Eur J Trauma Emerg Surg (2011) 37:209–213
DOI 10.1007/s00068-011-0104-7
REVIEW ARTICLE
The surgical anatomy and etiology of gastrointestinal fistulas
J. Pfeifer • G. Tomasch • S. Uranues
Received: 17 February 2011 / Accepted: 1 March 2011 / Published online: 22 April 2011
Ó Springer-Verlag 2011
Abstract
Background Fistulas are abnormal communications
between two epithelial surfaces, either between two por-
tions of the intestine, between the intestine and some other
hollow viscus, or between the intestine and the skin of the
abdominal wall. The etiology of intestinal fistulas is in
most cases a result of multiple contributing factors. Despite
significant advances in their management over the past
decades, intestinal fistulas remain a major clinical problem,
with a high overall mortality rate of up to 30% due to the
high rate of complications. This paper aims to describe
classification systems based on the anatomy, physiology
and etiology that may be helpful in the clinical manage-
ment of intestinal fistulas.
Methods On the basis of anatomical differences, fistulas
can be classified based by the site of origin, by site of their
openings, or as simple or complex. Physiologic classification
as low, moderate or high output fistulas is most useful for the
non-surgical approach. Concerning the etiology, we classi-
fied the possible causes as (postoperative) trauma, inflam-
mation, infection, malignancy, radiation injury or congenital.
Conclusion Fistula formation can cause a number of
serious or debilitating complications ranging from distur-
bance of fluid and electrolyte balance to sepsis and even
death. They still remain an important complication fol-
lowing gastrointestinal surgery.
Keywords Gastrointestinal fistula
Fistula
Anatomy

Etiology
J. Pfeifer
G. Tomasch
S. Uranues (&)
Department of Surgery, Section for Surgical Research,
Medical University of Graz, Auenbruggerplatz 29,
8036 Graz, Austria
e-mail: selman.uranues@medunigraz.at
Introduction
Fistulas are abnormal communications between two epi-
thelial surfaces, either between two portions of the intes-
tine, between the intestine and some other hollow viscus, or
between the intestine and the skin of the abdominal wall.
Despite significant advances in their management over the
past few decades, intestinal fistulas still present a major
clinical problem, with a disproportionally high overall
mortality rate of up to 30%, due to the high rate of com-
plications including sepsis, malnutrition, and electrolyte
imbalance [1]. Spontaneous fistula closures are reported to
lie between 19.9 and 81.4% [2, 3]. Operative intervention
is necessary in 13–80% of patients to achieve closure,
depending on the anatomical and physiological parameters
of the fistula [4]. The aim of this paper is to describe
classification systems used in terms of anatomy, physiol-
ogy, and etiology, that may be helpful in the clinical
management of intestinal fistulas.
General remarks
The treatment of gastrointestinal fistulas is a complex
challenge for every gastrointestinal surgeon. Such patients
are usually best managed by a multidisciplinary team,
consisting of a surgeon, gastroenterologist, dietitian,
enterostomal therapy nurse, and general nursing staff. The
team members must treat aggressively in order to prevent
mortality (which has decreased significantly worldwide in
recent decades), and to improve patients’ quality of life,
which can be significantly diminished for a long period of
time. Basically, surgical treatment is reserved for patients
whose fistulas do not resolve with medical and non-surgical
therapy.
210
Gastrointestinal fistulas are rare, and therefore random-
ized studies are lacking and management is usually based
on expert opinions. There are, however, a few generally
accepted empirical principles: (1) treatment of sepsis and
nutritional status are highly relevant for a good outcome,
(2) obstruction distal to the fistula usually prevents spon-
taneous healing of the fistula, (3) spontaneous closure is
uncommon in fistulas with Crohn’s disease or a malig-
nancy, (4) low-output fistulas have a greater chance of
healing than high-output fistulas, and (5) reconstructive
surgery should usually be postponed for 3–6 months [1, 4,
5].
Classification
Many classification schemes have been used to define fis-
tulas of the gastrointestinal tract. Anatomical, physiologi-
cal, and etiological classification schemes are the most
commonly used. Each type of classification system carries
specific implications, with regard to the likelihood of
spontaneous closure, prognosis, operative timing, and non-
operative care planning.
Anatomical classification
Site of origin
Gastrointestinal fistulas are generally named according to
the anatomical components involved, and virtually every
imaginable combination has been reported in the medical
literature. Anatomical information has prognostic signifi-
cance with regard to spontaneous healing of the fistula
tract. Anatomical segments with favorable closure rates
include oropharyngeal, esophageal, duodenal stump, pan-
creatobiliary, and jejunal. Anatomical features associated
with non-healing fistulas include large adjacent abscesses,
intestinal discontinuity, distal obstruction, poor adjacent
bowel, short fistula tracts (\2 cm in length), enteral defects
[1 cm, fistulas with complete epithelialization, and fistu-
las arising from special segments such as the stomach,
lateral duodenum, ligament of Treitz, and ileum [6].
Site of the openings
Acquired gastrointestinal fistulas can be categorized as
external or cutaneous if they communicate with the skin
surface, or internal if they connect to another internal organ
system or space, including elsewhere along the gastroin-
testinal tract itself. Internal gastrointestinal fistulas can be
further divided into two types: intestinal and extraintesti-
nal. Intestinal fistulas refer to a gut-to-gut connection and
may consist of any combination of stomach, small bowel,
J. Pfeifer et al.
and colon. An enteroenteric fistula may refer to any
intestinal fistula in the generic sense, although some may
restrict this term to small bowel fistulas only. Extraintes-
tinal internal fistulas imply communication of the gastro-
intestinal tract with another organ system, such as the
genitourinary system, biliary tree, or respiratory tract.
Severity classification
Fistulas can be classified in anatomical terms as simple or
complex. Simple fistulas have a short, direct tract; there are
no associated abscesses and no other organs are involved.
There are two types of complex fistulas. A Type 1 complex
fistula is associated with an abscess or involves multiple
organs. A Type 2 complex fistula opens into the base of a
disrupted wound (exposed fistula). By nature, complex
fistulas have higher morbidity and mortality rates, as well
as a lower rate of spontaneous closure [7].
Physiological classification
Physiological classification is most useful if a non-surgical
conservative treatment approach is selected. The most
useful parameter is the output of the fistula. We distinguish
among low output (\200 ml/24 h), moderate output
(200–500 ml/24 h), and high output fistulas ([500 ml/
24 h). The problem with high output secretion is the danger
of intestinal failure due to reduced intestinal absorption, so
that macronutrient and/or water and electrolyte supple-
ments are needed to maintain health or growth. By defi-
nition, in mild intestinal failure oral supplementation or
dietary modification is sufficient. In severe intestinal failure
parenteral nutrition and/or fluid replacement are needed.
Etiology
The etiology of intestinal fistula formation is important for
subsequent treatment. Table 1 provides an overview of the
etiology of acquired enterocutaneous fistulas. Not surpris-
ingly, many cases are the result of multiple contributing
factors; common examples include cancer patients who
have undergone radiation therapy and patients with Crohn’s
disease who have undergone prior bowel surgery.
Congenital
First, it is useful to differentiate between congenital and
acquired fistulas, since their clinical settings and implica-
tions obviously differ greatly. Congenital gastrointestinal
fistulas are best understood in the light of their embryo-
logical origin and include such entities as bronchial, tra-
cheoesophageal, and omphalomesenteric fistulas. The most
The surgical anatomy and etiology of gastrointestinal fistulas 211

Table 1 Etiology of acquired enterocutaneous fistulas Patients undergoing extensive adhesiolysis are at highest
(I) Post-operative occurrence
risk of inadvertent enterotomies. An enterotomy in and of
(A) Anastomotic problems
itself is not a complication, but failure to recognize and
adequately repair an enterotomy may lead to serious
(a) Technical factors Tension
problems. The result of leakage of bowel content into the
Blood supply
abdomen can be either peritonitis within 24–48 h or
Technique
abscess formation. The latter may erode the abdominal
(b) Intestinal factors Inflammation
wall, mainly at the incision or drainage site, leading to an
Ischemia
enterocutaneous fistula. Therefore, in cases with any form
Infection
of adhesiolysis, the entire bowel should be inspected at the
Malignancy
end of the procedure. In cases with multiple enterotomies
(c) Systemic factors Malnutrition
in a short bowel segment, resection of the involved seg-
Steroids
ment is recommended. The same is true for inadvertent
Immunosuppression
damage to the bowel mesentery, which otherwise can lead
Malignancy
to partial necrosis of the bowel wall and secondary fistula
(d) Systemic disease Diabetes mellitus formation.
Renal failure Anastomotic complications are the most feared in
(B) Incidental injury colorectal surgery. Often anastomotic complications are
(a) Lysis of adhesions related to technical factors such as ischemia, tension, poor
(II) Spontaneous occurrence technique, stapler malfunction or to a pre-existing condi-
(A) Intrinsic disease tion such as systemic hypotension, local sepsis, poor
(a) Inflammation e.g., IBD, diverticulitis nutrition, immunosuppression, morbid obesity, and/or
(b) Infection Tuberculosis sequelae to radiation exposure.
Actinomycosis The increased use of meshes and other biomaterials in
Amoebiasis general surgery, such as for closure of abdominal wall
Other defects or hernia repair, may lead to migration and erosion
(c) Malignancy of the bowel wall with enterocutaneous fistula formation
(d) Ischemia Embolus [9–11]. While older mesh materials must usually be ex-
Thrombosis planted to allow wound healing, newer materials can also
Low blood flow be used with good results in suspected contaminated
(e) Foreign body wounds, as in parastomal hernia repair [12].
(f) Collagen vascular disease Intraperitoneal drainage tubes can erode into the intes-
(g) Radiation tinal lumen and cause enterocutaneous fistulas. While sur-
(B) Extrinsic disease geons long believed that preventing collection of fluid or
(a) Trauma hematoma in the pelvis would minimize the risk of an
(b) Other organs anastomotic leak, more recent data have proven neither
benefit nor harm [13–15]. Penetration of the intestinal wall
by a foreign body (e.g., ingested metallic objects, toothpick,
frequently seen congenital enterocutaneous fistula is a chicken or fish bone) can lead to enteroenteric fistula for-
patent ductus omphaloentericus, whereby the appearance mation when adjacent bowel loops erode [16, 17]. Inter-
of feculent material at the umbilicus suggests the diagnosis estingly, penetrating trauma (i.e., stab wound) rarely causes
[8]. Otherwise, congenital fistulas are beyond the scope of enterocutaneous or enteroenteric fistula formation [18].
this review and will not be considered further here.
Infection
Trauma
Intestinal infections that erode through the wall cause an
The most common cause for intestinal fistula formation is abscess and may lead to fistula formation between adjacent
(post-operative) trauma, comprising more than 90% in viscus or solid organs, or externally. Intestinal fistula for-
some studies. Approximately 50% of small intestinal mation due to infection is more frequent in developing
fistulas form because of inadvertent enterotomies in countries [19]. The most common cause of non-traumatic
patients who have not undergone intestinal anastomosis. perforation of the small intestine is typhoid (46.4%), fol-
The remaining 50% are related to complete or partial dis- lowed by non-specific inflammation (39.2%), tuberculosis
ruption of intestinal anastomotic suture lines [7]. (12.8%), and malignant neoplasm (1.6%) [20]. Other
212
possible causes are salmonella, amebiasis, actinomycosis,
coccidioidomycosis, cryptosporidiosis, HIV, and possibly
hookworms [19, 20]. A solid organ abscess, such as an
amebic hepatic abscess, can erode into small bowel loops.
Similarly, rupture of a perinephric abscess can cause a
nephroenteric fistula. Diverticular and appendiceal
abscesses can also cause enteroenteric, enterovesical, en-
terovaginal or enterocutaneous fistulas. Appendico-cuta-
neous fistulas are uncommon and occur most frequently
after percutaneous drainage of an appendiceal abscess [21,
22]. In patients with Crohn’s disease, fistulas that occur in
the right lower quadrant after an appendectomy usually
arise from the involved terminal ileum and not from the
appendiceal stump [23, 24].
Inflammation
Fistula formation is a typical feature of Crohn’s disease,
occurring in up to 20–40% of patients described in surgical
literature [25, 26]. Sinus tracts and fistulas often involve the
distal small bowel, and peritoneal abscess or phlegmon may
be an associated finding. The chronic transmural inflam-
mation of the intestinal wall in Crohn’s disease causes
healthy organ structures to adhere to the serosa of the dis-
eased segment. When inflammation gradually progresses,
microabscess formation and internal perforation in the
ulcerated areas are the consequences. The ulcerated areas
may then penetrate through the bowel wall into the adjacent
involved structure, leading to formation of enteroenteric,
enterovesical, enterovaginal or perineal fistulas; most
commonly, adjacent bowel loops, bladder, colon, and
vagina are affected. Another possibility in Crohn’s disease
is the formation of interloop abscesses that may also erode
into adjacent bowel loops, resulting in fistula formation.
Radiation injury
Delayed or chronic radiation lesions can be seen from
6 months to 30 years after therapy, but usually manifest
themselves within 1–5 years. The pathophysiological
mechanism is mainly delayed submucosal damage to the
blood vessels and connective tissue of the bowel wall,
which causes progressive ischemia. Erosions and dense
adhesions can result in enteroentetric, enterovaginal or en-
terovesicular fistula. While several drugs are used to reduce
the side-effects of radiation therapy, reduction of radiation
dose and field size are still the most important factors in the
prevention of acute and chronic radiation enteritis [27].
Malignancy
As in the case of the destruction of tissue due to radio-
therapy, degeneration of malignant tumors of the intestine
J. Pfeifer et al.
or solid abdominal structures can lead to erosion into
adjacent bowel loops and subsequently to fistulas, which do
not usually heal spontaneously.
Radiological diagnosis
Radiology has come to play a prominent role in the diag-
nosis of gastrointestinal fistulas and has increasing thera-
peutic potential. This development is surely the result of
the application of modern diagnostic tools such as ultra-
sonography, computed tomography, and magnetic reso-
nance imaging. As an alternative to surgery, interventional
radiology and percutaneous techniques have been shown to
be advantageous, lowering the morbidity and mortality
rate, and allowing superior access to the fistulous tracts
with fistulography. Collaboration between the interven-
tional radiologist and surgeons can significantly improve
treatment results [28].
Enterocavitary fistulas occur or develop with an inci-
dence of 15–44% [29, 30]. More than 80% of these fistulas
can be treated with percutaneous drainage [31]. With
interventional radiology, it is also possible to drain com-
plications following enterocutaneous fistulas such as
residual abscesses or fluid collections that occur after the
removal of long-term surgical drains.
Discussion
Regardless of the cause, discharge of intestinal content
leads to a cascade of after effects from localized infection
to abscess formation, and finally to fistula formation at the
septic focus. According to their etiology, more than 60% of
gastrointestinal fistulas are accidental, if there is no distal
passage obstruction, no foreign body, and low-output
secretion without active infection.
The natural course of the underlying disease will usually
determine the further course. Some studies show that post-
operative fistulas develop more often after cancer surgery
than after operations for benign disease. Fistula formation
can cause a number of serious or debilitating complica-
tions, ranging from disturbance of fluid and electrolyte
balance to sepsis and even death. The patients will almost
always suffer from severe discomfort and pain. They may
also have psychological problems, including anxiety over
the course of their disease, and poor body image due to the
malodorous drainage fluid [32].
The most important therapeutic measures are adequate
nutrition, control and maintenance of the fistula drainage
site, appropriate treatment of infection, and avoidance of
sepsis. Spontaneous healing of gastrointestinal fistulas has
been well documented in quite a large proportion of
patients.
The surgical anatomy and etiology of gastrointestinal fistulas
Therapy has improved over time with the introduction of
parenteral nutrition, intensive post-operative care, and
advanced surgical techniques, which have reduced mor-
tality rates. The number of patients suffering from gastro-
intestinal fistulas has not, however, declined substantially.
This can partly be explained by the fact that with improved
care, more complex surgery is being performed on patients
with more advanced or complicated disease, who are
generally at higher risk. Gastrointestinal fistulas thus
remain an important complication following gastrointesti-
nal surgery [32].
Conflict of interest None.
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