You are on page 1of 8

Indian J Pediatr (December 2016) 83(12):14361443

DOI 10.1007/s12098-016-2219-7

REVIEW ARTICLE

Intestinal Failure in Children


Theodoric Wong 1 & Girish Gupte 2

Received: 21 October 2015 / Accepted: 11 August 2016 / Published online: 5 October 2016
# Dr. K C Chaudhuri Foundation 2016

Abstract Children with intestinal failure have had improved


survival, particularly those with extreme short bowel syndrome, over the last 1015 y. This has been attributed to better
understanding of the pathophysiology of intestinal failure, improvement in line care, recognition of the importance of a
team approach as well as the progress of intestinal transplant
as a viable option. Parenteral nutrition remains the cornerstone
for the continual survival of these patients. This review will
cover contemporary approaches to intestinal failure including
post surgical approaches, non-transplant surgery, dietetic and
medication approaches during the adaptation process, considerations for home parenteral nutrition and latest in intestinal
transplantation.
Keywords Intestinal failure . Parenteral nutrition . Growth .
Faltering growth . STEP procedure . Intestinal
transplantation . Total parenteral nutrition

Introduction
The intestine is an organ that has the potential to recover its
function from major insults in the majority of cases. The discovery of this potential has come about due to the advent of
parenteral nutrition (PN). In addition, development in surgical

* Girish Gupte
girish.gupte@bch.nhs.uk
1

Department of Gastroenterology and Nutrition, Birmingham


Childrens Hospital, Birmingham, UK

Liver Unit (Including Small Bowel Transplantation), Department of


Gastroenterology and Nutrition, Birmingham Childrens Hospital,
Steelhouse Lane, Birmingham B4 6NH, UK

techniques and intestinal transplantation has offered patients


with intestinal failure more options in their long-term
management.

Definition and Etiology of Pediatric Intestinal


Failure
Intestinal failure was previously classified in terms of intestinal length (hence, short bowel syndrome) and was thought to
be the most important determinant of intestinal function.
Currently, a functional definition is preferred and is defined
as failure of the gastrointestinal tract to fully support the absorption of fluids, nutrients and electrolytes to sustain life and
growth. This can be acute or chronic.
Acute intestinal failure usually lasts for a short period of
time (weeks) whilst chronic intestinal failure generally lasts
for months to years. Definitions which centre on parenteral
nutrition requirement/duration are also not favoured as the
threshold for using parenteral nutrition as well as the expertise
to promote the weaning of PN is extremely variable. Even so,
some have classified intestinal failure as reversible or irreversible using parenteral nutrition as part of the definition.
Reversible intestinal failure is defined as a temporary dependence on parenteral supplementation for fluids, electrolytes
and/or nutrients for metabolism with the eventual establishment on enteral feeds. Irreversible intestinal failure is where
the intestine has exhausted any potential to regain full function
and there is dependence on long-term parenteral nutrition.
There is currently no consensus on the classification of
pediatric intestinal failure although the consensus statement
from European Society for Parenteral and Enteral Nutrition
(ESPEN) for the definition of adult intestinal failure is used
as a basis (Fig. 1) and places intestinal failure into 3 types [1].

Indian J Pediatr (December 2016) 83(12):14361443


Fig. 1 Classification of intestinal
failure [1]

1437

Type I- Acute, short term and usually self limiting condition


Seen in peri-operative setting after abdominal surgery (ileus) or in association with critical illnesses
such as head injury, pneumonia and acute pancreatitis.
Type II- Prolonged acute condition, often in metabolically unstable patients, requiring complex multidisciplinary care and intravenous supplementation over periods of weeks or months
Uncommon, but seen in intra-abdominal catastrophe, septic, metabolic and complex nutritional
complications. Renal impairment might be present. May involve massive enterectomy and/or resulting
in one or more enterocutaneous fistulae, with or without a proximal stoma. acute on chronic intestinal
failure.
PN for more than 28 d.
Type III- Chronic condition, in metabolically stable patients, requiring intravenous supplementation over
months or years. It may be reversible or irreversible.
Metabolically stable patients usually require long term Home Parenteral Nutrition (HPN). It is a result of
progressive and devastating gastrointestinal or systemic benign diseases often requiring multiple intestinal
resections, congenital digestive diseases or end-stage intra-abdominal or pelvic cancer.

Etiology of Intestinal Failure


Surgical/Congenital Leading to Short Bowel Syndrome (SBS)
&
&
&
&
&
&
&

Malrotation
Volvulus
Necrotising enterocolitis (NEC)
Congenital SBS
Small bowel atresia
Gastroschisis
Long segment Hirschsprungs disease

These conditions are the most likely to require resection of


bowel and hence develop short bowel syndrome. As explained previously, although length is an important aspect of
intestinal absorption but the location of resection and associated factors as such dysmotility may play an important role in
the eventual gastrointestinal independence.
Patients with prematurity also feature prominently in
this group of patients as with modern medicine, newborns
born at 23 wk or above can now survive and these infants
are at risk of developing NEC. NEC can be a devastating
disease and result in extensive bowel necrosis and resection. Although there are many risk factors identified for
the development of NEC, it is often difficult to predict
individual infants disease path [2, 3].

(phenotypic diarrhea and autoimmune enteropathy) to


macroscopic epithelial abnormality (tufting enteropathy)
and epithelial intracellular transport defect (microvillous
inclusion disease). Other enteropathies do not generally
cause intestinal failure to the extent of needing parenteral
nutrition (e.g., abetalipoproteinemia).
Dysmotility and Others
&
&
&

Chronic intestinal pseudo-obstruction (CIPO)


Megacystis-microcolon- hypoperistalsis syndrome
Neuronal intestinal dysplasia

Dysmotility of the gastrointestinal tract can be caused


by a myopathy (smooth muscle), neuropathy (enteric nervous system) or idiopathic. There are a number of disorders that are not well categorised which includes chronic
intestinal pseudo-obstruction, megacystis-microcolonhypoperistalsis syndrome and neuronal intestinal dysplasia [4, 5]. These patients may present with obstructive

Enteropathies
&
&
&
&

Phenotypic diarrhea (trichohepatoenteric syndrome)


(Figs. 2 and 3)
Tufting enteropathy
Microvillus inclusion disease
Autoimmune enteropathy

Enteropathies comprise of a mixed group of conditions


with different etiologies with the common disease end
point being mucosal abnormality. Mucosal abnormalities
can range from villous atrophy and inflammatory infiltrates

Fig. 2 Trichorrhexis nodosa in hair strands in phenotypic diarrhea


patients

1438

Indian J Pediatr (December 2016) 83(12):14361443

Assessment of a Child with Intestinal Failure


Assessment of children with intestinal failure is a continual process. The initial assessment should include information regarding the etiology of the intestinal failure, extent and anatomy of
intestinal loss and co-morbidities (e.g., prematurity, chronic lung
disease). This will serve as a roadmap to tailor specific strategies
for that patient. As there is no single biomarker available, assessment of intestinal function requires the combination of different tools including clinical judgment, stool malabsorption
studies, hematology and biochemistry. Some of the common
symptoms encountered in intestinal failure, their causes, investigations and the management strategies are outlined in Table 1.

Management of a Child with Intestinal Failure


Nutrition Support Teams (NST)
Fig. 3 Typical facies of patient with phenotypic diarrhea with coarse hair

symptoms without radiological evidence of obstruction. In


the case of CIPO, dilated segments of small and/or large
bowel may be seen. These patients usually have intermittent symptoms where parenteral nutrition support may be
required during a pseudo- obstructive episode. Pain may
also be a feature which can be difficult to control.
Table 1

Evidence exists in the literature that supports a multidisciplinary team in managing children with intestinal failure (IF)
whilst in the hospital and supporting families discharged on
home PN [6, 7]. Improved outcomes such as reduced rates of
catheter-related sepsis and lower mortality might be attributed
to more and more units with NST, practicing evidence based
medicine in the area of clinical nutrition. Catheter management and preventing loss of venous access are especially

Common symptoms in children with intestinal failure, their investigations and management

Symptom

Possible causes

Investigations

Possible findings

Possible management

Vomiting

Obstruction

Dilated bowel

Surgery

Vomiting

Bacterial overgrowth

Raised serum D-lactate level

Vomiting

Foregut dysmotility

Plain X-ray
Contrast studies
Serum D-lactate +
blood gas
Contrast studies
Manometry

Diarrhea

Malabsorption

Fecal pH, fat,


reducing substance

-Reduce enteral carbohydrate


-Enteral non-absorbable antibiotics
Domperidone
Erythromycin
Coamoxiclav
Changes to feeds e.g., modular feeds

Diarrhea

Ulceration

Endoscopy

Diarrhea

Stricture

Growth failure

Total body sodium deficit

Plain X-ray
Contrast studies
Urinary sodium

Growth failure

Micronutrient deficiencies

Jaundice

IFALD

Hematochezia

Ulcerations
Allergic colitis
Cobalamin/
Iron deficiency

Tiredness

IFALD Intestinal failure associated liver disease

Serum trace elements/


Vitamin
Fractionated bilirubin
Liver biopsy
Endoscopy
Serum vitamin
B12/ iron/ferritin

Dilated segments of bowel


without obstruction
pH < 5.5
Fat globules
Reducing substance
Erosions
Dilated bowel

Antibiotics
Surgery
Surgery

Urinary Na <20 or < twice


Urinary K
Below normal range

Enteral or parenteral supplementation


Enteral or parenteral supplementation

Erosions
Eosinophils
Low vitamin B12, iron
and ferritin

Reduce overall dose of lipid provision


Use of fish oil containing emulsions
Antibiotics
Elemental feeds
Intramuscular vitamin B12
Parenteral iron

Indian J Pediatr (December 2016) 83(12):14361443

important in cases with prolonged or permanent intestinal failure. This is important as there are limited sites of venous
access for the children on long term parenteral nutrition.
Although the composition of the NST varies but they generally are composed of a medical practitioner (e.g., gastroenterologist with interest in clinical nutrition), nurse practitioner,
dietitian, pharmacist and a social worker/psychologist.

1439

not appear for sometime and so careful review of PN prescriptions is required. Iron deficiency is seen commonly in children
with IF. Many factors contribute to this: frequent blood letting
for blood tests, poor enteral absorption and incompatibility
preventing sufficient provision in PN. Separate parenteral iron
might be required (e.g., iron sucrose) but care must be taken as
frequent use might cause central venous catheters blockage.

Parenteral Nutrition
Intestinal Adaptation
PN is the mainstay therapy for children with intestinal failure.
PN provides fluid and nutrition whilst allowing the intestine
time to recover from surgery and for the adaptive response
(see below). This therapy has become widely available and
increasingly used, but remains a complex and specialised area.
Long-term PN can be associated with life-threatening
complications:
a) Catheter-related sepsis
b) Venous thromboembolism resulting in venous occlusion
c) Intestinal failure associated liver disease (IFALD)
PN should provide balanced combination of macronutrients
(carbohydrate, amino acids and lipids) and micronutrients (vitamins and trace elements). As requirements vary throughout
childhood, regular and detailed review of PN prescriptions to
tailor the PN to individual requirements with the NST is mandatory. This involves close monitoring of biochemical and nutritional parameters. Fluid and electrolyte imbalance is common
in SBS, particularly GI water and salt losses in patients with a
high jejunostomy for example. Assessment of urinary and stool
losses of sodium and potassium can help to guide managing
electrolytes in the prescription. If these are not accounted for in
the PN, then growth is unlikely to be supported, even if sufficient calories are provided e.g., renal conservation of sodium
and/or hydrogen ions may lead to low serum potassium, unresponsive to potassium supplementation.
Intestinal failure associated renal disease is an another complication although very rarely mentioned. Altered calcium,
phosphate and vitamin D metabolism due to changes in renal
tubular function can lead to nephrocalcinosis. Acid and base
metabolism can also be affected and so changes to chloride
and acetate content of the PN may be required.
Specific diagnoses as well as sepsis and post-operative
stress may result in reduced metabolic capacity for lipid oxidation and may be seen as hypertriglyceridemia. In these circumstances, reduction or change in lipid emulsion have been
advocated but care must be taken to avoid essential fatty acid
deficiency when lipid is completely ceased.
Micronutrient deficiency might arise when there are increased losses (e.g., zinc in high ileostomy output) or absence
of anatomical absorption site (e.g., vitamin B12 with terminal
ileal resection). Clinical signs of micronutrient deficiency might

Adaptation is the process in which there is intestinal architectural and functional changes post bowel resection to restore
normal function. Although there are some adult histological
evidences [8], little pediatric histological evidence is available
and most of the evidence has been from animal studies [9].
Even so, functional adaptation is seen in clinical practice when
children are weaned off parenteral nutrition. Hormonal factors
such as growth hormone, insulin like growth factor and glucagon like peptide 2, to name a few, have been shown to be
important in mediating this process. The preservation of the
terminal ileum, where stimulation of the production of these
factors is most potent, correlates with the clinical observation
of better adaptive responses [10].
The adaptive response must be stimulated by mucosal contact with enteral nutrition. There has been no consensus on the
type of enteral nutrition that would be beneficial for adaptation
[11] but the general strategy, in authors unit, is to use expressed
breast milk where available. When it is not available or when
malabsorption is demonstrated (particularly fat malabsorption),
a hydrolysed formula with a higher medium chain triglyceride
(MCT) content is used. Rarely would an elemental formula be
used due to its high osmotic content which can have an unintended effect to cause osmotic diarrhea.
Bolus feeding has been advocated as the most physiological way to deliver enteral nutrition. Vomiting related to
dysmotility and/or diarrhea caused by large osmotic load in
a shorten bowel may be a barrier to its success. A combination
of bolus feeding and continuous feeding might be an alternative to promote physiological responses (and if able to tolerate
oral feeding, also to support oromotor skills) whilst
maximising mucosal contact with enteral nutrition without a
large osmotic effect.

Medications Used in Intestinal Failure


Medications used in management of intestinal failure aim
mostly at symptom control rather than promoting the adaptation process with variable results [12]. The following is not an
exhaustive list but is an indication of the classes of medications used (doses are a guide and local recommendations
should be consulted):

1440

Gastric Hypersecretion
H2 receptor antagonist (e.g., ranitidine); Proton pump inhibitors (e.g., omeprazole).
The use of antacid has been particularly pushed in the immediate post operative phase. Its use during this phase has mostly
been based on the understanding of a hypersecretory phase post
intestinal surgery. This phase can last up to a month. Generally
speaking, if there is no effect on gastric output then they should
be stopped as suppression of gastric acid is thought to encourage
bacterial growth in the proximal gastrointestinal tract [13].
Foregut Dysmotility
Prokinetic agents: Erythromycin (1-3 mg/kg, po/iv tds);
Domperidone (100400 microgram/kg dependent on age po
*cautionary note below).
Erythromycin at low doses has been used as a prokinetic
agent. There is variable success with it and it should be used
on a trial basis and discontinued if no response is seen after a
reasonable period of time.
There has been a practice to use domperidone especially in
children with vomiting with variable success. Its use has now
been discouraged as there is an increased risk of prolonged QT
syndrome. The use of domperidone is not the usual practice in
authors unit in intestinal failure patients with vomiting.
Secretory Diarrhea
Octreotide 110 microgram/kg/day iv divided bd initially.
Convert to s/c if successful in symptom control.
Octreotide is a somatostatin analogue and reduces gastrointestinal motility by splanchnic vasoconstriction. It is often
used in its intravenous form with its initial dose being 1 mcg/
kg/h, increasing it to 10 mcg/kg/h. Again its success has been
variable in controlling gastrointestinal output i.e., diarrhea in
intestinal failure patients. It should be discontinued if there is
no response after a 23 wk trial.
Osmotic/Malabsorption Diarrhea
Loperamide (100200 microgram/kg 24 times a day dependent on age po); Cholestyramine (18 g in 24 divided doses
po depending on age); Tedeglutide (not licenced yet in children).
Loperamide Loperamide has antipropulsive action by binding of opiate receptors in the gut wall and thereby inhibiting
release of acetylcholine and prostaglandins. If there is no improvement within 25 d, its used should be discontinued.
Cholestyramine Cholestyramine is a bile acid resin, which
binds unabsorbed bile salts. This is especially useful in patients following terminal ileal resection with interrupted

Indian J Pediatr (December 2016) 83(12):14361443

enterohepatic re-circulation of bile acid. Measurement of stool


bile acid is often impractical and not available in most centres,
so empirical trial is often required in patients with susceptible
anatomy. Due to its highly effective binding capacity, other
medications should not be delivered one hour before and 4 h
after its administration. Caution should also be noted as overzealous administration have been implicated to cause obstruction in the gastrointestinal tract.
Tedeglutide Glucagon like peptide 2 (GLP2) is currently licenced to be used in a number of countries [14] and has been
shown to be successful in weaning adult patients with short
bowel syndrome off parenteral nutrition. Its effect is not
sustained once the medication is discontinued. Its use in the
pediatric intestinal failure population is not yet licenced but
clinical trials are being conducted at present.
Non Transplant Small Bowel Surgery
As shortened bowel is the primary pathology in those with
short bowel syndrome, surgical innovations have creating procedures that would increase the intestinal length. These are
generally classified as Blengthening^ procedures.
Longitudinal Intestinal Lengthening and Tailoring (LILT)
or Bianchi Procedure (Fig. 4)
The first of these procedures was described by Bianchi [15].
The principle centres on dividing a dilated loop of bowel into
two vascularised strips, by carefully splitting the mesentery.
The two strips are each then sutured to form tubes and anastomosed to regain continuity.
STEP (Serial Transverse Entero Plasty) (Fig. 5)
Since its first description in 2003 by Kim et al. [16], this
procedure has been performed widely around the world. Due
to its simplicity, many different variations have been
attempted including STEP of the duodenum [17] and repeated
STEP along the same segment of bowel as examples.
A STEP is not without its complications for example,
bleeding [18] and infection [19].
Its success has been reported with variable results. Oh et al.
reported that 25 % of patients achieved full enteral independence
at 6.5 mo after STEP and no change in enteral tolerance in 25 %
of patients with the rest having some improvement [20].
SILT (Spiral Intestinal Lengthening and Tailoring)
SILT is a recent technique that creates length by spiral incisions
along the length of the intestine [21]. Small incisions into the
avascular mesentery allowed spiral elongation and rotation
without vascular compromise. There has not been extensive
reporting of the use of this technique in the literature.

Indian J Pediatr (December 2016) 83(12):14361443

1441

Fig. 4 LILT (Bianchi procedure)


(courtesy of Mr. O Gee)

Non transplant intestinal lengthening procedures as a


group have been advocated for patients with SBS [22].
One of main issue is deciding which patient would be appropriate for such operations as patients with dysmotility,
such as those with complex gastroschisis, would be unlikely
to achieve enteral autonomy despite adequate length of bowel.
Fig. 5 STEP procedure (courtesy
of Mr. O Gee)

Intestinal Failure Associated Liver Disease (IFALD)


The term IFALD replaces the old terminology of PN
associated liver disease or total parenteral nutrition
(TPN) liver disease. It is a more appropriate term as
the liver disease in children with IF is due to a

1442

Indian J Pediatr (December 2016) 83(12):14361443

combination of factors, rather than due to parenteral


nutrition alone.
The exact incidence of IFALD is not known, but a 15 to
85 % incidence has been variably quoted in the literature.
The exact reason for development of liver disease in children with long-term PN is not known, but is believed to be
multifactorial due to the following factors:
i)
ii)
iii)
iv)
v)
vi)

Prematurity and low birth weight


Multiple laparotomies
Duration of PN
Lack of enteral feeding
Recurrent central venous catheter infections
Components of PN
& Choline deficiency
& Taurine deficiency
& Carnitine deficiency
& Glutamine deficiency
& Aluminium overload
& High dextrose concentrations (> 16 g/kg/d)
& Excess lipids (> 3 g/kg/d)

IFALD can develop in children with IF very quickly


after starting PN. Appropriate attention and early

Table 2 Indications and contraindications for intestinal


transplantation

recognition of IFALD needs to be done to manage these


children to prevent progression of IFLAD. IFALD can
sometimes rapidly progress and lead to death in children
if appropriate management is not started to reverse the
IFALD. In children with progressive IFALD, early contact with an experienced intestinal failure or transplant
centre is essential. The overall goal in management should be
to halt the progression of IFALD in young children and prevent them from developing end-stage IFALD and portal
hypertension.
One of the key steps in managing IFALD is to promote
enteral feeding as early as possible. Various medical and surgical treatment strategies are involved in management of
IFALD and choosing the correct strategy needs an experienced multidisciplinary team.
In recent studies use of fish oil PN based formulations has
been shown to halt the progression of IFALD and reverse the
process [23, 24]. A consensus is still not available regarding the
decision to commence fish oil based formulations in the neonatal period or soon after surgery. In authors institution children with IF are commenced on soy based lipid formulations
soon after surgery and changed over to fish oil based formulations if there is persistent conjugated hyperbilirubinemia over
50 micromol/L for 46 wk.

Indications for intestinal transplantation

Contra-indications for intestinal transplantation

Irreversible intestinal failure with major complications

Absolute

Recurrent or life threatening sepsis

Profound or progressive neurological dysfunction

Loss of 50 % or more central venous access sites

Non-correctable disease in organs outside GI tract

Recurrent and intractable fluid balance issues

Active systemic sepsis

Liver disease with portal hypertension

Malignancy
Psychosocial problems severe and irreconcilable
Relative
Intensive Care Unit (ICU) care
Immunodeficiency
Drug dependency
Loss of conventional venous access
Neoplasia, benign or of uncertain prognosis

per se age is not a contraindication


Working group consensus criteria for consultation or referral (in addition to the above)
Children with massive small bowel resection
Children with severely diseased bowel and unacceptable morbidity
Continuing prognostic or diagnostic uncertainty
Microvillous inclusion disease or intestinal epithelial dysplasia
Request by the patient or family
Isolated small bowel: Absent or reversible liver dysfunction
Combined liver/small bowel: Progressive moderate to severe liver disease and/or intestinal failure with hypercoagulability syndrome
(N.B. waiting list mortality rate is very high when synthetic dysfunction, GI bleeding, ascites, cirrhosis, have
occurred)

Indian J Pediatr (December 2016) 83(12):14361443

Intestinal Transplantation
Intestinal transplantation (ITx) is reserved for children developing life threatening complications secondary to the use of
parenteral nutrition. ITx should not be the first treatment option in children with intestinal failure. All children with IF
should initially be managed on parenteral nutrition and then
referral should be made for intestinal transplantation depending on the criteria laid down by the Intestinal Transplant
Association (Table 2) [25]. Intestinal transplantation is done
in limited centres around the world and at present there are 71
active intestinal transplant centres all over the world. The type
of intestinal transplantation depends on the severity of liver
disease and predominantly there are two types of intestinal
transplant: Liver + intestine transplant and isolated intestinal
transplantation [26, 27]. Further details about the procedure
are beyond the remit of this chapter. The survival of intestinal
transplantation is improving and the current survival rates
from experienced centres are: 1 y survival of 90 %. 5 y survival of 65 % and 10 y survival of 50 %. Re-transplantation is
a possibility and there are more and more number of retransplants being reported according to the reports from the
Intestinal Transplant Registry.
Acknowledgments The authors acknowledge the multidisciplinary
team in the gastroenterology and The Liver Unit at Birmingham
Childerns Hospital. They also thank Mr. Oliver Gee, Consultant
Paediatric Surgeon, BCH for providing diagrams in this article.

1443
8.

9.

10.
11.
12.

13.

14.

15.
16.

17.
18.

19.

Compliance with Ethical Standards


20.
Conflict of Interest None.
Source of Funding None.
21.

References
1.

2.
3.
4.
5.
6.
7.

Pironi L, Arends J, Baxter J, et al; Home Artificial Nutrition &


Chronic Intestinal Failure; Acute Intestinal Failure Special Interest
Groups of ESPEN. ESPEN endorsed recommendations. Definition
and classification of intestinal failure in adults. Clin Nutr. 2015;34:
17180.
Neu J. Neonatal necrotizing enterocolitis: an update. Acta Paediatr
Suppl. 2005;94:1005.
Lin PW, Stoll BJ. Necrotising enterocolitis. Lancet. 2006;368:
127183.
Gabbard SL, Lacy BE. Chronic intestinal pseudo-obstruction. Nutr
Clin Pract. 2013;28:30716.
Antonucci A, Fronzoni L, Cogliandro L, et al. Chronic intestinal
pseudo-obstruction. World J Gastroenterol. 2008;14:295361.
Schneider PJ. Nutrition support teams: an evidence-based practice.
Nutr Clin Pract. 2006;21:627.
DeLegge MH, Kelly AT. State of nutrition support teams. Nutr Clin
Pract. 2013;28:6917.

22.
23.

24.

25.

26.
27.

Williamson RC. Intestinal adaptation (first of two parts). Structural,


functional and cytokinetic changes. N Engl J Med. 1978;298:1393
402.
Aunsholt L, Thymann T, Qvist N, Sigalet D, Husby S, Sangild PT.
Prematurity reduces functional adaptation to intestinal resection in
piglets. J Parenter Enter Nutr. 2015;39:66876.
Spencer AU, Neaga A, West B, et al. Pediatric short bowel syndrome:
redefining predictors of success. Ann Surg. 2005;242:4039.
Welters CF, Dejong CH, Deutz NE, Heineman E. Intestinal adaptation in short bowel syndrome. ANZ J Surg. 2002;72:22936.
Rodrigues CA, Lennard-Jones JE, Thompson DG, Farthing MJ.
The effects of octreotide, soy polysaccharide, codeine and
loperamide on nutrient, fluid and electrolyte absorption in the
short-bowel syndrome. Aliment Pharmacol Ther. 1989;3:15969.
Ukleja A, Scolapio JS. Abnormalities in fluid and electrolyte absorption in intestinal failure. In: Matarese LE, Steiger E, Seidner
DL, editors. Intestinal failure and rehabilitation: a clinical guide.
USA: CRC Press LLC; 2004. p. 4965.
Jeppesen PB, Pertkiewicz M, Messing B, et al. Teduglutide reduces
need for parenteral support among patients with short bowel syndrome with intestinal failure. Gastroenterology. 2012;143:1473
81.e3.
Bianchi A. Intestinal loop lengtheninga technique for increasing
small intestinal length. J Pediatr Surg. 1980;15:14551.
Kim HB, Fauza D, Garza J, Oh JT, Nurko S, Jaksic T. Serial transverse enteroplasty (STEP): a novel bowel lengthening procedure. J
Pediatr Surg. 2003;38:4259.
Bueno J, Redecillas S, Garca L, et al. Duodenal lengthening in
short bowel with dilated duodenum. J Pediatr Surg. 2015;50:4936.
Fisher JG, Stamm DA, Modi BP, Duggan C, Jaksic T.
Gastrointestinal bleeding as a complication of serial transverse
enteroplasty. J Pediatr Surg. 2014;49:7459.
Fujioka WK, Cowles RA. Infectious complications following serial
transverse enteroplasty in infants and children with short bowel
syndrome. J Pediatr Surg. 2015;50:42830.
Oh PS, Fingeret AL, Shah MY, et al. Improved tolerance for enteral
nutrition after serial transverse enteroplasty (STEP) in infants and
children with short bowel syndromea seven-year single-center experience. J Pediatr Surg. 2014;49:158992.
Alberti D, Boroni G, Giannotti G, et al. Spiral intestinal lengthening and tailoring (SILT) for a child with severely short bowel.
Pediatr Surg Int. 2014;30:116972.
Iyer KR. Surgical mangement of short bowel syndrome. J Parenter
Enter Nutr. 2014;38:53S9.
Gura KM, Duggan CP, Collier SB, et al. Reversal of parenteral
nutrition-associated liver disease in two infants with short bowel
syndrome using parenteral fish oil: implications for future management. Pediatrics. 2006;118:e197201.
Diamond IR, Sterescu A, Pencharz PB, Kim JH, Wales PW.
Changing the paradigm: omegaven for the treatment of liver failure
in pediatric short bowel syndrome. J Pediatr Gastroenterol Nutr.
2009;48:20915.
Kaufman SS, Atkinson JB, Bianchi A, et al; American Society of
Transplantation. Indications for pediatric intestinal transplantation:
a position paper of the American Society of Transplantation. Pediatr
Transplant. 2001;5:807.
Fishbein TM. Intestinal transplantation. New Engl J Med.
2009;361:9981008.
Kato T, Tzakis A, Selvaggi G, Madariaga JR. Surgical techniques
used in intestinal transplantation. Curr Opin Organ Transpl. 2004;9:
20713.

You might also like