| - Colon | |
| - Biliary tree | |
| - Pancreas | |
| Prognosis | |
| Conclusion | |
| Recommendations | |
Introduction
Acquired gastrointestinal fistulae are amongst the most dreaded complications
in abdominal surgery. Sadly, every surgeon is familiar with the patient who,
after intestinal resection and anastomosis, develops a low-grade fever and
prolonged ileus and in whom the subsequent discharge of bile stained fluid
through the incision heralds the onset of an enterocutaneous fistula. While
post-operative iatrogenic fistulae still account for 80% of cases, spontaneous
intestinal fistulae occur as complications of a wide variety of pathologic
processes. Together, these gastrointestinal fistulae pose extremely complicated
problems for the clinician and are associated with a great deal of morbidity.
Prior to the advent of nutritional therapy and intensive care, mortality rates
of over 40% were common. This review will discuss the management of those
acquired gastrointestinal fistulae common in the developing world. Excellent
reviews are available (1-4). Despite their
importance, we will not deal with obstetric fistulae, congenital fistulae
or fistulae in ano. Neither will we devote much time to the two most common
causes of spontaneous intestinal fistulae in the industrialized world –
Crohn’s disease (5-7) and colonic
diverticulitis (8). Aortoenteric fistulae are similarly ignored.
Classification
A fistula is defined as an abnormal communication between two epithelialised
surfaces (1). Intestinal fistulae can be internal or external
(enterocutaneous). This differentiation is clinically important because, properly
managed, 70% of external fistulae will close spontaneously, whereas internal
fistulae seldom do so. Similarly, fistulae can be divided into end or lateral
- based on their relation to the viscus from which they arise. Of even greater
significance is whether intestinal continuity is maintained. Furthermore external
fistulae can be classified as to output. High-output fistulae discharge more
than 500ml/day; low-output less than this. In the case of pancreatic fistulae
a high-output fistula is one which produces more than 200 ml/day. High output
fistulae lead to more serious metabolic disturbances and have higher mortality
rates.
Appropriate classification is important because it is predictive of whether
spontaneous closure can be anticipated (9). Spontaneous closure
is more likely if: bowel continuity is maintained, there is an end fistula,
there is no abscess, the adjacent bowel is healthy and there is no distal
obstruction, the fistula tract is not epithelialized or more than 2 cm in
length and the bowel defect is less than 1 cm in diameter. Gastric, lateral
duodenal, ligament of Treitz and ileal fistulae are the least likely to close
with non-operative therapy.
Aetiology
The aetiology of acquired gastrointestinal fistulae is extremely broad (10).
Of the spontaneous disease processes which may result in fistulization, inflammation
is the most important. All the standard organ diseases: peptic ulcers, cholecystitis,
neonatal enterocolitis (11;12), appendicitis
(13), pancreatitis and late presentation of strangulated
inguinal hernia (14) can give rise to fistulae. Radiation
(15;16) is a prominent source. Certain
infections such as tuberculosis (17;18)
are known to cause fistulae. The known association of abdominal tuberculosis
and HIV infection creates a particularly dangerous setting in which gastrointestinal
fistulae may occur. In a report of 46 patients with enterocutaneous fistulae
from India, tuberculosis and enteric fever were the most common underlying
pathologies (19). In a report from Nigeria of 17 cases of
post-operative fistulae appendicitis and surgery for obstruction were the
commonest antecedents (20). Trauma,(21)
including burns (22) and foreign bodies (23)
are recognized causes; as is malignancy (24;25).
The causes of the iatrogenic or post-operative intestinal fistula are felt
to be technical errors, poor suture material, shock and intra-operative blood
loss, ischemia and/or tension on the suture line, and distal obstruction (3).
Whether the routine use of drains after intestinal resection is of benefit
or is a source of complications is much debated. Gonzalez-Pinto (9)
is an advocate. However, there is now good evidence that prophylactic drains
do not reduce complications after hepatic, colon or rectal resection, cholecystectomy
and possibly pancreatic resection and do harm after appendectomy (26).
There is a lack of evidence on which to make recommendations about the use
of prophylactic drains after upper GI resection.
A wide variety of surgical procedures have been implicated in the development
of gastrointestinal fistulae: minimal access approaches and the placement
of foreign bodies (27); pancreaticoduodenectomy which carries
the greatest risk; surgery for obstruction, cancer and inflammatory bowel
disease; even herniorraphy (28-30). Damage
control surgery using the open abdomen technique for trauma and the abdominal
compartment syndrome is associated with a 8% risk of fistula formation (31;32).
Malnutrition, underlying infection, immunosuppression and advanced age play
their role; as does surgeon inexperience.
Clinical Spectrum
The clinical presentation may be obvious when bile stained fluid discharges
from the operative wound. The prodrome to this disaster may be subtle. The
patient with a developing post-operative iatrogenic fistula is one who is
not recovering normally, suffers from excessive abdominal pain and tenderness,
ileus, fever and leukocytosis. Wound changes develop with swelling, infection
and discharge. Wound discharge usually commences 7-10 days after initial surgery.
The enteric nature of the discharge is diagnostic. If there is doubt, methylene
blue ingestion may confirm the initial suspicion.
Patients with post-operative intestinal fistulae need to be distinguished
from those with peritonitis from anastomotic dehiscence. These latter are
toxic and sick with an acute abdomen. They require prompt resuscitation and
laparotomy with lavage and either repair or exteriorization of the defect
(33). In contra-distinction fistula patients will be harmed
by immediate surgery to repair the defect.
Internal fistulae are likely to be more subtle with symptoms of sepsis, diarrhea,
rectal bleeding, weight loss and exacerbation of the underlying disease. Obstruction
may arise from gallstone ileus through a cholecystoduodenal fistula (34);
pneumaturia and recurrent UTI are indicative of an enterovesicle fistula (35).
Sometimes, extensive investigation results in the diagnosis of an otherwise
unsuspected fistula.
Diagnosis
The goal of diagnostic efforts is the precise anatomic classification of the
fistula. In an external fistula the discharge should be accurately measured
and analyzed for amylase and bacteriology. The patient’s general condition,
haemoglobin and WBC, electrolytes including acid-base balance, and nutritional
status including albumin and where possible transferrin; all should be assessed
(9).
Further diagnostic work-up includes upper and lower GI endoscopy, upper and
lower intestine radiography with water soluble contrast medium, fistulography,
ultrasound and CT (36) or MRI scanning where available (10).
Fistulography with flourosocopy is especially useful and is likely to be most
widely available. Water soluble contrast should be used, recognizing the risk
of barium contamination of the peritoneum. When fistulalization to extraintestinal
viscera is suspected, additional imaging techniques may be necessary: biliary
tree – ERCP and cholangiography; bladder – cystoscopy, pyelography
and cystograms.
General Principles of Management
The management of gastrointestinal fistulae, particularly enterocutaneous
ones, require an integrated multi-disciplinary approach aimed at fluid resuscitation,
controlling sepsis, controlling and reducing fistula output, protecting skin
and wound care, providing nutritional support followed by the planning and
institution of definitive surgical repair, when necessary. Various protocols
have been developed based on the time course of the different treatment phases
(1;4).
Phase 1- Recognition and
Stabilization
The following problems need to be addressed within the first 48 hours after
fistula recognition (37):
Resuscitation
Restoration of circulatory volume in a dehydrated or shocked patient is the
sine qua non of surgical care. Generally crystalloid infusion is adequate.
Anemia should be corrected to recognized standards (usually > 7g/dL). Gastric
fistulae result in acid losses and hypokalemic metabolic alkalosis; pancreatic
and upper small bowel fistulae may cause significant bicarbonate deficits,
hyponatremia, hypokalemia and metabolic acidosis. The importance of correcting
serum electrolytes and acid base imbalances cannot be overemphasized.
Sepsis
Untreated sepsis is the major cause of mortality in all studies of fistula
patients and undrained abscesses are recognized as a major impediment to fistula
closure. Empiric broad spectrum antibiotics should be instituted early on
in febrile or septic patients. However adequate drainage of intra-abdominal
abscesses is mandatory. This can be achieved either through percutaneous techniques
or through open drainage. In Kaur’s study from India where tuberculosis
and enteric fever predominate as causes, early ileostomy for control of sepsis
seemed to be useful in reducing mortality rates (38). Ongoing
sepsis from indwelling lines and catheters also needs to be considered.
Wound care and control of drainage
Fistula effluent contains potent digestive enzymes which can cause maceration
of the surrounding skin and preventing this is an immediate priority. Fortunately
a wide variety of products are available (1;39;40).
The participation of an enterostomal therapist, if available, is strongly
recommended. Various powders, ointments and sealants are used to protect the
skin from fistula effluent. Stomahesive and karaya paste ought to be commonly
available. Very low output fistulae (< 150ml.day) may respond to skin protection
and hydrofiber dressings alone (39). Larger volume fistulae
require the application of pouches to collect the effluent. The system needs
to be adaptable to deformities of the abdominal wall. Control of larger volume
fistulae may require insertion of catheters, such as foley catheters, or even
sump systems (4) using suction to control the discharge.
Bowel rest and nasogastric suction are often necessary as early measures to
control ileus and reduce drainage. The ongoing need for nasogastric suction
in the absence of ileus has been questioned (4). The use
of proton pump inhibitors to reduce gastric acid secretion is recommended.
Anticholinergic agents may be used to decrease GI motility. The use of somatostatin
and its analogue, octreotide, will be discussed further below. These agents
reduce gastric, pancreatic, biliary and enteric secretions and GI motility
through blocking the release of gastrointestinal hormones.
A new concept which addresses both wound care and fistula drainage is the
vacuum-assisted closure (VAC) system. Introduced initially to handle chronic
large open wounds, this system (41) has a number of components:
a) a sterile black polyurethane (PU) foam dressing which is a dense, hydrophobic,
open pore foam with high tensile strength applied directly to the wound; b)
an occlusive dressing; c) tubing applied to the foam under the dressing at
a continuous negative pressure of 125 mmHG. This system has been shown to
improve granulation and wound healing in a number of acute and chronic conditions.
While enterocutaneous fistulae were initially considered to be a contraindication
to VAC, they have subsequently been shown to respond well to this treatment
(42-44). This is especially useful because
enterocutaneous fistulae are often associated with large, dehisced, often
infected abdominal wounds, which themselves respond to this treatment. Unfortunately
the commercial systems are expensive, but the basic components are not. Adapted
systems should be possible with locally available materials. (see
AllHeal)
Nutrition
The single most important factor in improving outcome in patients with gastrointestinal
fistulae has been the development of nutritional support - both enteral and
parenteral (45;46). It is recognized that
fistulae will not close if the albumin is <3.5gm/l. The sources of malnutrition
in these patients are: a) inadequate nutrient intake, b) hypercatabolism resulting
from sepsis, and c) losses of protein-rich gastrointestinal secretions from
the fistula (47).
After the patient is stabilized and sepsis controlled, the patient’s
nutritional needs can be addressed. Nutritional assessment begins with weighing
the patient and measuring other anthropometric data, monitoring Hb, electrolytes,
albumin and transferrin and by calculating ongoing losses. From this assessment
nutritional requirements can be derived. Evenson (4) recommends
25-35 kcal/kg/day, and a calorie to nitrogen ratio of 150-200:1 with a protein
intake of at least 1.5gm/kg/day. Gonzalez recommends the following: “In
general, patients with low output fistulae should receive the full basal energy
requirement and between 1 and 1.5 g of protein per kg body weight every day,
with a minimum of 30% of the caloric intake supplied as lipid. With high output
fistulae, patients should receive 1.5–2 times their basal energy expenditure
plus 1.5–2.5 g of protein per kg body weight per day. This nutritional
regimen should also include twice the recommended daily allowance (RDA) for
vitamins and trace minerals, up to 10 times the RDA for vitamin C, and zinc
supplements. Fistulae from the small intestine that have been established
for a number of weeks are often associated with considerable zinc and copper
deficiency, and patients may also be deficient in folic acid and vitamin B12.”
(9) This therapy is best managed by a nutritional support
team. Meguid (48) provides a comprehensive review of the
practical details of nutritional assessment and support.
Enteral nutrition is the preferred route, for cost and safety, but it is often
not practical, especially in patients with small bowel fistulae. Even partial
enteral feeding is of value as it protects the mucosal integrity of the bowel
as well as the immunologic and hormonal function of the gut (4).
It may be used in upper GI fistulae, if access to the GI tract distal to the
fistula is possible through jejunostomy, or in distal terminal ileal or colonic
fistulae. Elemental diets are probably the most suitable but they are expensive
and may not be available (49). Feeding must be initiated
gradually because the hyperosmolar fluids may cause diarrhea. Enteral feeding
may also be used as fistuloclysis, if the distal aspect of the fistula can
be cannulised (50;51). This precludes
the possibility of spontaneous closure.
Total parenteral nutrition (TPN) has been used more commonly in the West for
gastrointestinal fistulae. On its own parenteral nutrition will reduce fistula
output by 30-50%. Its expense may preclude its use in many African settings.
Usually the central route is required to provide the high calorie/high osmolar
solutions. Central venous catheterization is associated with increased risk
of systemic sepsis, as well as other complications (48).
The use of lipid solutions as the primary calorie source may allow the peripheral
route to be used in some cases.
Phase 2- Investigation
and Assessment
After the patient’s condition has stabilized, approximately 7-10 days
after recognition, an assessment is made of the precise nature of the fistula.
Here the fistulogram is the most important procedure. Evenson (4) recommends
that the following information be derived: “(1) the source of the fistula;
(2) the nature (length, course, and relationships) of the fistula tract; (3)
the absence or presence of bowel continuity; (4) the absence or presence of
distal obstruction; (5) the nature of the bowel adjacent to the fistula (inflammation,
stricture); and (6) the absence or presence of an abscess cavity in communication
with the fistula.” CT scanning and endoscopy may supplement this information.
A conclusion can then be drawn as to the likelihood of spontaneous fistula
closure (Table 1) (4). In all cases
where the patient is stable, conservative therapy should be continued for
at least 4-6 weeks. Decreasing fistula output gives a measure of the likelihood
of closure. Ninety percent of fistulae that close spontaneously do so within
4-5 weeks (4). Evenson recommends waiting 16 weeks before
definitive surgery. One reason for delaying surgery is to allow the obliterative
peritonitis associated with intra-abdominal sepsis to resolve.
Somatostatin-14 and analogues
Somatostatin and its analogues have been intensively investigated in the treatment
of gastrointestinal fistulae (52;53).
Two meta-analyses of the clinical trials have shown that neither somatostatin
nor octreotide increased the number of fistulae which closed spontaneously.
However, various trials did show a decrease in time to closure when these
agents used with other treatments, such as nutritional support. The recommendation
is that, if available, they should be used in high output fistulae. If there
is no reduction in fistula output in 48 hours they should be stopped (52).
A recent Canadian study showed an improved spontaneous closure rate (54).
When used prophylactically, somatostatin and its analogues do seem to reduce
complications after pancreatic surgery (55).
Definitive surgery
Surgery is necessary in the 20-30% of enterocutaneous fistulae which do not
close spontaneously. At some time during the clinical course, emergency surgery
may have been necessary to drain abscesses, exteriorize leaking bowel or arrest
secondary hemorrhage (1). For definitive surgery all authors
caution that the patient’s nutritional status be optimized, sepsis controlled
and sufficient time transpired to be assured that spontaneous closure will
not occur and that the consequences of previous surgery have resolved (4;49).
While specific approaches will be discussed below the general principles are
as follows: a) clear plan for the surgery; b) appropriate antibiotics; c)
the team should be well rested with sufficient time held in the theatre; d)
where possible the abdomen should be entered via a new incision far from the
areas of disease (56); e) the entire bowel should be freed
from the ligament of Treitz to the cecum with sharp meticulous dissection;
f) the fistula itself is best handled with resection and primary anastomosis;
g) exteriorization, bypass, serosal patch may be reserved for inability to
resect the diseased bowel; h) decompressive gastrostomy and feeding jejunostomy
may be of value; i) repair of the abdominal wall needs to be carefully planned.
Good reviews on abdominal wall closure in these cases are available. Surgeons
may use prosthetic mesh, the component separation method (57),
staged management (58), the use of tissue expanders (59),
etc. to achieve abdominal closure. Given the difficult nature of this surgery
it is surprising to find a number of papers on the laparascopic repair of
GI fistulae (60-62).
Human fibrin sealant
There have been sporadic reports of the use of human fibrin sealant to close
gastrointestinal fistulae (63;64).
Specific sites
In a large 30 year study involving more than 1000 patients from China the
following anatomic distribution of fistulae was found: stomach 1.7%, duodenum
22%, small bowel 51%, colon 24% (65).
Stomach
In the West probably the most common causes of gastric fistulae today are
after surgery for morbid obesity and percutaneous endoscopic gastrostomy (PEG)(66).
Spontaneous internal gastrocolic fistulae occur as a late consequence of benign
or malignant gastric ulcers (67). Spontaneous gastrojejunocolic
fistulae arise as a result of stomal ulcers after incomplete gastric resection
or vagotomy for peptic ulcer disease (68). Although gastric
fistulae are unlikely to close on their own, access to the distal bowel for
enteric feeding is usually possible.
Duodenum
Duodenal fistulae, as well, can often be managed without TPN (69).
Fistulae arise after duodenal trauma, spontaneously with malignant disease
(70), after duodenal surgery such as pyloroplasty, transduodenal
sphincterotomy and classically as a result of a blown duodenal stump after
gastrectomy and BilrothII reconstruction (71). Although
good stomal care (72) and drainage of infection is important,
most of these will close spontaneously. In the event that surgery is needed
the serosal patch (1) and myocutaneous flaps have been used
(73).
Small Bowel
Since small bowel fistulae form the majority of GI fistulae there is no need
to repeat the management details described above (74). Appendiceal
fistulae are surprisingly common in the developing world and a number of reports
have been published (13;75;76).
Colon
Colonic fistulae arise as a result of colon trauma (16% risk in one Nigerian
study (77)), failure of colon anastomoses, spontaneously
from diverticulitis,where colovesical fistulae predominate (78),
or from malignant disease. Enteocutaneous fistulae are associated with considerable
local sepsis, which needs to be drained. Proximal diversion may be necessary
with transverse colostomy or preferably ileostomy (79).
Distal obstruction needs to be ruled out.
Biliary tree
The classic case of internal biliary fistula occurs with gallstone ileus (34).
Here chronic cholecystitis results in a cholecystoduodenal fistula which allows
passage of gallstones into the small intestine causing obstruction. The terminal
ileum is the usual site of obstruction. The radiologic signs are obstruction
with air in the biliary tree. Management consists of enterotomy and removal
of stones. Cholecystecomy and repair of fistula should be carried out in good
risk patients. Bouveret’s syndrome or duodenal obstruction is a variant
(80).
The most common cause of external biliary fistula is leak from a cystic duct
stump or injury to the biliary tree after cholecystectomy (81).
The risk is increased after laparoscopic cholecystectomy (82).
Many of these can be managed with ERCP. Biliary-colonic fistula is another
complication of cholecystectomy (83). Drainage of the biliary
system into a Roux-en-Y loop of small bowel may be necessary.
Pancreas
Pancreaticoduodenectomy, Whipple’s procedure, is fraught with complications
related to anastomotic breakdown (84;85).
Somatostatin and its analogues used prophylactically reduce complications
(55). Trauma, either spontaneous or surgically induced,
as after splenectomy, and complications of pancreatitis (86)
are responsible for most of the other external fistulae. If sepsis can be
resolved, these fistulae usually resolve spontaneously with bowel rest and
nutritional support. Drainage into a Roux loop may be necessary.
Prognosis
The outcome of gastrointestinal fistulae has changed dramatically over the
years with the introduction of intensive care and the provision of nutritional
support. Chapman’s study in 1964 showed a decrease in morality from
55% to 12% with improved nutrition. Of all the factors correlating with high
mortality the most important is the volume of fistula output (87).
In Haffejee’s study of 494 patients from South Africa the overall mortality
rate was 13% and the spontaneous closure rate was 75% (49).
Li’s large study from China with over 1000 patients had a remarkable
mortality of rate of only 5.5% but a spontaneous closure rate of only 37%
(65). Hollington’s study from Australia, where one
half of patients suffered from inflammatory bowel, the spontaneous closure
rate was even lower, 19.9%.
Conclusion
Acquired gastrointestinal fistulae are amongst the most complicated problems
in general surgery. They require a multidisciplinary approach combined with
skilled clinical acumen to identify the precise nature of the fistula, support
the patient nutritionally and eradicate sepsis. Expert judgment is crucial
in determining the necessity of emergency surgical intervention to drain infection
and control discharge. However, definitive fistula repair should almost always
be deferred until non-operative measures have proved unsuccessful and the
patient’s general condition has been optimized. Definitive repair requires
experience and meticulous surgical skills.
Recommendations
1. Gastrointestinal fistulae are best prevented by meticulous surgical technique,
proper sutures, following appropriate indications for exteriorization as opposed
to primary anastomosis and the appropriate use/avoidance of drains.
2. Prophylactic use of somatostatin and its analogues in pancreatic surgery
will reduce complications.
3. The priorities on diagnosis of an enterocutaneous fistula are: fluid resuscitation,
control of discharge, protection of skin, control of sepsis and provision
of nutrition. These should be assessed and acted upon within the first 48
hours of diagnosis.
4. Vacuum assisted closure (VAC) may be of value for those GI fistulae associated
with large open wounds.
5. Enteral feeding is cheaper and safer than parenteral feeding and should
be used if adequate nutrition can be provided - in upper GI fistulae if it
is possible to obtain access to the GI tract below the fistula or in small
bowel fistulae if elemental diets are available.
6. In resource-poor countries it may be of value to centralize TPN services.
7. Emergency surgery in GI fistulae should be confined to draining abscesses,
exteriorizing bowel and inserting feeding tubes.
8. Fistulography is the most important investigation and should be performed
when the patient is stable. The following information should be derived: (1)
the source of the fistula; (2) the nature (length, course, and relationships)
of the fistula tract; (3) the absence or presence of bowel continuity (end
vs. side fistula); (4) the absence or presence of distal obstruction; (5)
the nature of the bowel adjacent to the fistula (inflammation, stricture);
and (6) the absence or presence of an abscess cavity in communication with
the fistula.
9. If available, stomatostatin or analogue may be used to reduce effluent
volume in high output fistulae.
10. Definitive surgery for enterocutaneous fistulae should be delayed for
at least 4-6 weeks to see if spontaneous closure will occur. If there has
been significant peritonitis it may be wise to wait 12-16 weeks.
11. Definitive surgery should not be undertaken if there is undrained sepsis
or serum albumin<3.5gm/L.
AllHeal
There are 12.5 million worldwide cases of chronic, and potentially
debilitating, wounds. Wounds that do not heal within three months are considered
chronic. Some of these wounds take years to heal, as others may never heal,
causing great emotional, physical, and financial stresses. Negative-Pressure
Wound Therapy (NPWT) is a revolutionary technology that has been medically
proven to successfully treat these chronic wounds. However, current NPWT treatments
are completely unavailable to the third world, as the only application that
exists in the developed world is currently implemented with a $10K-$20K vacuum-assisted
closure (VAC) device and $180 per day disposable dressings. Aiming to impact
medical technology available to serve the third world, AllHeal has developed
low-cost VAC solutions for under $3 per unit and less than $1 per day for
disposables.
Currently, two VAC concepts have been developed into functional designs,
and have working prototypes that were analyzed on clean skin: the Wound Sucker
and Wound Flush. Both of these prototyped devices focus on third world applications,
as their designs are very robust, reusable, and cleanable. As the AllHeal
team pushes for a third world solution, Dr. Sheridan is helping the team to
design for third world environments, as he often volunteers in third world
clinics that treat chronic wounds. He is also assisting the team in obtaining
clinical trials at MGH of the current solutions. allheal@mit.edu
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