Enterocutaneous Fistula

Also known as: ECF

An enterocutaneous fistula is an abnormal communication between the gastrointestinal tract and the skin.

Most arise after abdominal surgery from anastomotic failure or unrecognised bowel injury. Other causes include Crohn disease, malignancy, radiation injury, tuberculosis, bowel ischaemia and intra abdominal infection.

Output predicts fluid loss and likelihood of spontaneous closure:

Low output: below 200 mL per 24 hours
Moderate output: 200 to 500 mL per 24 hours
High output: above 500 mL per 24 hours

Proximal high output fistulas produce the greatest water, sodium, magnesium and nutritional losses.

The immediate threats are sepsis, fluid and electrolyte depletion, malnutrition and destruction of surrounding skin.

The usual postoperative presentation is unexpected enteric drainage through the wound, drain site or abdominal wall.

High output proximal fistulas may rapidly cause thirst, oliguria, hypotension, acute kidney injury, hypokalaemia, hypomagnesaemia and metabolic disturbance.

Persistent fever, tachycardia or failure to recover should raise concern for an associated intra abdominal abscess. Sepsis remains one of the major causes of mortality.

The fistula opening should be assessed for site, number, output and character of effluent. Daily measured output is essential.

The diagnosis is usually clinical once enteric output appears externally.

CT abdomen and pelvis with enteric and IV contrast where appropriate: define the fistula anatomy and identify undrained abscess, distal obstruction or ongoing intra abdominal disease.

Definitive anatomical definition with fistulography or contrast studies is usually performed after initial sepsis and fluid problems have been controlled.

Check renal function, sodium, potassium, magnesium, phosphate, calcium, full blood count and inflammatory markers. Monitor weight and nutritional status.

Management follows four priorities: control sepsis, replace losses, provide nutrition, then define anatomy and plan closure.

Sepsis control comes first. Drain intra abdominal abscesses percutaneously whenever feasible. Antibiotics treat sepsis but do not close the fistula and should not be continued indefinitely once source control is achieved.

Replace fistula losses according to measured volume and electrolyte composition. High proximal losses commonly require substantial sodium, potassium and magnesium replacement. Match IV fluid replacement to ongoing measured losses rather than relying on maintenance fluids alone.

Protect the skin aggressively with ostomy appliances, wound management systems and specialist stoma care.

Enteral nutrition is preferred whenever sufficient functioning bowel is available and feeding does not produce uncontrolled fistula output. Feeding distal to the fistula through a tube or fistuloclysis may preserve intestinal function in suitable anatomy. Parenteral nutrition is required when enteral intake cannot meet requirements, particularly with proximal high output fistulas, severe malabsorption or distal obstruction. ESPEN recognises intestinal fistula as one of the major mechanisms of intestinal failure.

For troublesome high output, reduce gastrointestinal secretion and transit.

A practical starting regimen is:

Loperamide 4 mg orally three to four times daily, preferably before meals and at bedtime, then titrated according to measured response. ESPEN recommends loperamide as first line because it reduces water and sodium losses without central opioid effects.

A proton pump inhibitor such as omeprazole 20 to 40 mg orally once or twice daily is useful when proximal output is driven by gastric hypersecretion, especially early after major bowel resection.

Factors that prevent spontaneous closure include distal obstruction, active Crohn disease, malignancy, radiation injury, foreign body, uncontrolled sepsis, epithelialised tract and major bowel discontinuity.

Do not rush definitive surgery into a hostile postoperative abdomen. Early reoperation through dense adhesions carries substantial enterotomy and recurrent fistula risk.

Definitive surgery is considered when spontaneous closure has failed and the patient is free of sepsis, nutritionally restored and the abdomen has softened sufficiently for safe dissection. This often requires several months. Tertiary fistula centres frequently delay reconstruction approximately 6 to 12 months in complex postoperative cases.

Definitive repair usually requires complete adhesiolysis, resection of the fistula bearing segment and restoration of healthy bowel continuity rather than simple oversewing of the fistulous opening.

Strangulated Bowel Obstruction

Strangulated obstruction is mechanical bowel obstruction accompanied by compromised blood supply.

Venous obstruction initially produces oedema and haemorrhage within the bowel wall and mesentery. Progressive pressure then compromises arterial inflow, resulting in transmural ischaemia, necrosis, bacterial translocation, perforation and septic shock.

Strangulation can complicate adhesive obstruction, closed loop obstruction, hernia, volvulus or intussusception.

It is an operative emergency.

Pain often changes from intermittent colic to persistent severe pain.

Suspicious findings include:

Continuous abdominal pain
Focal or generalised guarding
Persistent tachycardia
Fever
Localised severe tenderness
Gastrointestinal bleeding in some ischaemic processes
Haemodynamic deterioration

Late findings include rigidity, shock, metabolic acidosis and organ dysfunction.

Absence of fever or leukocytosis does not exclude early strangulation.

Obtain full blood count, renal function, electrolytes, coagulation, blood gas and lactate. Crossmatch blood when bowel resection or major contamination is likely.

CT abdomen and pelvis with IV contrast: confirms obstruction and should be assessed specifically for impaired bowel enhancement or other evidence of ischaemia. CT evidence of ischaemia should prompt a low threshold for immediate exploration.

Do not undertake prolonged conservative management.

Begin resuscitation immediately with balanced crystalloid, correction of electrolyte abnormalities, nasogastric decompression and urinary output monitoring where systemic compromise is present.

Start broad spectrum antibiotics because loss of mucosal integrity and necrosis expose the patient to enteric Gram negative and anaerobic organisms.

A suitable adult regimen is:

Ceftriaxone 2 g IV every 24 hours plus metronidazole 500 mg IV every 12 hours.

For severe sepsis or extensive necrosis:

Piperacillin tazobactam 4.5 g IV every 8 hours by extended infusion, adjusted for renal function.

Resuscitation must not become a reason to postpone source control. Correct major physiological abnormalities while theatre preparation proceeds.

At laparotomy or laparoscopy, relieve the constricting lesion and assess the entire affected segment. Necrotic bowel requires resection back to clearly perfused margins.

Primary anastomosis is reasonable in a stable patient with viable margins and limited contamination. Shock, high vasopressor requirement, gross contamination, severe bowel oedema or questionable perfusion should lower the threshold for diversion or staged reconstruction.

Where viability remains uncertain after reperfusion, second look laparotomy is appropriate, particularly when extensive bowel resection would otherwise be required.

Postoperatively, persistent acidosis, rising lactate, vasopressor requirement, worsening abdominal findings or ongoing organ dysfunction should raise concern for residual ischaemic bowel or inadequate source control.

Enterocutaneous Fistula

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management