G.P.Chakravarthy

Moderator – Dr.Viswanath

INTRODUCTIONINTRODUCTION

Fistula is defined as an abnormal communication between two epithelialized surfaces. (fistula means a “pipe” or “flute” in Latin)

Enterocutaneous fistula is an abnormal communication between the skin with various parts of the gut, for example duodenum, jejunum etc.

The ileum is the most common site of origin of Enterocutaneous fistula.

ETIOLOGYETIOLOGY

Webster and Carey proposed five mechanisms of fistula formation :

1) Congenital : - Rare

- Due to the complete failure of Vitellointestinal duct to obliterate.

- Fecal matter at umbilicus after post natal slough of umbilicalcord.

2) Trauma : - Major penetrating trauma to the abdomen may lead to Fistula. but rare

- Damage control laparotomy techniques have higher risk of delayed ECF formation(2% to 25%).because there will be prolonged exposure and dessication of multiple intestine loops

3)Infection : - Abscess or invasive intestinal infections like amoebiasis, coccidiomycosis, tuberculosis etc.

- Intestinal perforation in ileum from tuberculosis or enteric fever esp in endemic countries.

- Actinomyces is a cause of enterocutaneous fistulas after appendectomy..

4) Perforation or Injury with Abscess & Operative complications :

- 60% to 90% of enterocutaneous fistulas were caused by operative complications. - In addition, enterocutaneous fistulas are caused by leakage from an intestinal anastomosis or enterotomy closure. - may also develop as a result of percutaneous drainage of an intraabdominal abscess.

5) Inflammation, Irradiation or Tumour :

-spontaneous external fistula can develop in Crohn disease, But most occur only after a surgery

it causes diseased intestine to adhere to the abdominal wall

- Fistula formation after laparotomy is usually an early complication, especially when arising from an anastomosis, whereas a late fistula generally indicates recurrent Crohns Fistulas that arise secondary to radiation injury rarely close spontaneously.

PREVENTION OF FISTULAPREVENTION OF FISTULA

- Acute intra-operative perforations should be identified and closed.

- Serosal tears should be examined carefully and repaired if required.

- Aggressive interloop adhesion break-up should be avoided to prevent serosal tears.

- Intraluminal instillation of methylene blue and saline or direct endoscopy helps to identify small perforations

-Post operatively anastomotic leaks/unrecognised perforations and subsequent fistulae may manifest as instability or patient’s failure to improve.

-Fever, abdominal pain followed by exiting of intestinal contents from drain or incision site.

-Occasionally,heavily purulent discharge may mask an ECF like in enteric perforations.

IDENTIFICATION OF PERFORATION AND FISTULAIDENTIFICATION OF PERFORATION AND FISTULA

STAGING AND CLASSIFICATIONSTAGING AND CLASSIFICATION1. Anatomical Classification : Internal or External fistula(ECF).

- Internal fistulae are named after the structures it communicates like gastrocolic, jejunoileal, aortoenteric fistula.

- External fistulae like gastric, duodenal, jejunal, ileal or fecal.

2. Physiologic classification : Based on output

- High-output > 500 ml/day (Difficulties in fluid management and skin care) - Moderate-output 200-500 ml/day

- Low-output < 200 ml/day (Usually colonic)

The anatomic and etiologic factors are much more important in predicting spontaneous closure than the actual output of the fistula.

External or enterocutaneous fistulas are by far the most common type of small intestinal fistula- readily recognizable.

In contrast, internal fistulas - may not be suspected for

some time because the symptoms may be minimal or may mimic the underlying disease

Etiologic classification – webster and carey

Fluid and electrolyte imbalance.

Malnutrition

Sepsis

Abdominal wall and wound abnormalities

The mortality diminished from 40% to 60% to approximately 15% to 20% (malnutrition and electrolyte imbalance were the causes of death in the majority of these patients)

attributable to general advances in fluid and electrolyte/acid–base therapy, blood administration, critical care, ventilatory management, antibiotic regimens, and nutritional management.

In the present era of fistula treatment, mortality is largely attributable to uncontrolled sepsis and sepsis-associated malnutrition

Fluid and electrolyte imbalance :

The degree of volume depletion and electrolyte imbalance depends on the anatomic location of the fistula and can vary from 50 to 3000 mL/day.

High-output duodenal or jejunal fistulas continue to carry a mortality rate of approximately 35%.

arising from the terminal ileum is usually associated with less fluid loss.

The most common abnormalities seen are hypovolemia, hypokalemia, and metabolic acidosis.

Hypokalemia occurs primarily from potassium loss in the fistula efflux

Hypovolemia - renal retention of sodium in exchange for potassium secretion.

Metabolic acidosis - loss of pancreatic juice rich in bicarbonate - more common with proximal intestinal fistulas

MALNUTRITION : small intestine contains fluid rich in ingested

nutrients and endogenous proteins, such as enzymes and albumin.

protein–calorie malnutrition and mineral and micronutrient depletion develops.

Before the introduction of TPN, 74% of patients - malnutrition, and 59% of these patients died.

SEPSIS Major cause of death in fistulas

Uncontrolled abdominal sepsis can lead to bacteremia, local and distant infection, and multisystem organ failure.

Large defects in the abdominal wall predispose the patient to repeated episodes of sepsis and a high mortality rate.

Sepsis contributes to the hypovolemic state by altering the metabolic rate and increasing insensible water loss.

Nutritional deficiency may be exacerbated by the extra metabolic demands of sepsis

OTHERS :

Abdominal wall excoriations

Massive GI hemorrahges in case of fistula b/w bowel and blood vessel

Colonization and overgrowth of the small intestine by colonic bacteria can occur with enterocolic fistulas

Five stages :

1. Stabilization,2. investigation,3. decision,4. definitive therapy,5. Healing. The ultimate goal when treating gastrointestinal fistulas is

restoring continuity of the gastrointestinal tract.

MANAGEMENTMANAGEMENT

STABILIZATIONSTABILIZATION

Resuscitation nutrition control of sepsis pharmacological support

> Needs to be accomplished within the first 24 to 48 hours of management.

> Initial efforts directed towards intravenous fluid resuscitation, control of infection, protection of surrounding skin & measuring and replacing ongoing losses.

> Attention should also be given to any intra-abdominal/subcutaneous abscesses & if present they should be drained.

> Identification of fistula source.

A. RESUSCITATIONA. RESUSCITATION

> Restoration of normal circulating blood volume and correction of electrolyte and acid-base imbalances are a top priority.

>Rehydration usually requires isotonic fluid(NS/RL) until the patient is euvolemic.

> Strict input and output measurements are essential and CVP monitoring and urinary catheterization are especially helpful.

> Ongoing fluid losses should be fully replaced and electrolyte imbalances must be corrected.

> High-output fistulas - highest mortality rate, up to 35%,because of malnutrition ,electrolyte imbalance and sepsis

RESUSCITATIONRESUSCITATION

> Small bowel, pancreatic, and biliary lossesare isotonic.> Colonic losses -hypotonic > Gastric fistulas -classic hypokalemic, hypochloremic metabolic alkalosis.

> Electrolyte measurement of the fistula output helps in planning of replenishment of ongoing losses.

> Urine output > 0.5mL/kg/hr.

> Requirement of blood transfusion depends upon overall hemodynamic status, patient’s oxygen carrying capacity and oxygen delivery.

B. NUTRITIONB. NUTRITION

> In 1972, Roback and Nicholoff reported closure of 73% of enteric fistulae in adequately nourished patients, as against 19% in inadequate ones.

> Nutritional support needs to begin as soon as the patient is stabilized.

> Nutrition can be given by parenteral or enteral route,based on the anatomy of the fistula.

> Its advisable to provide atleast a part of the daily nutritional requirement through enteral route.(Even 25% of daily requirement given enterally)

Enteral tube feeding is much more efficacious way

1. maintaining the intestinal mucosal barrier

2. immunologic integrity

3. stimulating hepatic protein synthesis - found to be essential in determination of the outcome in patients

WHO’s ORS should be given when oral intake is possible.- contains high conc. of Na+ and K+

Hypotonic fluids are to be restricted in proximal fistulas as they increase fistula effluent , electrolyte disturbances and worsens dehydration

> In proximal fistulae, the enteral feeding tube may be entered beyond the fistula to provide enteral nutrition(fistuloclysis).

> It is advisable to enter feeding tube beyond ligament of Treitz for a gastric or duodenal fistula to prevent the risk of aspiration .

NUTRITIONNUTRITION

these patients are in a severe catabolic state and have extremely low protein and albumin levels.

patients will have low capillary oncotic pressure, which may contribute to profound edema, especially after resuscitation has begun.

Severe hypoalbuminemia will take weeks to correct through nutritional repletion alone.

Short-term supplemental intravenous salt-poor albumin administration will help increase oncotic pressure and minimize edema

NUTRITIONNUTRITION

> Twice the daily requirement of vitamins, trace elements, zinc and upto 10 times the daily requirement of Vitamin C should be provided.

> Short turnover proteins like retinol-binding protein, prealbumin, ferritin can be used to monitor the weekly efficacy of protein delivery. [Alb half life is 20 days].

> Mortality rate of 42% with alb <2.5 mg/dl vs 0% if >3.5 mg/dl.

TYPE OF FISTULA CALORIE REQ PROTEIN REQ

Low Output 30-35 kcal/kg/day 1-2 gm/kg/day

High Output 45-50 kcal/kg/day 1.5-2.5 gm/kg/day

C. CONTROL OF SEPSIS AND FISTULA EFFLUENTC. CONTROL OF SEPSIS AND FISTULA EFFLUENT Sepsis is still responsible for almost 80% of all deaths in fistula patients

Persistent fever, tachycardia and leukocytosis along with failure to improve adequately points towards possible sepsis or abscesses.

require surgical drainage of abscess, if any along with adequate antibiotic

Local skin care and prevention of skin excoriation by using stomahesive paste or aluminium paint etc along with stoma bags.

Excessive fistula output can be controlled by nasogastric tube placement, withdrawal of oral feeds, initiation of parenteral nutrition or placement of sump suction catheter.

C. CONTROL OF SEPSIS AND FISTULA EFFLUENT C. CONTROL OF SEPSIS AND FISTULA EFFLUENT

> Vacuum assisted closure [VAC] device drainage system maybe used too.

> Due to the negative pressure application, VAC device helps to control drainage, minimizes the size of the abdominal wound, reduces frequency of dressing and protects the skin while helping to promote fistula healing.

> For majority of ECFs, VAC devices have become the method of choice for controlling fistula drainage and skin protection.

D. PHARMACOLOGICAL SUPPORTD. PHARMACOLOGICAL SUPPORT

> Somatostatin analogue Octreotide, at doses of 100 – 250 mcg TDS reduces fistula output by 40 – 60% by the end of 24 hrs.

> Should be discontinued if ineffective for 48 hrs as it has side effects like hyperglycemia, elevated cholesterol and reduced bowel motility.

> Octreotide and TPN seem to have a synergistic effect on reduction of effluent volume and improvement in fistula closure rates.

> Proton-pump inhibitors and H2 receptor antagonists also help reduce fistula output especially in proximal fistulas.

D. PHARMACOLOGICAL SUPPORTD. PHARMACOLOGICAL SUPPORT

> Cyclosporine in doses of 4 mg/kg/day for 6 – 10 days followed by oral doses of 8 mg/kg/day helps to treat refractory fistulae associated with Crohn’s disease.

> Other drugs used include Tacrolimus, Azathioprine, 6-MP, Infliximab(mAb TNFα).

> Infliximab administered at a dose of 5 mg/kg iv at 0,2,6 weeks helped in partial resolution of 68% of multiple lesions and complete closure in 55% of patients.

> Complications include URTI, headache, fatigue etc.

INVESTIGATIONSINVESTIGATIONS

> Investigations are done for the next 7 to 10 days following stabilization.

> They are carried out to determine the presence and location of the fistula, its cause and presence of comorbidities.

> Oral administration of Indigo Carmine/ Charcoal helps in diagnosing the presence of a fistula,but not its location, cause or anatomy.

> USG abdomen helps in locating intra-abdominal abscesses, apart from helping in performing guided aspiration of intra-abdominal collections.

> Fistulography helps in defining the length & width of the fistula, its anatomical location, the presence of any distal obstructions etc.

> It can be performed by entering a small cathter into the fistulous tract and then injecting the water-soluble contrast under fluoroscopy.

> Fistulogram should be performed before an upper GI series or CT scan with oral contrast or contrast enema as it poses difficulty in interpretation.

> Fistulography should be followed up with a complete contrast study of the GI tract.

CT scan of the abdomen with IV and oral contrast is highly sensitive and specific for locating the fistula, defining its anatomy, commenting on the gut surrounding fistula, presence of any intra-abdominal abscess or distal obstruction/pathology.

CT scan is highly recommended for duodenal and pancreatic fistula.

CT scan can be therapeutic by helping in CT-guided aspiration of intra-abdominal abscesses,if any.

Endoscopy may also be used occasionally though its principal use is in internal fistulas.

Endoscopy is usually delayed till acute inflammation gets reduced.

DECISIONDECISION

Factor Favorable UnfavorableOrgan of origin Esophageal, Duodenal stump,

Pancreatic, Biliary, Jejunal, Colonic

Gastric, Lateral duodenal, Ligament of Treitz, Ileal

Etiology Postop (anast leak), Appendicitis, Diverticulitis

Malignancy, IBD

Output Low (<200-500cc/day) High (>500cc/day)Nutritional status Well nourished, Transferrin

>200Malnourished, Transferrin <200

Sepsis Absent Present State of bowel Intestinal continuity, absence

of obstructionDiseased adjacent bowel, Distal obstruction, Abscess, Discontinuity, Irradiation

Fistula characteristics

Tract >2 cm, Defect <1cm Tract <1cm, Defect >1cm

Miscellaneous Original operation at same institution

Referred from outside institution

FACTORS RESPONSIBLE FOR SPONTANEOUS CLOSURE

> Reber et al reported that more than 90% of small intestinal fistula which closed spontaneously,did so within a month.

> Spontaneous closure rates dropped to less than 10% after 2 months and none after 3 months.

> Factors possibly responsible for failure of spontaneous closure are: a. Foreign Body b. Radiation c. Inflammation/ infection d. Epithelialisation e. Neoplasm f. Distal intestinal obstruction g. Steroids.

DEFINITIVE THERAPYDEFINITIVE THERAPY

> Majority (80-90%) will close within 6 weeks with conservative management.

> Surgery between 10 days and 6 weeks post-op will encounter the worst adhesions.

> Preferably wait upto 6 weeks before open exploration and repair of defect, but in case of faecal fistula, due to intense inflammation, it is prudent to wait upto 10-12 weeks.

> The patient should,by then, be nutritionally optimized, patient should not be septic and patient should be vitally stable.

> Definitive operative correction remains the final step in the treatment of non-healing small intestinal fistulas.

> In majority of the cases, preferred operation is resection of the involved segment with primary end-to-end anastomosis. (Reber HA, 1978)

> However if primary anastomosis is not possible,then both the proximal and distal ends of intestine are exteriorized.

> In case the fistula is deemed inappropriate for resection, such as when it develops after a deep pelvic procedure, staged approach involving bypass should be considered.

> In a staged procedure, the fistulous segment is left in-situ or the ends are exteriorized as mucous fistula and the afferent and efferent bowel loops are anastomosed to restore intestinal continuity.

> The staged procedure is completed when the fistula segment is removed at a later date,although it may not always be possible.

> Enteroatmospheric fistulas, which are associated with large abdominal defects are very difficult to manage and are associated with high mortality rates.

> Mortality rates may vary from 20% to 60%. (Schein M, Decker GA 1991)

> Enteroatmospheric fistulas usually require multiple staged operations.

ENTEROATMOSPHERIC FISTULAENTEROATMOSPHERIC FISTULA

> Enterocutaneous fistula treatment is complicated due to various factors like open abdominal wound leading to desiccation of gut loops, presence of multiple fistulous openings, dressings adhering to the gut loops etc.

> VAC devices are used initially to approximate the large abdominal defect along with isolation of the fistula(s) by ostomy bags.

> After proper granulation tissue formation, the stabilized patient can be considered for SSG, if his nutritional status is favourable.

> After 6 to 12 months recovery time to replenish protein and calorie stores, resection of the fistula as definitive therapy can be provided to the patient.

> Musculocutaneous flaps, abdominal wall reconstruction by component separation technique, use of prosthetic materials,esp biologics may also be necessary. (human acellular dermal matrix)

> In 1995, Ho HS and Frey CF used primary closure of gastric fistula with delayed external drainage as treatment for gastric fistulas.

> If the gastric fistula defect is too large to allow primary closure,then a Roux-en-Y gastrojejunostomy may be done.

> Duodenal fistulas are usually treated with tube duodenostomy or Roux-en-Y duodenojejunostomy.

> A feeding jejunostomy distal to the enteroenterostomy should always be considered.

Roux-en-Y DuodenojejunostomyRoux-en-Y Duodenojejunostomy

CONCLUSIONCONCLUSION

> Enterocutaneous fistulas are abnormal communication between the gut and skin.

> Majority of the ECF are due to iatrogenic causes (70-85%). Others include trauma, congenital causes. Spontaneous ECF may arise due to Crohn’s disease.

> Malnutrition, Electrolyte imbalances, acid-base imbalances and sepsis are the major causes of mortality in ECF.

> After initial stabilization of the patient by resuscitation( fluid, electrolytes, blood transfusions etc), the patient is subjected to various investigations to determine the location& anatomy of fistula, presence of distal obstruction etc.

> Enteral nutrition is always preferable to parenteral nutrition provided the patient tolerates enteral feeds.

> Local wound care by application of ostomy bag and pastes are essential.

> Drainage of intra-abdominal abscesses, treatment of sepsis is of utmost importance.

> After proper optimization, patient undergoes definitive therapy which includes resection of the fistulous segment of the gut.

> ECF with large abdominal defects may require VAC devices/ biologic mesh SSG to help close the defect.

THANK YOUTHANK YOU