminus. The single amino acid substitution relative to nat-
urally occurring GLP-2 results in resistance to in vivo degrada-
tion by the enzyme dipeptidyl peptidase-IV (DPP-IV). Adult
trials have shown decreased PN dependence in adults with
SBS.47,48 There is currently no pediatric study evaluating the
effectiveness and safety of long-term use of GLP-2/teduglu-
tide. Teduglutide is the most recently approved drug for use in
adults with intestinal failure due to SBS.
Glutamine, a nonessential amino acid that is a primary
energy source for the enterocyte, has been shown in animals
and adults to prevent mucosal atrophy and deterioration in gut
permeability in patients receiving PN. Glutamine administra-
tion improves the growth and function of human gut epithe-
lial cells.49,50 PN-dependent individuals, when administered
glycyl-glutamine–supplemented PN, demonstrated signifi-
cantly increased duodenal villous height and decreased intesti-
nal permeability compared with individuals with standard
nonsupplemented PN.49 In a large multicenter prospective
study, addition of glutamine to the PN of extremely low birth
weight neonates (birth weight <1000 g) did not decrease sepsis
or shorten the duration of PN use. Parenteral glutamine had no
effect on the tolerance of enteral feeds, recurrence of NEC, or
growth in these infants.51 In adults, using a combination of
enteral glutamine (0.6 g/kg/d), subcutaneously administered
human growth hormone, and a high-fiber (apple pectin), low-
fat diet (20% fat, 20% protein, and 60% carbohydrate sources)
led to improvement of intestinal absorptive capacity and wean-
ing or reducing the need for PN.52 An ongoing, multicenter
phase 3 trial to evaluate the safety and efficacy of enteral glu-
tamine in infants with SBS is currently in progress insofar as
glutamine is currently not approved for use in pediatrics.
Soluble fiber slows gastric emptying and decreases overall
gut transit, resulting in a mild antidiarrheal effect. In the colon,
soluble fiber is fermented by bacteria, yielding short-chain
fatty acids (butyrate, propionate, and acetate), which serve as
an energy source for the colonocytes.53 Short-chain fructo-
oligosaccharides are the preferred fiber source as they undergo
rapid hydrolysis, which is advantageous in patients with
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Table 3.  Recommended Strategies for Preventing Recurrent
Central Line–Associated Bloodstream Infections.
Chlorhexidine skin prep and chlorhexidine-impregnated dressing
Heparin and antibiotic-impregnated central venous catheters
Ethanol and antibiotic lock therapy
Chlorhexidine-heparin central venous catheter cap
Strategic education tools
Event analysis
surgical SBS. Short-chain fatty acids also stimulate sodium and
water absorption in the colon, thereby decreasing fluid loss.54-56
Soluble fiber added to the diet of patients with an intact colon
has a significant impact on enteral tolerance.56 This is indicated
when feeding advancement is impeded by increased stool loss.
Prevention of CLA-BSIs
Central line care is an important component of the nutrition
management of children who require central venous access for
long-term PN. This becomes critical if the child is going to
need home PN. The educational process of the primary care-
givers needs to start as soon as home PN is identified as a pos-
sibility. Patient care educators need to evaluate the caregivers
with regard to the type of teaching technique that will be used
to educate them about caring for the catheter to prevent recur-
rent CLA-BSIs. The rate of CLA-BSIs reported in this popula-
tion from a multicenter consortium was 8.9 per 1000 catheter
days.7 The rates of home-acquired CLA-BSIs are highest dur-
ing the first month of home PN and decrease as the caregivers
become more knowledgeable and confident with the tech-
niques of appropriately taking care of the line at home.57 The
risk for CLA-BSIs was higher in patients from a lower socio-
economic group and if the child was younger than 1 year on
discharge.57
The American Pediatric Surgical Association recommends
specific strategies outlined in Table 3 for preventing recurrent
CLA-BSIs.58 These strategies need to be initiated prior to the
insertion of the central line and continued as long as the patient
has a central venous catheter. As reviewed by the American
Pediatric Surgical Association, the use of antimicrobial/antibi-
otic impregnated catheters has become standard in most insti-
tutions when long-term access is required in children.58
Antibiotic and ethanol locks may be recommended in patients
with recurrent CLA-BSIs. The use of ethanol lock therapy for
preventing CLA-BSIs has been shown to be very effective if
used appropriately.59,60 It is recommended that ethanol lock
therapy should be used only with silicone-based catheters as
there is evidence suggesting that polyurethane-based catheters
are susceptible to breakdown when exposed to ethanol.61 A
meta-analysis of 4 small studies has shown that in comparison
to heparin locks, ethanol locks reduced CLA-BSIs by 81% and
decreased the need to replace lines by 72%.62 Thus, the use of
ethanol locks is indicated in children with intestinal failure
6 Nutrition in Clinical Practice XX(X)
with a silicone-based catheter who have a previous history of
CLA-BSIs and have caregivers who are capable of performing
the required care. Antibiotic locks are used less frequently in
children compared with adult patients, and more data are
needed regarding the type and indication for the use of specific
antibiotics as lock therapy in children.
Bacterial Overgrowth
Small bowel bacterial overgrowth is a relatively common
problem in patients with surgical SBS.63 Many patients toler-
ate bacterial overgrowth quite well, and indeed, in some, the
anaerobic flora overgrowing the small bowel live in symbiosis
with the host, producing short-chain fatty acids that have a
caloric value and improve colonic integrity. Furthermore, they
acidify the colonic contents, thereby inhibiting the putrefac-
tive gram-negative aerobes, which are prone to translocate
across the damaged intestinal lining to produce bloodstream
infections.
However, at times, excessive quantities of small bowel bac-
teria can produce deleterious consequences. In such a case, the
patient has small bowel bacterial overgrowth syndrome. The
symptoms suggestive of bacterial overgrowth syndrome
include feeding intolerance, abdominal distention, gassiness,
diarrhea or increased ostomy output, early satiety, or impaired
mental status from D-lactic acidosis. The diagnosis is usually
made based on symptoms, although occasionally breath hydro-
gen studies or small bowel aspirates can be obtained to confirm
the role of excessive small bowel bacteria in this syn-
drome.13,63-65 Preventing and treating bacterial overgrowth in
these postsurgical patients with injured gut is important for
promoting mucosal health and feeding tolerance. Metronidazole
is the most popular agent for eradicating anaerobes. This can
be used in the context of D-lactic acidosis, whose pathogenesis
depends on anaerobic synthesis of D-lactate. It can also be
used when the clinician suspects excessive bile salt deconjuga-
tion resulting in steatorrhea due to failure of bile acids to
achieve a critical micellar concentration in the proximal small
bowel. Nitazoxanide and rifaximin also cover obligate anaer-
obes quite effectively.66,67 Putrefactive, gram-negative aerobes
may be treated with trimethoprim-sulfamethoxazole, amino-
glycosides (such as gentamicin) given orally, and extended-
spectrum penicillins and cephalosporins. Intermittent
monitoring of serum gentamicin levels to avoid ototoxicity and
nephrotoxicity may be necessary.68 The use of antibiotics
effective against gram-negative flora is especially useful in
patients with recurrent gram-negative infections presumably
due to translocation of bacteria across the gut. Amoxicillin–
clavulanic acid was effective against more than 90% of the iso-
lated species in bacterial overgrowth.69 There are no large-scale
clinical trials evaluating the timing and effectiveness of the
antibiotics used in this condition. Experts recommend cycling
specific antibiotics or antibiotic combinations for 1–2 weeks
every month in patients with suspected bacterial overgrowth.64
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The improvement in symptoms following therapy is then retro-
spectively used as evidence for the diagnosis.
Conclusion
Nutrition management of the infant or young child with sig-
nificant injury to the GI tract that requires resection and long
term use of PN is complex. Each patient is unique, and man-
agement should be individualized based on the initial injury,
amount and site of resection, and duration of PN. Early focus
on engaging and educating the primary caregivers is a key pre-
dictor for success. Early, aggressive introduction and advance-
ment of enteral feeds are critical for promoting intestinal
adaptation, preventing IFALD, and weaning the patient off PN.
There is an urgent need for more clinical trials and the estab-
lishment of benchmarks that will assist care teams in identify-
ing processes of care that can lead to excellent outcomes.
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