Official reprint from UpToDate®

www.uptodate.com © 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved.

Enterocutaneous and enteroatmospheric fistulas

AUTHOR: Sharon L Stein, MD, FACS, FASCRS
SECTION EDITORS: Eileen M Bulger, MD, FACS, J Thomas Lamont, MD, David I Soybel, MD
DEPUTY EDITOR: Wenliang Chen, MD, PhD

All topics are updated as new evidence becomes available and our peer review process is complete.

Literature review current through: Nov 2023.

This topic last updated: Dec 03, 2020.

INTRODUCTION

A fistula is an abnormal connection between two epithelialized hollow spaces or organs. Strictly
speaking, an enterocutaneous fistula connects the small bowel to the skin. A more liberal
interpretation of the term, however, also includes enteric fistulas originating from the colon,
stomach, and esophagus. (See 'Classification' below.)

The clinical features, diagnosis, and management of enterocutaneous fistulas are reviewed
here. Enteroatmospheric fistulas, which are a subset of enterocutaneous fistulas that occur in
the setting of an open abdomen, are also discussed here.

Fistulas that occur in other areas of the body are discussed in other topics, including:

● Colovesical fistulas (see "Colovesical fistulas")

● Urogenital tract fistulas in women (see "Urogenital tract fistulas in females" and
"Rectovaginal and anovaginal fistulas")

● Anorectal fistulas (see "Anorectal fistula: Clinical manifestations and diagnosis" and
"Operative management of anorectal fistulas" and "Perianal Crohn disease")

● Pancreatic fistulas

● Duodenal fistulas (see "Postgastrectomy duodenal leak")

 ● Tracheoesophageal fistulas (see "Tracheo- and broncho-esophageal fistulas in adults")

● Bronchopleural fistulas (see "Bronchopleural fistula in adults")

CLASSIFICATION

Enterocutaneous fistulas can be classified according to source, output volume, and etiology.

By source — The most common method of defining a fistula is by its organ of origin (eg,
gastro-, duodeno-, entero-, jejuno-, ileo-, colo-, recto-) followed by the point of its termination
(eg, -cutaneous, -atmospheric). However, at initial presentation, the specific segment of bowel
involved (ie, the enteric origin of the fistula) is often unknown, and a broader designation (eg,
enterocutaneous rather than jejunocutaneous) is used until the anatomy of the fistula can be
delineated. (See 'Diagnosis' below.)

Fistulas originating from different organ systems will have very different outputs. Electrolyte
and nutritional losses can vary greatly between organs of origin. As an example, gastric output
has a higher acidity. This information may prove essential in the management of
enterocutaneous fistulas. (See 'Fluid therapy' below.)

By output volume — The physiologic consequences of enterocutaneous fistulas may depend

on the quantity of fluid put out by the fistula, which may differ by the location (proximal versus
distal) and the length or diameter of the fistula. An alternative classification defines fistulas by
the quantity of their output:

● A low-output fistula drains less than 200 mL/day.

● A moderate-output fistula drains between 200 and 500 mL/day.
● A high-output fistula drains more than 500 mL/day.

In general, high-output fistulas are less likely to heal spontaneously, and patients with high-
output fistulas are at a higher risk for metabolic disturbances, fluid loss, and malnutrition. For
such patients, controlling external fistula output is as important as replacing fluid and
electrolyte loss during the chronic phase of management. (See 'Fistula output reduction' below.)

By etiology — Enterocutaneous fistulas can also be classified according to their etiologies (eg,
iatrogenic, spontaneous), which are further discussed below. (See 'Etiology and risk factors'
below.)

EPIDEMIOLOGY
Although a few studies have reported postoperative prevalences of enterocutaneous fistulas in
patients undergoing surgery for trauma (1.5 percent [1]), general surgery (3.6 percent [2]), and
Crohn disease (15 to 35 percent [3,4]), the prevalence of enterocutaneous fistulas in the general
population (including both iatrogenic and spontaneous cases) is not well known. The National
Inpatient Sample (NIS) noted 317,000 admissions between 2004 and 2014 with a diagnosis of
enteric fistula, costing the United States hospital systems more than 500 million dollars
annually [5].

ETIOLOGY AND RISK FACTORS

Various etiologies can lead to fistula formation ( table 1). Most enterocutaneous fistulas are
iatrogenic/postoperative (75 to 85 percent); a minority (15 to 25 percent) develop spontaneously
[6].

Iatrogenic fistulas — Iatrogenic causes of enterocutaneous fistula include trauma and surgery
(ie, postoperative fistulas). Postoperative fistulas develop from either a bowel anastomotic leak
(50 percent) or a missed enterotomy (45 percent), with a small percentage from erosion of
foreign material (eg, mesh for hernia repair, vascular graft) into adjacent bowel [7]. Preoperative
factors that increase the likelihood of the development of a postoperative fistula include Crohn
disease, malnutrition, immunosuppression, traumatic injury, infection, smoking, and
emergency procedures [8,9].

Enteroatmospheric fistulas — Enteroatmospheric or exposed fistulas occur in the midst of an

open abdomen with no overlying soft tissue ( picture 1). The open abdomen is usually the
result of a damage control laparotomy, which leaves the abdomen open after trauma or
emergency surgery to prevent intra-abdominal hypertension/abdominal compartment
syndrome [10,11]. (See "Abdominal compartment syndrome in adults".)

A review of 517 patients from the American Association for Surgery in Trauma (AAST) registry
with open abdomen found that 111 patients (21 percent) developed an enterocutaneous fistula,
an enteroatmospheric fistula, or intra-abdominal sepsis. Independent risk factors included
large bowel resection, large-volume resuscitation, and an increasing number of abdominal re-
explorations [12]. The risks of open abdomen are further discussed separately. (See
"Management of the open abdomen in adults", section on 'Complications of open abdomen'.)

Spontaneous fistulas — The mnemonic "FRIEND" describes common etiologies for

spontaneous enterocutaneous fistulas, which include foreign body, radiation, inflammation (eg,
Crohn disease) or infection (eg, tuberculosis, actinomycosis), epithelialization, neoplasia, and
distal obstruction [10]. These etiologies also describe conditions in which fistulas are less likely
to heal spontaneously. Diverticular disease and appendicitis are also reported as uncommon
etiologies of fistulas.

Crohn disease is the most common etiology for spontaneous fistulas; the prevalence varies by
patient populations [10,13]. Between 27 and 35 percent of patients undergoing surgery for
Crohn disease had a fistula [3,4], while 15.4 percent of patients with complicated Crohn disease,
but who had not had surgery, had a fistula [14]. Crohn-related fistulas are typically treated
initially with immunosuppressive drugs (thiopurines), biologic agents (TNF inhibitors), and
antibiotics (metronidazole) to reduce inflammation and diarrhea. Medical treatment of Crohn-
related fistulas is discussed in another topic. (See "Clinical manifestations, diagnosis, and
prognosis of Crohn disease in adults", section on 'Features of transmural inflammation'.)

CLINICAL FEATURES

The most common presentation of an enterocutaneous fistula is in a postoperative patient who

fails to recover normally from abdominal surgery. The patient often presents first with
abdominal symptoms, including increased pain, nausea and vomiting, obstipation, and fullness
or induration of the abdominal wall. These may be accompanied by fever and leukocytosis. A
wound infection is then typically recognized 7 to 10 days postoperatively, and following
incisional drainage, enteric contents appear in the surgical wound [7]. An enteric fistula can be
distinguished from a wound infection by the presence of bile in the wound. As opposed to
infection or seroma, bilious output will stain gauze and dressings an orange/brown or green
color. Frank stool can also be noted in the wound of a colonic fistula.

Enterocutaneous fistulas are characterized by leakage of enteric or bowel contents through the
abdominal wall. The leakage is also referred to as effluent. Depending upon the location and
origin of the fistula, it can be through a prior abdominal wound, incision, or an area of "virgin"
abdomen. Leakage of effluent can cause irritation of the skin, loss of fluids and electrolytes,
malnutrition, and infection. In addition, as a fistula is forming, the patient may become acutely
ill secondary to leakage of effluent into the abdominal cavity.

DIAGNOSIS

The diagnosis of an enterocutaneous fistula is clinical. It should be suspected in a postoperative

patient who fails to recovery normally from abdominal surgery and has bilious wound drainage.
The diagnosis of enterocutaneous fistula can be confirmed by the appearance of enteric
contents draining from the abdominal wall. If in doubt, bilirubin levels can be sent from the
wound drainage to determine if contents are enteric.

By definition, an enteroatmospheric fistula can only be diagnosed in a patient with an open

abdomen. Similar to enterocutaneous fistulas, the diagnosis can be confirmed by the presence
of enteric contents draining from an opening in a segment of bowel within the open abdominal
wound.

However, the organ of origin of an enterocutaneous or enteroatmospheric fistula is often not

defined until imaging studies can be performed. (See 'Diagnostic evaluation' below.)

Diagnostic evaluation — For stable patients with an enterocutaneous or enteroatmospheric

fistula, we perform abdominal computed tomography (CT) with and without oral and
intravenous contrast at least 7 to 10 days after fluid and electrolyte resuscitation, infection
control, and appropriate wound care [15]. CT can not only help delineate the anatomy of the
fistula but also demonstrate associated intra-abdominal abscesses, fluid collections, or areas of
distal intestinal obstruction. These are all risk factors for fistula formation and persistence. (See
'Etiology and risk factors' above.)

If abdominal CT does not elucidate fistula anatomy, a gastrointestinal contrast study is

performed. Either a small bowel follow-through or contrast enema is selected depending upon
the suspected level of the fistula (upper versus lower gastrointestinal tract). It should be noted
that only the portion of the bowel in continuity will be evaluated by traditional contrast studies.
As an example, a mass or stricture (inflammatory or malignant) distal to the fistula may not be
well demonstrated, because most of the contrast is drained via the fistula.

Alternatively, for enterocutaneous fistulas that have a well-defined cutaneous opening, a

fistulogram can be performed by injecting a water-soluble contrast agent into the opening to
define the fistula tract. Although a fistulogram can document intestinal continuity and evaluate
for distal obstruction [7,16,17], it rarely identifies the specific origin of the tract [10].

Small fistulas or low-output fistulas may not be apparent on imaging. Another simple method to
determine whether or not an enterocutaneous or enteroatmospheric fistula is indeed present is
by the administration of dye (eg, indigo carmine, methylene blue, charcoal), which can be
ingested or added to enteric feeding or instilled as a solution into the gastrointestinal tract
during endoscopy. The presence of dye in the effluent confirms the diagnosis of an enteric
fistula.

Differential diagnosis — Drainage from an abdominal incision following gastrointestinal

surgery may represent a surgical site infection rather than an enterocutaneous fistula. The
character of the drainage, and whether drainage persists once the wound has been opened,
usually makes the distinction as the presence of feces or bile is definitive evidence of an
enterocutaneous or enteroatmospheric fistula. (See "Wound infection following repair of
abdominal wall hernia".)

TREATMENT OVERVIEW

The treatment of enterocutaneous and enteroatmospheric fistulas requires a systematic

approach and is carried out in phases ( table 2 and algorithm 1).

Initial acute management focuses on control and treatment of sepsis, which requires surgery in
some patients but can be accomplished nonoperatively in others (eg, with antibiotics and
catheter drainage). (See 'Acute management' below.)

Once sepsis is controlled, the treatment enters a chronic phase, which focuses on wound
management, fluid/electrolyte replacement, and nutritional optimization. It may be appropriate
to transfer patients to a specialized center for this phase of the care and beyond [18], where
improved outcomes, including a lower mortality rate, have been realized [10,19,20]. This phase
of fistula management optimizes the condition for spontaneous healing while simultaneously
preparing the patient for possible definitive management. Most contemporary studies report
that approximately one-third of enterocutaneous fistulas will close spontaneously within five to
six weeks with conservative measures [13,21-27]. (See 'Chronic management' below.)

For fistulas that fail to close spontaneously, the final stage of management is definitive fistula
repair, which may be endoscopic or surgical. As long as fistula output is gradually decreasing
and the wound (or tract) shows signs of healing, surgery should be delayed. Surgical fistula
repair should not be attempted for at least three to six months from the inciting event to allow
time for spontaneous healing and patient conditioning. Specialized centers often delay
definitive operations for 6 to 12 months [6]. Prerequisites to definitive fistula repair include
eradication of infection, optimization of nutrition, and clinical evidence of softening scars and
abdominal wall on physical exam. (See 'Nonoperative fistula closure' below and 'Operative
fistula closure' below.)

ACUTE MANAGEMENT

Initial treatment of enterocutaneous and enteroatmospheric fistulas focuses on the

identification and management of sepsis, especially in the case of acute postoperative fistulas.
In this acute phase, the etiology of the fistula is often not important.
Fistula-associated abdominal sepsis (eg, intra-abdominal abscess, gastrointestinal perforation,
or subcutaneous infection) needs to be recognized and promptly treated with antibiotics,
percutaneous catheter drainage, and/or operative drainage or source control. Prompt
treatment of abdominal sepsis will reduce the risk of mortality as well as progressive organ
dysfunction [28,29]. Infection and sepsis account for over 70 percent of mortality associated
with these fistulas [13].

Treatment of sepsis — Patients who have diffuse peritonitis or evidence of free

gastrointestinal perforation on imaging studies require urgent surgical exploration. It is rare
that an enterocutaneous fistula can be resected or closed primarily in the acute phase,
particularly if it is a postoperative complication. Thus, operative sepsis control should focus on
infection drainage and exteriorization of any leaking small or large intestine. A common
mistake is to repair or primarily redo the anastomosis in the infected field in order to avoid a
stoma. No new anastomoses should be created in a critically ill patient or in the presence of
significant intra-abdominal contamination. Diversion of the fecal stream by ostomy is often
required and is the preferred approach. In the setting of acute sepsis, diversion is highly
recommended to prevent further complications. Resection of healthy bowel that may be
involved in an inflammatory process should also be avoided.

Hemodynamically stable patients without diffuse peritonitis should undergo abdominopelvic

computed tomography (CT) to identify any intra-abdominal source of sepsis, such as intra-
abdominal abscess or fluid collection. Patients with a contained fluid collection or abscess may
undergo image-guided percutaneous drainage (ultrasound or CT) [30]. Drainage is usually
performed through the anterior abdominal wall. However, abscesses deep in the pelvis or
obscured by other organs may be accessed with a variety of other approaches, including
transgastric, transrectal, transvaginal, and transgluteal [18]. The drainage catheter is usually left
in place until output is less than 10 mL in 24 hours or until definitive fistula surgery. Catheter
fistulogram during this period permits assessment of resolution of the abscess cavity and
determination of direct communication of drainage catheter with the bowel. Operative drainage
is needed if sepsis does not resolve with catheter drainage.

Antibiotic management in septic patients should follow the Surviving Sepsis Guidelines [31].
Once source control is obtained by operative or catheter drainage, empirical antibiotics should
be discontinued after another five to seven days. (See "Antimicrobial approach to intra-
abdominal infections in adults", section on 'Duration of therapy'.)

Antibiotic management in nonseptic patients with an enterocutaneous fistula is controversial.

Because no studies have demonstrated improved outcomes with antibiotic therapy in these
patients and there are increasing concerns for multidrug-resistant bacteria, we do not suggest
routine antibiotic coverage for patients who are not septic and have no acute signs of infection.

Restoration of hemodynamic stability — Treatment of sepsis in the acute phase also requires
restoration of hemodynamic stability. Resuscitation with fluids, repletion of electrolytes, and
restoration of normotension may be required on a case-by-case basis; some may require
vasopressors in an intensive care unit (ICU) setting. (See "Evaluation and management of
suspected sepsis and septic shock in adults".)

CHRONIC MANAGEMENT

Chronic management of fistulas entails evaluation and treatment of fluid, electrolyte, and
nutritional losses and specialized wound care to manage the intestinal effluent ( table 2 and
algorithm 1). In those with high-output fistulas, drug therapies may be instituted to reduce
fistula output.

Fluid therapy — Aggressive correction of hypovolemia and electrolyte loss should occur early
in treatment. Hyponatremia, hypokalemia, and hypomagnesium are the most common
electrolyte abnormalities. Ongoing fluid losses from moderate-output upper gastrointestinal
fistulas should be replaced with saline and potassium supplementation with serial
measurements of serum electrolytes. The composition of replacement fluid should mimic that
of fluid lost as much as possible ( table 3) [32]. Replacing fluid losses cc per cc may be
necessary to help prevent dehydration and hypovolemia.

High-output fistulas may require direct electrolyte analysis of the fistula effluent to make an
appropriate choice of replacement fluid. The St. Mark's Intestinal Failure Unit has created a
worksheet to help calculate daily losses for patients with high-output fistulas [33]. (See
"Treatment of severe hypovolemia or hypovolemic shock in adults" and "Clinical manifestations
and treatment of hypokalemia in adults".)

Duodenal or pancreatic fistulas may require bicarbonate replacement to prevent metabolic

acidosis. (See "Approach to the adult with metabolic acidosis", section on 'Overview of therapy'.)

Nutritional support — Nutritional optimization is critical to successful resolution of the fistula.

Data demonstrate that nutritionally optimized patients with serum albumin of ≥4 mg/dL have
lower mortality from surgical interventions [34]. In addition, the spontaneous healing rate of
the fistula improves from 7 to 81 percent when nutrition is optimized [35]. The nutritional needs
of a patient with an enterocutaneous or enteroatmospheric fistula are met with enteral feeding,
parenteral feeding, or a combination of the two. The decision is primarily dependent upon
fistula output ( algorithm 1).

Nutritional goals — Depending on the amount of output, the baseline energy requirement
for a patient with an enterocutaneous or enteroatmospheric fistula may be 1 to 2.5 times that
of a healthy adult [36]. The requirement may be even higher for patients with ongoing infection,
large open abdominal wounds, and high-output fistulas.

The estimated nutrition needs for a patient with a low-output fistula range from 20 to
30 kcal/kg per day of total caloric intake and 1 to 1.5 g/kg per day of protein intake. Those with
a high-output fistula require 25 to 35 kcal/kg per day of total caloric intake and 1.5 to
2.5 g/kg per day of protein intake (due to up to 75 g of protein loss in the effluent) [6]. Required
doses of vitamins and trace elements, such as vitamin C, zinc, copper, and selenium, which
promote healing, may be increased substantially [6]. The addition of fish oil or omega-3 fatty
acids has also been shown to improve immune function [37] after severe injury [38], abdominal
operation [39], and in patients in the intensive care unit [40]. There are no trials directly
investigating the effect of omega-3 fatty acid nutritional supplements specifically in the
treatment of enterocutaneous fistula.

It may be necessary to carefully calculate the composition and quantity of daily output to
determine repletion requirements. Ongoing assessment of the patient's nutritional, electrolyte,
and fluid status may be necessary for patients with high-output fistulas [41]. Serum albumin,
prealbumin, transferrin, C-reactive protein, weight, and anthropometrics should be followed
over time [6].

Low-output fistulas (<200 mL/day) — Enteral feeding is always preferred to parenteral

nutrition because this route preserves the intestinal mucosal barrier and has positive effects on
immunologic and hormonal gut functions. However, although the patient may eat well,
absorption of nutrition may be compromised by the fistula to the degree determined by its
output and location. With proximal fistulization (jejunal), the patient may not have adequate
absorptive capacity in the functioning intestines to maintain nutrition. Additionally, the output
from the fistula may increase in quantity with enteral feeding and become excessive, requiring
fluid supplementation. For patients trying enteral feeding, the goal enteric output is <1.5 L/day.
The following is our protocol for managing nutrition in patients with low-output fistulas
( algorithm 1):

● After the patient has been stabilized and sepsis treated, we generally try a short period of
bowel rest (days) to see if the fistula output would reduce and/or if the fistula would
 spontaneously close. During this brief period of bowel rest, the patient may or may not
need total parenteral nutrition (TPN) depending on his/her baseline nutritional status.

● If the fistula output does not decrease with bowel rest and the fistula does not close, the
patient is then started on an oral diet while we continue to monitor and manage output.

● If the fistula output increases substantially with oral diet, we will generally stop oral diet
and start TPN to see if that decreases output. TPN has been known to reduce fistula
output [6].

Moderate- or high-output fistulas (>200 mL/day) — Patients with moderate- to high-output

enteric fistulas may be intolerant to oral nutrition secondary to inability to control sepsis, poor
absorption, greater fluid and nutrient loss from fistula output, or difficulty with infection or
excoriation of the skin.

Output from the fistula may decrease with an elemental diet [42]. One specialized intestinal
failure unit reported lowering fistula output by limiting the intake of low-sodium fluids (free
fluids) to 500 mL/day and encouraging the patient to drink an electrolyte solution containing
high concentrations of sodium and glucose (up to 1000 mL per day) [43]. Drug therapies may
also be successful, including anticathartics (eg, loperamide, diphenoxylate, codeine), histamine-
2 receptor antagonists and proton pump inhibitors [21], cholestyramine, and somatostatin
analogues. (See 'Fistula output reduction' below.)

In general, patients with output greater than 1.5 L/day, less than 75 cm of intestinal length prior
to the fistula, or intestinal discontinuity may require parenteral nutritional supplementation. In
these cases, parenteral nutrition may be required exclusively or as an adjunct to oral nutrition.
Parenteral nutritional support should be initiated slowly after correction of fluid, electrolyte, and
vitamin deficits has been completed [36,44,45]. (See "Nutrition support in critically ill patients:
An overview".)

Wound care — The main goal in wound care is to protect the skin near the external fistula
opening from the corrosive effects of the enteric or pancreatic contents and promote wound
healing. Wound care for most low-output fistulas requires nothing more than a gauze cover.
Moderate-output fistulas can be controlled with an ostomy appliance. The real challenge is
management of high-output fistulas and enteroatmospheric fistulas.

Bag drainage — Skin protection creams and effluent collection bags must be tailored to the
unique characteristics of each fistula, but the principles are similar to those used in the care of a
colostomy or ileostomy [22]. The assistance of a skilled enterostomal therapist is helpful. (See
"Ileostomy or colostomy care and complications".)
 ● For enterocutaneous fistulas, a pouch should be placed around the fistula. The adjacent
skin should be protected with semipermeable barrier dressing or other skin protectants.
Wound protectors and wound managers may be used to minimize skin irritation and
collect effluent as with surgical ostomy. (See "Ileostomy or colostomy care and
complications", section on 'Pouch systems and routine ostomy care'.)

Effluent from the fistula is often acidic and copious and can result in significant
denudation and excoriation of the surrounding skin. Cellulitis or fungal infection is not
uncommon with poorly controlled fistula output. Sophisticated pouching systems
available at specialty centers that care for these patients can protect the skin, divert the
effluent, and are key to allowing patients to function prior to surgery. Good pouching can
convert an inflamed, painful wound into a functional stoma.

● Control of intestinal contents from an enteroatmospheric fistula will minimize damage to

the healing bed of granulation tissue until definitive closure of the fistula can be
undertaken 6 to 12 months later. Management options include the creation of a "floating
stoma" by sewing exposed bowel mucosa circumferentially to a plastic sheet that is used
as an interface to attach the stoma appliance and be placed on the surface of the exposed
bowel [46]. A similar technique has also been described using an abdominal closure
device, progressively approximating and inverting the edges of the skin to convert an
open wound to a pouchable stoma [47].

Negative pressure wound therapy — Although there are no high-quality studies comparing
negative pressure wound therapy ( figure 1) with traditional drainage bags, the use of
negative pressure wound therapy in fistula management has become widespread because
surgeons are familiar with the technology from its successful application to other problematic
wounds [48]. (See "Negative pressure wound therapy", section on 'Mechanism of action'.)

While many case series reported that negative pressure wound therapy accelerated fistula
closure [49-51], none reported improved rates of fistula closure. In a few case reports, negative
pressure wound therapy led to new fistula formation [52]. Nevertheless, most would agree that
negative pressure wound therapy may be effective for high-output fistulas and hard-to-pouch
fistulas and may improve the patient's quality of life by protecting surrounding skin and
gathering effluent [6].

Negative pressure wound therapy can also simplify management of enteroatmospheric fistulas.
Continuous suction of the fistula output minimizes contact time between intestinal fluid and
exposed peritoneum by effectively controlling intestinal spillage. A useful technique for
superficial enteroatmospheric fistulas is to intubate the fistulas and bring the tubes out
perpendicularly through the sponge of the negative pressure dressing ( picture 2) [53]. With
this technique, the majority of intestinal effluent is collected in the tubes. The sponge serves as
a stable rig that anchors the tubes, prevents dislodgement, and collects any residual fluid that
might leak around the tubes. Care must be used when applying a negative pressure wound
dressing in the setting of exposed but uninvolved bowel because the dressing can cause
formation of additional fistulas, especially if fresh suture or staple lines in the bowel are
exposed [52,54]. Additional protection can be provided by placing another layer of plastic or a
biologic dressing between the bowel and the negative pressure sponge [55]. (See "Negative
pressure wound therapy", section on 'Enterocutaneous fistula'.)

Fistula output reduction — In patients with a high-output fistula, fistula output reduction is
critical to simplifying fluid management, optimizing wound care, and enabling enteral nutrition.
Anticathartics, somatostatin and analogues, antisecretories, and cholestyramine have been
used to reduce the output from intestinal fistulas, especially when the output exceeds 1.5 L/day
( table 4) [32].

Anticathartics — Anticathartics such as loperamide hydrochloride (Imodium) and

diphenoxylate-atropine (Lomotil) may be used for diarrhea and high-output fistulas.
Loperamide is available in 2 mg tablets over the counter, while diphenoxylate requires a
prescription for 2.5 mg tablets. Patients should titrate the dosage to output, with a typical
maximal dose of 16 mg of loperamide and 20 mg of diphenoxylate daily. Both are also available
in liquid form, which may be more useful for patients with poor absorption. Both medications
are best used approximately 20 minutes prior to the consumption of foods.

In a British intestinal failure unit, higher doses of loperamide (up to 40 mg/day) and codeine (up
to 240 mg/day) have been used to control otherwise refractory high-output fistulas [13,43].

Opiates, such as tincture of opium and codeine, have also been used for their anticathartic
property to treat high-output fistulas [32,56].

Somatostatin and analogues — Intestinal fistula output can be reduced with somatostatin
and its analogues (eg, octreotide). Somatostatin reduces fistula output, but its clinical use is
limited by a very short half-life. Octreotide, with a half-life of two hours, reduces pancreatic
secretions and may facilitate absorption of water and electrolytes. Somatostatin and its
analogues are generally renally cleared, so attention must be paid to renal function in these
patients.

A systematic review identified eight trials and found that somatostatin analogues decrease the
duration of enterocutaneous fistulas (weighted mean difference [WMD] -6.37 days, 95% CI -8.33
to -4.42) and duration of hospital stay (WMD -4.53 days, 95% CI -8.29 to -0.77) but did not
increase the rate of spontaneous closure [57]. A separate review found similar results but noted
that somatostatin had a more significant effect compared with somatostatin analogues [58].
Octreotide does not significantly reduce the need for operation in patients with Crohn disease
fistulas [59,60]. Octreotide may adversely affect immune function as a result of growth
hormone inhibition [61,62], but there are no clinical data to confirm this possibility. It is also
important to keep in mind that if the patient has one of the barriers to spontaneous closure
( table 5), such as distal obstruction, octreotide will be futile and will delay the surgical
procedure ultimately needed to obtain definitive closure.

Specialized centers typically try somatostatin analogues for three days in an effort to decrease
output in a fistula that produces >1 L/day. If the output decreases within those three days, the
treatment is continued for a longer period of time [13,43].

Antisecretories — Proton pump inhibitors and histamine-2 receptor antagonists decrease the
volume and acidity of gastric output and have been a part of standard drug treatment for high-
output fistulas [13]. However, none of the acid reduction therapies have been shown to increase
the rate of spontaneous fistula closure.

Cholestyramine — For the uncommon bilioenteric fistula (eg, biliary-colonic), cholestyramine

can be tried. It is available in powder form and dosed at 9 mg twice daily prior to meals. Each of
these medications can be used for the treatment of diarrhea, with anecdotal evidence of
decreased fistula output. In addition, patients with a fistula proximal to the terminal ileum may
find reduced output after the addition of cholestyramine.

NONOPERATIVE FISTULA CLOSURE

The following nonsurgical treatments have been attempted to close or better control fistulas
that do not close spontaneously. These methods are generally appropriate after the patient has
been stabilized from the acute phase of an enterocutaneous or enteroatmospheric fistula.

Endoscopic therapies — Endoscopic therapy may be used to temporarily control the initial leak
and limit infection, or as a definitive technique to close the fistula. The ability to intervene
endoscopically is limited by endoscopic accessibility, which is determined by the location of the
fistula. Fistulas in the esophagus, stomach, or colon are most amenable to endoscopic closure.
Endoscopic manipulation may transiently increase intraluminal pressure, which may increase
the risk of sepsis acutely. Thus, endoscopic therapy should only be pursued in stable, nonseptic
patients by experienced providers.
 ● Covered enteric stents have been used to treat early postoperative leaks of the colon and
esophagus. Success rates vary by location, and a major concern of stenting is
postplacement migration. When temporary stents were used to treat esophageal leaks,
fistulas, and perforations, primary closure was achieved in 74 percent of patients, but
stent migration rate occurred in 28 percent [63]. A study of 22 patients with colonic fistulas
treated with stents noted a closure rate of 86 percent, but 69 percent of patients had
diversion during the healing phase [64].

● Endoscopic clipping of the intraluminal end of the fistula has also been successful. Over-
or through-the-scope clips can be deployed endoscopically to close the internal opening of
the fistula, preventing further soilage and promoting sealing of the fistula. Data are
limited, but the largest series of 108 patients demonstrated a fistula closure rate of 42.9
percent at a median follow-up of about five months [65]. This technology is primarily used
for acute fistulas and postoperative perforations and is not well suited for chronic fistulas.
Potential complications include increasing the size of the fistula and causing further
damage to surrounding tissues.

● Fistula plugs can also be used to close the internal opening of the fistula. Plugs are
generally made from porcine submucosa. Placement is also limited by endoscopic access,
but case reports demonstrate success rates of up to 80 percent [66-68].

Fibrin sealant — Small series also demonstrated successful fistula closure with multiple
applications of fibrin glue. Placement of fibrin glue reduced median time to closure and
increased rate of closure when compared with control groups [69]. Several applications may be
necessary to achieve closure, and success is limited by the ability to treat the entire tract prior to
drying of the glue. Ideal fistulas for fibrin glue treatment are long, narrow, low output, and
devoid of distal obstruction and Crohn disease.

OPERATIVE FISTULA CLOSURE

Approximately one-third of enterocutaneous fistulas will close spontaneously within five to six
weeks with conservative measures [22-25]. In one retrospective review of 79 patients with
enterocutaneous fistulas, spontaneous closure occurred in 23 (29 percent) after a median of 39
days (range 7 to 163) [70].

Predictors of spontaneous closure are given in the table ( table 5) [34,71]. Generally, fistulas
with low output, long track, or proximal location are most likely to heal with conservative
measures. Barriers to closure include distal obstruction, a short epithelialized fistula tract,
infection, and malignancy [21,71]. Given that an enteroatmospheric fistula is an exposed hole in
the bowel lumen without overlying skin or soft tissue, there should be no realistic expectation of
its spontaneous closure.

Timing of surgery — Patients with enterocutaneous fistulas that do not close with five to six
weeks of nonoperative management are unlikely to heal spontaneously and will likely need
surgery to definitively manage the fistula. In a review of patients with enterocutaneous fistulas,
90 percent of spontaneous closures occurred in the first month after resolution of sepsis and 10
percent during the second month [21]. No patients achieved spontaneous closure after two
months [70].

Although the timing of definitive surgery to close the fistula is a matter of judgment, surgery
should be delayed as long as fistula output is gradually decreasing and the wound (or tract)
shows signs of healing [51]. Surgery should generally be postponed for at least three to six
months to allow for resolution of inflammation, which may reduce the risk of bowel injury.
Specialized centers often delay the definitive surgery for 6 to 12 months ( algorithm 1).

The presence of a fistula is usually associated with a severe inflammatory response that leads to
dense adhesions, known as "obliterative peritonitis," which make early surgery hazardous
[34,72]. Dense adhesions begin to form in the open abdominal wound after approximately one
week of exposure and remain treacherous for at least six to eight weeks. In one study, the
mortality rate associated with surgery between days 11 and 42 after presentation of the fistula
(21 percent) was significantly higher than the mortality rate of either operating before day 11
(13 percent) or after day 42 (11 percent) [34]. Recurrence rates of postoperative fistula also
appear to be higher with earlier surgery [73].

Preoperative preparation — Before any definitive operative closure of an enterocutaneous

fistula, the patient should be nutritionally replete, free of infection, and have supple, soft tissues
adjacent to the fistula [10,74].

Nutritionally, data suggest that raising serum albumin level to >3.5 mg/dL reduces
perioperative mortality rate to 0 percent [34]. Definitive surgical management of a fistula
should also be delayed until the initial scar or incision is mobile and can be pinched between
the examining thumb and index fingers, which signifies the existence of a plane between the
skin/skin graft and underlying bowel [75].

Prior to surgery, abdominal computed tomography (CT) imaging should be repeated to rule out
any residual intra-abdominal fluid collection or a distal obstruction and assess for evidence of
Crohn disease, radiation enteritis, malignancy, or any other pathologies that could increase the
likelihood of recurrence ( table 5). Fluoroscopic exams, such as small bowel follow-through
series and fistulograms, image contrast passage through the fistula in real time, which may
help define the fistula anatomy. In addition, contrast injected retrograde through the fistula,
drain, or rectum may help identify distal disease (eg, obstruction, stricture, or tumor) that will
need to be addressed at the time of surgery. Endoscopic evaluation of the distal colon should
also be considered prior to surgery. (See 'Diagnostic evaluation' above.)

Patients should also be mentally prepared for the surgery. They should be forewarned that the
recurrence rate after surgery for enterocutaneous fistula can be as high as 20 to 36 percent [73]
and that a diverting stoma may be required. Prior to surgery, the surgeon should mark
potential stoma sites, particularly in patients with Crohn disease or diverticular disease, and
consider placing ureteral stents if colon mobilization is anticipated. (See "Overview of surgical
ostomy for fecal diversion", section on 'Preparation and counseling' and "Placement and
management of indwelling ureteral stents", section on 'Prophylactic'.)

Surgical techniques — The aim of the surgery is to eliminate the fistula, which usually requires
resection of the segment of bowel that is the origin of the fistula, reestablishment of
gastrointestinal continuity, and tension-free closure of the abdomen with well-vascularized soft
tissue [10]. Fecal diversion and bowel rest during the postoperative healing period can be used
to minimize recurrence.

Since studies evaluating surgical techniques for managing enterocutaneous fistulas are
generally heterogeneous and of low quality [76], the surgical approach described below is
derived from expert opinions and our clinical experience.

Incision and adhesiolysis — For patients with an intact abdominal wall, the incision should be
placed remote from prior incisions where bowel loops may be adherent to the abdominal wall.
The incision should also preserve vascular supply to the soft tissue of the abdominal wall, which
is critical to any successful complex abdominal wall reconstruction (eg, component separation).

Once the incision is made, lysis of adhesions is performed to free the abdominal wall
circumferentially from adherent bowel. Expert surgeons recommend working laterally first to
take down adhesions and deliver the bowel from the side of the abdomen least involved [7,77].
The adhesions are often dense, and the dissection should be slow and careful. The surgeon
must be prepared to spend hours performing meticulous adhesiolysis and mobilizing the entire
length of the gastrointestinal tract from the ligament of Treitz to the rectum, if necessary, to
identify the fistula and approach it safely [10]. It is usually not advisable to schedule other major
elective operations on the same day, because these demanding procedures often take all day.

During the surgery, the surgeon should identify normal areas of small bowel that are free from
injury and primary disease where the fistula and any other pathology are found. In addition,
there may be segments of bowel where serosal injuries or small iatrogenic full-thickness injury
occurred during adhesiolysis. Each of these areas should be evaluated before decisions can be
made about resection or repair based on the available bowel reserve. Issues with
malabsorption and short bowel syndrome may occur with less than 100 cm of viable small
bowel remaining, depending on whether the ileocecal valve is present and the remaining length
of the colon. (See "Management of short bowel syndrome in adults".)

Fistula resection — Once the fistula and primary pathology (ie, source of
infection/obstruction) have been clearly defined, the segment of bowel that contains the origin
of the fistula is resected and gastrointestinal continuity reestablished. (See "Bowel resection
techniques".)

We suggest a segmental resection of the bowel containing the fistula, rather than a wedge
resection of the fistula. In a large series of patients with fistulas, patients who underwent
segmental resection of the primary disease had a significantly lower rate of fistula recurrence
than patients who had wedge resection (18 versus 33 percent) [73]. For patients with Crohn
disease, complete resection of the enterocutaneous fistula, as well as the adjacent diseased
bowel, is necessary to prevent recurrence [73].

Abdominal wall closure or reconstruction — Once an enterocutaneous fistula is resected

and gastrointestinal continuity restored, the abdomen should be closed using standard
techniques, provided this will not result in undue tension. (See "Principles of abdominal wall
closure".)

The goal of the definitive surgery in the management of enteroatmospheric fistulas, besides
closing the fistula, is to reconstruct the abdominal wall with durable, well-vascularized tissue. A
two-team approach has the advantage of providing a well-rested plastic surgeon focused on
reconstruction after a long and tedious visceral dissection by the general surgery team [10].
Closure of large or complex abdominal wall defects associated with enteroatmospheric fistulas
may require advancement flap techniques. One option for abdominal closure is the component
separation technique, provided the rectus abdominis muscle remains intact [78]. Defects up to
10 cm in the upper abdomen, 20 cm in the midabdomen, and 8 cm in the lower abdomen can
be closed using this technique. Other options may include random, pedicle, or free flaps with
microvascular reconstruction. (See "Overview of abdominal wall hernias in adults" and
"Overview of component separation".)

MORTALITY
Historically, mortality rates after developing an enterocutaneous fistula were as high as 65
percent in some series. Sepsis is responsible for 70 percent of case fatalities [13]. However,
specialized care centers have been able to reduce morbidity and mortality greatly. With modern
management strategies, most modern series report a mortality rate of 10 to 20 percent
( table 6) [7,10,13,19,59,70,79].

INFORMATION FOR PATIENTS

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics."
The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading
level, and they answer the four or five key questions a patient might have about a given
condition. These articles are best for patients who want a general overview and who prefer
short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more
sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading
level and are best for patients who want in-depth information and are comfortable with some
medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print
or e-mail these topics to your patients. (You can also locate patient education articles on a
variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Enteric fistula (The Basics)")

SUMMARY AND RECOMMENDATIONS

● A fistula is an abnormal connection between two epithelialized hollow spaces or organs.

Enterocutaneous fistulas communicate between the lumen of the gastrointestinal tract
and the skin. Enteroatmospheric fistulas communicate between the lumen of the
gastrointestinal tract and the wound of an open abdomen. (See 'Introduction' above.)

● The majority of enterocutaneous fistulas occur in the postoperative setting, usually as a

result of a bowel anastomotic leak or missed enterotomy. Approximately 20 to 30 percent
of enterocutaneous fistulas arise spontaneously, most commonly due to Crohn disease.
Other etiologies of spontaneous enteric fistula formation and persistence include foreign
body, radiation, inflammation or infection (eg, tuberculosis, actinomycosis),
epithelialization, neoplasia, and distal obstruction ( table 1). (See 'Etiology and risk
factors' above.)
● The most common clinical presentation of an enterocutaneous fistula is in a postoperative
patient who fails to recover normally from abdominal surgery. The patient often presents
first with abdominal symptoms and signs of bowel obstruction. A wound infection is then
typically recognized 7 to 10 days postoperatively, and following incisional drainage, enteric
contents appear in the surgical wound. (See 'Clinical features' above.)

● By definition, an enteroatmospheric fistula can only be diagnosed in a patient with an

open abdomen. The diagnosis can be confirmed by the presence of enteric contents
draining from an opening in a segment of bowel in the open abdominal wound. (See
'Diagnosis' above.)

● The organ of origin of an enterocutaneous or enteroatmospheric fistula is often not

defined until imaging studies can be performed. We prefer abdominal computed
tomography (CT) as the initial study for patients suspected to have an enterocutaneous or
enteroatmospheric fistula, but only after the patient has been stabilized and sepsis
treated. Other methods of identifying and characterizing enteric fistulas include
gastrointestinal contrast studies, a fistulogram, and enteric administration of dye (eg,
indigo carmine, methylene blue, charcoal). (See 'Diagnostic evaluation' above.)

● Acute management of enterocutaneous and enteroatmospheric fistulas focuses on fluid

therapy to correct volume and electrolyte deficits and treatment of infection/sepsis
( algorithm 1). In this acute phase, the etiology of the fistula is often not important.
Fistula-associated abdominal sepsis (eg, intra-abdominal abscess, gastrointestinal
perforation, or subcutaneous infection) needs to be recognized and promptly treated with
antibiotics, percutaneous catheter drainage, and/or operative drainage or source control.
However, we suggest against routine antibiotic coverage for patients with a nonseptic
enterocutaneous or enteroatmospheric fistula (Grade 2C). (See 'Acute management'
above.)

● Chronic management of enterocutaneous and enteroatmospheric fistulas entails

evaluation and treatment of fluid, electrolyte, and nutritional losses, and specialized
wound care to manage the intestinal effluent ( table 2 and algorithm 1).

• Patients with low- and high-output fistulas have different caloric and nutritional goals.
(See 'Nutritional goals' above.)

• For patients with a low-output fistula (<200 mL/day), a trial of bowel rest for several
days after initial fluid and electrolyte resuscitation ( table 3) and sepsis control may
lead to spontaneous closure of the fistula. (See 'Low-output fistulas (<200 mL/day)'
above.)
 • For patients with a low-output fistula that does not close with bowel rest, oral diet
should be started. If the fistula output increases with oral diet, and for patients with a
moderate- or high-output fistula (>200 mL/day), medical therapies to reduce fistula
output may be instituted with the goal of limiting output to <1.5 L/day. Choices of such
medications include anticathartics, somatostatins and analogues, antisecretories, and
cholestyramine ( table 4). (See 'Fistula output reduction' above.)

• For patients with fistula output >1.5 L/day, less than 75 cm of intestinal length prior to
the fistula, or intestinal discontinuity, total parenteral nutrition is required, either
exclusively or to supplemental enteral nutrition. (See 'Moderate- or high-output fistulas
(>200 mL/day)' above.)

● Approximately one-third of fistulas heal spontaneously with conservative measures within

five to six weeks. For patients with a persistent enterocutaneous or enteroatmospheric
fistula, definitive surgical fistula closure is required but should be delayed for at least three
to six months from the inciting event. High-volume centers often delay definitive
operations for 6 to 12 months ( algorithm 1). Before consideration of definitive operative
repair of fistulas, patients should be nutritionally replete, free of infection, and have
supple soft tissues adjacent to the fistula. (See 'Operative fistula closure' above.)

● The goals of definitive surgery are to resect the fistula, reestablish gastrointestinal
continuity, and provide a tension-free closure of the abdomen with well-vascularized soft
tissue. We suggest a segmental resection of the bowel containing the fistula, rather than a
wedge resection of the fistula (Grade 2C). Segmental bowel resection is associated with a
lower recurrence rate. (See 'Surgical techniques' above and 'Fistula resection' above.)

● Modern care of enterocutaneous/enteroatmospheric fistulas, often provided at specialized

centers, has reduced the mortality rate from 65 percent to 10 to 20 percent. (See
'Mortality' above.)

ACKNOWLEDGMENT

The editorial staff at UpToDate would like to acknowledge William Schecter, MD, who
contributed to an earlier version of this topic review.

Use of UpToDate is subject to the Terms of Use.

REFERENCES
 1. Teixeira PG, Inaba K, Dubose J, et al. Enterocutaneous fistula complicating trauma
laparotomy: a major resource burden. Am Surg 2009; 75:30.
2. Wercka J, Cagol PP, Melo AL, et al. Epidemiology and outcome of patients with
postoperative abdominal fistula. Rev Col Bras Cir 2016; 43:117.

3. Michelassi F, Stella M, Balestracci T, et al. Incidence, diagnosis, and treatment of enteric and
colorectal fistulae in patients with Crohn's disease. Ann Surg 1993; 218:660.
4. Annibali R, Pietri P. Fistulous complications of Crohn's disease. Int Surg 1992; 77:19.

5. Brooks NE, Idrees JJ, Steinhagen E, et al. The impact of enteric fistulas on US hospital
systems. Am J Surg 2021; 221:26.
6. Gribovskaja-Rupp I, Melton GB. Enterocutaneous Fistula: Proven Strategies and Updates.
Clin Colon Rectal Surg 2016; 29:130.
7. Osborn C, Fischer JE. How I do it: gastrointestinal cutaneous fistulas. J Gastrointest Surg
2009; 13:2068.
8. Burlew CC, Moore EE, Cuschieri J, et al. Sew it up! A Western Trauma Association multi-
institutional study of enteric injury management in the postinjury open abdomen. J Trauma
2011; 70:273.
9. Hu D, Ren J, Wang G, et al. Persistent inflammation-immunosuppression catabolism
syndrome, a common manifestation of patients with enterocutaneous fistula in intensive
care unit. J Trauma Acute Care Surg 2014; 76:725.
10. Schecter WP, Hirshberg A, Chang DS, et al. Enteric fistulas: principles of management. J Am
Coll Surg 2009; 209:484.
11. Majercik S, Kinikini M, White T. Enteroatmospheric fistula: from soup to nuts. Nutr Clin Pract
2012; 27:507.
12. Bradley MJ, Dubose JJ, Scalea TM, et al. Independent predictors of enteric fistula and
abdominal sepsis after damage control laparotomy: results from the prospective AAST
Open Abdomen registry. JAMA Surg 2013; 148:947.
13. Hollington P, Mawdsley J, Lim W, et al. An 11-year experience of enterocutaneous fistula. Br
J Surg 2004; 91:1646.
14. Schwartz DA, Loftus EV Jr, Tremaine WJ, et al. The natural history of fistulizing Crohn's
disease in Olmsted County, Minnesota. Gastroenterology 2002; 122:875.
15. Evenson AR, Fischer JE. Current management of enterocutaneous fistula. J Gastrointest
Surg 2006; 10:455.

16. Alexander ES, Weinberg S, Clark RA, Belkin RD. Fistulas and sinus tracts: radiographic
 evaluation, management, and outcome. Gastrointest Radiol 1982; 7:135.
17. Kwon SH, Oh JH, Kim HJ, et al. Interventional management of gastrointestinal fistulas.
Korean J Radiol 2008; 9:541.
18. Schein M, Decker GA. Gastrointestinal fistulas associated with large abdominal wall defects:
experience with 43 patients. Br J Surg 1990; 77:97.

19. Irving M, White R, Tresadern J. Three years' experience with an intestinal failure unit. Ann R
Coll Surg Engl 1985; 67:2.

20. Sansoni B, Irving M. Small bowel fistulas. World J Surg 1985; 9:897.
21. Reber HA, Roberts C, Way LW, Dunphy JE. Management of external gastrointestinal fistulas.
Ann Surg 1978; 188:460.
22. Martinez JL, Luque-de-Leon E, Mier J, et al. Systematic management of postoperative
enterocutaneous fistulas: factors related to outcomes. World J Surg 2008; 32:436.
23. Aguirre A, Fischer JE, Welch CE. The role of surgery and hyperalimentation in therapy of
gastrointestinal-cutaneous fistulae. Ann Surg 1974; 180:393.
24. Prickett D, Montgomery R, Cheadle WG. External fistulas arising from the digestive tract.
South Med J 1991; 84:736.

25. Schein M. What's new in postoperative enterocutaneous fistulas? World J Surg 2008; 32:336.
26. Rahbour G, Gabe SM, Ullah MR, et al. Seven-year experience of enterocutaneous fistula
with univariate and multivariate analysis of factors associated with healing: development of
a validated scoring system. Colorectal Dis 2013; 15:1162.

27. Li J, Ren J, Zhu W, et al. Management of enterocutaneous fistulas: 30-year clinical

experience. Chin Med J (Engl) 2003; 116:171.
28. Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines
for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296.
29. Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe
sepsis and septic shock. N Engl J Med 2001; 345:1368.

30. Fulcher AS, Turner MA. Percutaneous drainage of enteric-related abscesses.

Gastroenterologist 1996; 4:276.
31. Rhodes A, Evans LE, Alhazzani W, et al. Surviving Sepsis Campaign: International Guidelines
for Management of Sepsis and Septic Shock: 2016. Intensive Care Med 2017; 43:304.
32. Bleier JI, Hedrick T. Metabolic support of the enterocutaneous fistula patient. Clin Colon
Rectal Surg 2010; 23:142.
33. Samad S, Anele C, Akhtar M, Doughan S. Implementing a Pro-forma for Multidisciplinary
Management of an Enterocutaneous Fistula: A Case Study. Ostomy Wound Manage 2015;
61:46.
34. Fazio VW, Coutsoftides T, Steiger E. Factors influencing the outcome of treatment of small
bowel cutaneous fistula. World J Surg 1983; 7:481.
35. CHAPMAN R, FORAN R, DUNPHY JE. MANAGEMENT OF INTESTINAL FISTULAS. Am J Surg
1964; 108:157.

36. Polk TM, Schwab CW. Metabolic and nutritional support of the enterocutaneous fistula
patient: a three-phase approach. World J Surg 2012; 36:524.

37. Kudsk KA. Immunonutrition in surgery and critical care. Annu Rev Nutr 2006; 26:463.
38. Kudsk KA, Minard G, Croce MA, et al. A randomized trial of isonitrogenous enteral diets
after severe trauma. An immune-enhancing diet reduces septic complications. Ann Surg
1996; 224:531.
39. Schilling J, Vranjes N, Fierz W, et al. Clinical outcome and immunology of postoperative
arginine, omega-3 fatty acids, and nucleotide-enriched enteral feeding: a randomized
prospective comparison with standard enteral and low calorie/low fat i.v. solutions.
Nutrition 1996; 12:423.

40. Bower RH, Cerra FB, Bershadsky B, et al. Early enteral administration of a formula (Impact)
supplemented with arginine, nucleotides, and fish oil in intensive care unit patients: results
of a multicenter, prospective, randomized, clinical trial. Crit Care Med 1995; 23:436.

41. Lloyd DA, Gabe SM, Windsor AC. Nutrition and management of enterocutaneous fistula. Br
J Surg 2006; 93:1045.
42. Bury KD, Stephens RV, Randall HT. Use of a chemically defined, liquid, elemental diet for
nutritional management of fistulas of the alimentary tract. Am J Surg 1971; 121:174.

43. Datta V, Engledow A, Chan S, et al. The management of enterocutaneous fistula in a

regional unit in the United kingdom: a prospective study. Dis Colon Rectum 2010; 53:192.

44. Dudrick SJ, Maharaj AR, McKelvey AA. Artificial nutritional support in patients with
gastrointestinal fistulas. World J Surg 1999; 23:570.

45. Stanga Z, Brunner A, Leuenberger M, et al. Nutrition in clinical practice-the refeeding

syndrome: illustrative cases and guidelines for prevention and treatment. Eur J Clin Nutr
2008; 62:687.

46. Subramaniam MH, Liscum KR, Hirshberg A. The floating stoma: a new technique for
controlling exposed fistulae in abdominal trauma. J Trauma 2002; 53:386.
47. Freund MR, Reissman P, Spira RM, Topaz M. Innovative approach to open abdomen:
converting an enteroatmospheric fistula into an easily manageable stoma. BMJ Case Rep
2020; 13.
48. Boulanger K, Lemaire V, Jacquemin D. Vacuum-assisted closure of enterocutaneous fistula.
Acta Chir Belg 2007; 107:703.
49. Cro C, George KJ, Donnelly J, et al. Vacuum assisted closure system in the management of
enterocutaneous fistulae. Postgrad Med J 2002; 78:364.

50. Banwell P, Withey S, Holten I. The use of negative pressure to promote healing. Br J Plast
Surg 1998; 51:79.
51. Wainstein DE, Fernandez E, Gonzalez D, et al. Treatment of high-output enterocutaneous
fistulas with a vacuum-compaction device. A ten-year experience. World J Surg 2008;
32:430.
52. Fischer JE. A cautionary note: the use of vacuum-assisted closure systems in the treatment
of gastrointestinal cutaneous fistula may be associated with higher mortality from
subsequent fistula development. Am J Surg 2008; 196:1.

53. Al-Khoury G, Kaufman D, Hirshberg A. Improved control of exposed fistula in the open
abdomen. J Am Coll Surg 2008; 206:397.
54. Rao M, Burke D, Finan PJ, Sagar PM. The use of vacuum-assisted closure of abdominal
wounds: a word of caution. Colorectal Dis 2007; 9:266.
55. Jamshidi R, Schecter WP. Biological dressings for the management of enteric fistulas in the
open abdomen: a preliminary report. Arch Surg 2007; 142:793.
56. Parli SE, Pfeifer C, Oyler DR, et al. Redefining "bowel regimen": Pharmacologic strategies
and nutritional considerations in the management of small bowel fistulas. Am J Surg 2018;
216:351.
57. Coughlin S, Roth L, Lurati G, Faulhaber M. Somatostatin analogues for the treatment of
enterocutaneous fistulas: a systematic review and meta-analysis. World J Surg 2012;
36:1016.

58. Rahbour G, Siddiqui MR, Ullah MR, et al. A meta-analysis of outcomes following use of
somatostatin and its analogues for the management of enterocutaneous fistulas. Ann Surg
2012; 256:946.

59. Draus JM Jr, Huss SA, Harty NJ, et al. Enterocutaneous fistula: are treatments improving?
Surgery 2006; 140:570.

60. Alivizatos V, Felekis D, Zorbalas A. Evaluation of the effectiveness of octreotide in the

conservative treatment of postoperative enterocutaneous fistulas. Hepatogastroenterology
 2002; 49:1010.

61. Wiedermann CJ, Reinisch N, Braunsteiner H. Stimulation of monocyte chemotaxis by

human growth hormone and its deactivation by somatostatin. Blood 1993; 82:954.

62. Lattuada D, Casnici C, Crotta K, et al. Inhibitory effect of pasireotide and octreotide on
lymphocyte activation. J Neuroimmunol 2007; 182:153.
63. El Hajj II, Imperiale TF, Rex DK, et al. Treatment of esophageal leaks, fistulae, and
perforations with temporary stents: evaluation of efficacy, adverse events, and factors
associated with successful outcomes. Gastrointest Endosc 2014; 79:589.

64. Lamazza A, Fiori E, Schillaci A, et al. Recurrent rectovaginal fistula: treatment with self-
expanding metal stents. Endoscopy 2015; 47 Suppl 1 UCTN:E149.

65. Haito-Chavez Y, Law JK, Kratt T, et al. International multicenter experience with an over-the-
scope clipping device for endoscopic management of GI defects (with video). Gastrointest
Endosc 2014; 80:610.

66. Truong S, Böhm G, Klinge U, et al. Results after endoscopic treatment of postoperative
upper gastrointestinal fistulas and leaks using combined Vicryl plug and fibrin glue. Surg
Endosc 2004; 18:1105.

67. Böhm G, Mossdorf A, Klink C, et al. Treatment algorithm for postoperative upper
gastrointestinal fistulas and leaks using combined vicryl plug and fibrin glue. Endoscopy
2010; 42:599.
68. Filgate R, Thomas A, Ballal M. Treatment of foregut fistula with biologic plugs. Surg Endosc
2015; 29:2006.
69. Wu X, Ren J, Gu G, et al. Autologous platelet rich fibrin glue for sealing of low-output
enterocutaneous fistulas: an observational cohort study. Surgery 2014; 155:434.
70. Visschers RG, van Gemert WG, Winkens B, et al. Guided treatment improves outcome of
patients with enterocutaneous fistulas. World J Surg 2012; 36:2341.

71. Campos AC, Andrade DF, Campos GM, et al. A multivariate model to determine prognostic
factors in gastrointestinal fistulas. J Am Coll Surg 1999; 188:483.

72. Hill GL. Operative strategy in the treatment of enterocutaneous fistulas. World J Surg 1983;
7:495.

73. Lynch AC, Delaney CP, Senagore AJ, et al. Clinical outcome and factors predictive of
recurrence after enterocutaneous fistula surgery. Ann Surg 2004; 240:825.

74. Becker HP, Willms A, Schwab R. Small bowel fistulas and the open abdomen. Scand J Surg
2007; 96:263.
 75. Jernigan TW, Fabian TC, Croce MA, et al. Staged management of giant abdominal wall
defects: acute and long-term results. Ann Surg 2003; 238:349.
76. Owen RM, Love TP, Perez SD, et al. Definitive surgical treatment of enterocutaneous fistula:
outcomes of a 23-year experience. JAMA Surg 2013; 148:118.

77. Marinis A, Gkiokas G, Argyra E, et al. "Enteroatmospheric fistulae"--gastrointestinal

openings in the open abdomen: a review and recent proposal of a surgical technique.
Scand J Surg 2013; 102:61.

78. Shestak KC, Edington HJ, Johnson RR. The separation of anatomic components technique
for the reconstruction of massive midline abdominal wall defects: anatomy, surgical
technique, applications, and limitations revisited. Plast Reconstr Surg 2000; 105:731.

79. Fischer JE, Evenson AR. Gastrointestinal-cutanous fistulae. In: Mastery of Surgery, 5th, Fisch
er JE, Bland KI (Eds), Lippincott, Philadelphia 2007. Vol 2, p.1401.
Topic 15157 Version 26.0
GRAPHICS

Causes of enterocutaneous fistulae

Cause Frequency (percent)

Postoperative 85

Spontaneous 15

Crohn disease 39

Ulcerative colitis 13

Malignancy 9

Radiation 6

Diverticular disease 5

Other* 27

* "Other" includes rare conditions such as enteric vasculitis or myopathy or no associated condition.

Reproduced with permission from: Fischer JE, Evenson AR. Gastrointestinal-cutaneous fistulae. In: Mastery of Surgery, Fischer JE
(Ed), Lippincott Williams & Wilkins 2007. Copyright © 2007 Lippincott Williams & Wilkins. www.lww.com.

Graphic 76953 Version 7.0

Enteroatmospheric fistula

Enteroatmospheric or exposed fistulas occur in the midst of an open abdomen with no overlying soft
tissue. These fistulas occur when the abdomen is left open after trauma or emergency surgery. This
photograph shows the appearance of superficial exposed fistulas draining atop the granulating wound of
a frozen abdomen with an obliterated peritoneal cavity.

Graphic 58058 Version 2.0

Phases of management for enterocutaneous fistulae

Phase Description Timing

Stabilization Rehydration 24-48 h

Correction of anemia
Electrolyte repletion
Drainage of sepsis
Control of fistula drainage
Local skin care measures
Commencement of nutritional support

Investigation Fistulogram to define anatomy 7-10 d

CT/US/MRI to localize collections and guide
drainage

Decision Assess likelihood of nonoperative closure 7-10 d to 4-6 wk

Plan therapeutic course
Decide optimal surgical timing

Definitive Plan operative approach 4-6 wk or if spontaneous closure

therapy Bowel resection with end-to-end anastomosis unlikely

Secure abdominal closure (+/- flap)

Gastrostomy
Jejunostomy

Healing Continue nutrition support 5-10 d after closure

Transition to total oral/enteral feedings
Physical and emotional rehabilitation

CT: computed tomography; US: ultrasound; MRI: magnetic resonance imaging.

Reproduced with permission from: Fischer JE, Evenson AR. Gastrointestinal-cutaneous fistulae. In: Mastery of Surgery, Fischer JE
(Ed), Lippincott Williams & Wilkins 2007. Copyright © 2007 Lippincott Williams & Wilkins. www.lww.com.

Graphic 57027 Version 7.0

Management of enterocutaneous and enteroatmospheric fistulas
TPN: total parenteral nutrition.

Graphic 118853 Version 1.0

Gastrointestinal tract secretions, electrolyte composition, and suggested
replacement

Sodium Potassium Bicarbonate Chloride Volume

Source Replacement
(mEq/L) (mEq/L) (mEq/L) (mEq/L) (mL/d)

Gastric 60 10 0 90 2000 to 0.45 NS + 10 K

2500

Pancreatic 140 5 90 to 110 30 to 45 1000 NS + 10 K +

HCO3

Bile 140 5 35 100 1500

Small 100 to 130 15 25 to 35 100 to 140 3500 NS + 10 K

bowel

Colon 50 30 50 50 1000 to 0.45 NS + 20 K

(diarrhea) 4000

Original figure modified for this publication. From: Parli SE, Pfeifer C, Oyler DR, et al. Redefining "bowel regimen": Pharmacologic
strategies and nutritional considerations in the management of small bowel fistulas. Am J Surg 2018; 216:351. Table used with the
permission of Elsevier Inc. All rights reserved.

Graphic 119174 Version 2.0

Negative pressure wound therapy

Negative pressure wound therapy. The foam insert (sponge) is placed within the wound and covered by a
clear, vapor-permeable, plastic dressing. Continuous subatmospheric pressure (suction) applied through
the tube causes fluid to flow out of the wound (arrows).

Graphic 50588 Version 5.0

Negative pressure wound dressing in situ

Reproduced with permission from: Fischer JE, Evenson AR. Gastrointestinal-cutaneous fistulae. In: Mastery of Surgery, Fischer JE
(Ed), Lippincott Williams & Wilkins 2007. Copyright © 2007 Lippincott Williams & Wilkins. www.lww.com.

Graphic 63582 Version 8.0

Antimotility agents used for high-output fistulas

Initial
Drug Route Frequency Titration Max dose Cost
dose

Loperamide 4 mg PO Three times By 2 mg 16 mg/day $

daily with
meals or
every 6
hours with
enteral
nutrition

Diphenoxylate/atropine 2.5 PO Three times By 1 tablet 2 tablets four $$

mg/0.025 daily with times daily
mg meals or (20 mg
(1 tablet) every 6 diphenoxylate)
hours with
enteral
nutrition

Pantoprazole 40 mg IV Twice daily None 40 mg twice $$$

daily

Codeine 15 mg PO Three times By 15 mg 45 mg four $$

daily with times daily
meals, up to
four times
daily

Octreotide 100 mcg SC Three times None None $$$

daily

Clonidine 0.3 mg Transdermal Every 7 days None 0.3 mg every 7 $$$$

days

PO: oral; IV: intravenous; CNS: central nervous system; SC: subcutaneous; HR: heart rate; BP: blood
pressure.

* Prices estimated based on approximate inpatient acquisition cost:

$: less than $1 per day
$$: more than $1 per day
$$$: more than $5 per day
$$$$: more than $10 per day
Reproduced from: Parli SE, Pfeifer C, Oyler DR, et al. Redefining "bowel regimen": Pharmacologic strategies and nutritional
considerations in the management of small bowel fistulas. Am J Surg 2018; 216:351. Table used with the permission of Elsevier Inc.
All rights reserved.

Graphic 119176 Version 1.0

Predictors of spontaneous closure of enterocutaneous fistulas

Factor Likely to close Unlikely to close

Anatomical location Oropharyngeal Gastric

Esophageal Ligament of Treitz
Duodenal stump Ileal
Lateral duodenal
Pancreaticobiliary
Jejunal

Tract length >2 cm <2 cm

Defect size <1 cm 2 >1 cm 2

Fistula output Decreasing Stable or increasing

Surrounding bowel Healthy Distal obstruction or stricture

Abscess
Active inflammation
Bowel discontinuity

Etiology Appendicitis Crohn disease

Diverticulitis Malignancy
Postoperative Radiation
Foreign body (mesh)

Nutritional status Well nourished Malnourished

Sepsis Absent Present

Reproduced with permission from: Fischer JE, Evenson AR. Gastrointestinal-cutaneous fistulae. In: Mastery of Surgery, Fischer JE
(Ed), Lippincott Williams & Wilkins 2007. Copyright © 2007 Lippincott Williams & Wilkins. www.lww.com.

Graphic 76451 Version 10.0

Mortality of gastrointestinal-cutaneous fistulae

1946-1959 45 percent (138 patients - MGH)

1960-1970 15 percent (119 patients - MGH)

1970-1975 19 percent (145 patients - MGH)

1982-1991 20 percent (79 patients - UH)

Reproduced with permission from: Fischer JE, Evenson AR. Gastrointestinal-cutaneous fistulae. In: Mastery of Surgery, Fischer JE
(Ed), Lippincott Williams & Wilkins 2007. Copyright © 2007 Lippincott Williams & Wilkins. www.lww.com.

Graphic 54412 Version 8.0

Contributor Disclosures
Sharon L Stein, MD, FACS, FASCRS No relevant financial relationship(s) with ineligible companies to
disclose. Eileen M Bulger, MD, FACS Equity Ownership/Stock Options: Opticyte [Shock].
Consultant/Advisory Boards: Opticyte [Shock]. All of the relevant financial relationships listed have been
mitigated. J Thomas Lamont, MD Equity Ownership/Stock Options: Allurion [Weight loss].
Consultant/Advisory Boards: Teledoc [Gastrointestinal diseases]. All of the relevant financial relationships
listed have been mitigated. David I Soybel, MD No relevant financial relationship(s) with ineligible
companies to disclose. Wenliang Chen, MD, PhD No relevant financial relationship(s) with ineligible
companies to disclose.

Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must
conform to UpToDate standards of evidence.

Conflict of interest policy