malnutrition from inability to feed via the GI tract and loss of protein-rich fluid
sepsis
Factors Preventing Spontaneous Fistula Closure
high output
severe disruption of intestinal continuity (>50% of bowel circumference)
active inflammatory bowel disease
cancer
radiation enteritis
distal obstruction
undrained abscess cavity
foreign body in the fistula tract
fistula tract < 2.5 cm long
epithelialization of the fistula tract
Management
prevention is the best treatment: optimize preoperative nutrition, mechanical bowel preparation,
meticulous hemostasis, technically sound anastomoses, avoidance of bowel injuries
once a fistula is established, goal is to reestablish the continuity of the GI tract
~ 1/3 of fistulas close spontaneously with supportive care only
Stabilization
Sepsis Control
lack of source control can lead to multiorgan failure and death
CT scanning is necessary to look for abscesses and distal obstructions
abscesses can usually be drained percutaneously
infected mesh or retained foreign bodies will require operative removal
antibiotics alone will not clear the infection
Fluid and Electrolyte Replacement
most patients are dehydrated and will require several liters of isotonic fluid administration
on presentation
volume deficits can be large
anemic patients should be transfused to improve oxygen carrying capacity
hypokalemia and hypophosphatemia, which are important for cardiac and pulmonary function,
should be corrected quickly
metabolic acidosis requires replacement of sodium bicarbonate
Nutritional Support
malnutrition can be determined by total protein, serum albumen, transferrin levels
mortality is high for patients with a serum albumen < 2.5 g/dL
enteral nutrition is preferred if it is tolerated and does not cause conversion to a high output
fistula
however, in cases of increased fistula output, ileus, or distal obstruction, TPN may be necessary
baseline nutritional needs are 20 kcal/kg/d of carbohydrate and fat, and 0.8 g/kg/d of protein
in high output fistulas, requirements may be as high as 30 kcal/kg/d of carbohydrate and fat,
and 1.5 to 2.5 g/kg/d of protein
occasionally, the distal limb of a proximal fistula can be intubated to provide enteral feeds
(fistuloclysis)
Pharmacologic Management of Fistula Output
converting high output fistulas to low or moderate output fistulas makes wound management and
fluid and electrolyte management easier
bulking agents (psyllium) have value if the patient is on enteral feeds
antimotility agents such as loperamide may reduce fistula output
octreotide can reduce fistula output, but there is no evidence that it improves spontaneous closure
proton pump inhibitors can limit damage to the skin and assist in acid-base regulation
Wound Care
maintaining skin integrity is a critical aspect of fistula management
wound care teams and enterostomal therapists are an invaluable part of the management team
corrosive properties of the fistula output are detrimental to skin integrity
skin barriers, adhesives, dressings, pouches are all useful for protecting the patient’s skin
and collecting the output
wound VAC dressings now have an important role in fistula management
in a superficial EA fistula, STSGs can be place around the fistula and covered with a VAC;
appliances can then be placed over the fistula
Surgical Management
if a fistula does not spontaneously close, surgical repair is necessary
preferred operation is fistula tract excision, resection of the involved segment of bowel,
and primary anastomosis
simple closure of the fistula almost always results in fistula recurrence
Timing of Operation
nutrition must be optimized: goal is serum albumen > 3 g/dL
surgeon should wait at least 12 weeks from time of fistula formation to operation –
this allows the inflammatory adhesions time to become more manageable
if a skin graft was placed over an open abdominal wound, it should pass the ‘pinch test’
before operation
Technical Details
incision should be made away from the fistula and in virgin tissue if possible
adhesions will be extensive, and great care must be taken to avoid enterotomies
the small bowel should be entirely freed up, and an assessment for a distal obstruction
must be made
fistula closure requires bowel resection and anastomosis
suture lines should be covered by omentum and separated from the incision
Abdominal Wall Closure
amount of abdominal wall resection may preclude a primary abdominal closure
since fistula closures are not clean cases, permanent mesh such as proline must
be avoided
midline can often be medialized with a component separation, and reinforced with an
underlay of biologic material such as Alloderm or Stratice
Short Bowel Syndrome (SBS)
Etiology
defined as disabling malabsorption of both macronutrients and micronutrients
in adults, it is usually caused by extensive small bowel resection from Crohn’s disease, trauma,
mesenteric ischemia, or malignancy
in infants and children, necrotizing enterocolitis or congenital anomalies such as mid-gut volvulus, atresias,
or gastroschisis are the most common causes
Pathophysiology
there are four main factors that determine whether SBS develops after massive small bowel resection:
residual small bowel length, loss of the ileum and ileocecal valve, loss of all or part of the colon,
and whether the intestines are in continuity or not
Residual Small Bowel Length
adults with residual small bowel length of less than 200 cm are at risk for SBS
jejunal resection is better tolerated than ileal resection since the ileum is better able
to adapt and take over the functions of the jejunum
certain functions are specific to the ileum (bile salt, vitamin B12, and fluid reabsorption)
Loss of the Ileocecal Valve
an intact ileocecal valve slows small intestine transit time and increases nutrient absorption
loss of the ileocecal valve also leads to bacterial overgrowth, which can further reduce bile salt
and vitamin B12 absorption
Loss of the Colon
the colon is capable of absorbing large amounts of fluid and electrolytes
the colon is also capable of absorbing short-chain fatty acids and some complex carbohydrates
patients with an end jejunostomy are at high risk of lifelong TPN dependence
Gastric Acid Hypersecretion
results from gastric hypergastrinemia
a high acid load in the duodenum inhibits pancreatic enzyme function
typically lasts for 1 - 2 years postoperatively and is treated with acid-reducing drugs
Intestinal Adaptation
usually occurs during the first two years after intestinal resection in adults
most of the adaptive changes are in the ileum, and to a lesser extent, the jejunum and colon
Structural and Functional Changes
the remaining small bowel dilates and elongates, and the mucosal absorptive capacity greatly increases
in addition, there is an upregulation in brush border enzyme activity and carrier-mediated transport
Nutrient Effects
intestinal adaptation requires enteral feeding and will not occur with exclusively parenteral feeding
biliary and pancreatic secretions are important mediators of intestinal adaptation
long-chain triglycerides and omega-3 fatty acids promote intestinal adaptation through release
of growth factors
Glucagon-Like Peptide 2 (GLP-2)
GLP-2 is an intestinal growth factor produced by the ileum and colon and is released in response to enteral fat
induces villus hyperplasia of the remaining jejunum and ileum
teduglutide is a long-acting GLP-2 analogue that is modestly beneficial in weaning patients off of
parenteral nutrition
Management
the clinical course of SBS can be divided into two phases, the acute phase and the adaptive phase
Acute Phase
starts immediately after surgery and lasts for 3 – 4 weeks
characterized by high intestinal fluid and electrolyte losses
Fluid Management
stomal and fecal losses should be measured and replaced with an isotonic fluid
potassium, magnesium, and bicarbonate losses can be large and must be aggressively replaced
Gastric Acid Suppression
gastric acid hypersecretion is common in SBS and should be suppressed with proton pump inhibitors
gastric hypersecretion increases fluid losses and decreases fat absorption by deactivating pancreatic enzymes
Parenteral Nutrition (TPN)
should be started once the patient is hemodynamically stable
Enteral Feeding
should be started once the patient is stable
initial feedings are via an NG tube or gastrostomy
continuous feedings are better tolerated than bolus feedings
standard formulas are better tolerated than elemental formulas
Adaptative Phase
Oral Diet
oral feedings should be introduced slowly over weeks to months
if the colon is present, a diet high in complex carbohydrates, low in fat, and unchanged in
protein is recommended
for patients with an end jejunostomy, avoidance of hypertonic fluids and carbohydrates is required
(anti-dumping diet)
Antidiarrheals
necessary in most SBS patients
reduce intestinal motility and prolong transit time, increasing nutrient absorption
Octreotide
reserved for patients with IV fluid requirements > 3 L/day (high output end jejunostomy)
should only be used after the period of maximal intestinal adaptation
is expensive, painful to administer, inhibits intestinal adaptation, and causes the development
of gallstones
Weaning TPN
TPN should be reduced as oral intake increases
TPN can be discontinued when > 60% of the patient’s fluid and caloric needs are met orally
TPN-associated complications include catheter sepsis, central vein thrombosis, and liver failure
Persistent Intestinal Failure
defined as patients chronically dependent on TPN two years after resection
significant addition intestinal adaptation rarely occurs after two years
ultimately, intestinal or liver/intestinal transplant may be required
References
Sabiston, 20th ed., pgs 1286 – 1289
Cameron, 11th ed., pgs 142 – 145
Whelan, J,F., Ivatury, R. R., Eur J Trauma Emerg Surg (2011) 37:251-258
UpToDate. Dibaise, John. Pathophysiology of Short Bowel Syndrome. May 22, 2019. Pgs 1 – 20
UpToDate. Dibaise, John. Management of the Short Bowel Syndrome in Adults. Sep 24, 2018. Pgs 1 – 22
