High output gastrointestinal fistula management

Preview:

Citation preview

High output gastrointestinal fistula management

B86401103Ri 烏惟新

Definition Fistula:

Abnormal pathological communication between two epithelialized surfaces.

Categorization Anatomical Physiological Etiological

Anatomy External Internal Proximal Distal Simple Complicated

Physiology High-output fistula

Pancreatic fistulae >200 ml/24 hours

Intestinal fistulae >500 ml/24 hours

Low-output fistula Pancreatic fistulae

<200 ml/24 hours Intestinal fistulae

<500 ml/24 hours

Etiology Abdominal surgical procedure

Leading cause, 67-85% Inflammatory bowel disease Diverticular disease Malignancy Radiation enteritis Trauma Congenital Other causes

Abdominal surgical procedures Predisposing factor

Cancer Inflammatory bowel disease Lysis of adhesions Peptic ulcer Pancreatitis Emergency Technical failure

Complications Loss of GI contents

Hypovolemia Acid-base and electrolyte abnormalities

Malnutrition Lack of food intake, loss of protein in fistula

discharge, hypercatabolism associated with sepsis

Sepsis Skin excoraiation Hemorrhage Psychological effect

High output fistula Fistula output

A predictor of morbidity and mortality Not an independent indicator of

spontaneous closure Fistula mortality rates have decreased

over the past few decades from as high as 40–65% to 5.3–21.3%

High output fistulae continue to have a mortality rate of approximately 35%.

Clinical/physical signs Slow or unusual course of post-

operative recovery Abdominal pain or tenderness Fever, and leukocytosis Skin:

Cellulitic appearance Excessive drainage Abscess formation

Evaluation History Physical examination Radiographic studies Laboratory studies

Image study Contrast radiography

fistulography, oral contrast , contrast enema, pyelography, cystography

Endoscopy Abdominopelvic CT scan, MRI,

ultrasound X-ray

Management Conservative

Fluid resuscitation Correct acid-base and electrolyte abnormalities Complete bowel rest Nutritional support Infection control Fistula drainage Skin protection

Surgery

Fluid resuscitation Correct hypovolemia Accurate measurement of ongoing

fluid losses Intravenous fluid administration

Iso-osmotic and high in potassium Replaced with a balanced salt

solution that contains added potassium

Sample of fistula fluid

Correct acid-base and electrolyte abnormalities Site of the fistula Quantity of fluid loss

High-output gastric fistulas Hydrochloric acid

Biliary and pancreatic fistula Hypertonic Large bicarbonate and sodium losses

Complete bowel rest Reduce fistula drainage

Solid food stimulates secretion of digestive juices and therefore

increases fistula output, exacerbating poor nutritional status and limiting healing

Simplify the evaluation

Nutritional support Early, aggressive parenteral

nutritional therapy has dramatically decreased mortality from fistulas from 58% to 16% (am J surg 108:157, 1964).

Therapeutic role Decrease in fistula output Modify the composition of

gastrointestinal pancreatic secretions

Role of TPN Conservative treatment with TPN

Reduce the maximal secretory capacity of the gastrointestinal tract by 30–50%

Not suppress basal or cephalic secretions Long term administration the presence of

lipids and amino acids can stimulate GI secretions

TPN complications Bacterial translocation, superinfection of

central venous access, and metabolic disorders as a result of fistula losses

Nutritional support Enteral feeding

Primary method of choice Esophagus, distal ileum, and colon Given below proximal fistula if accessible

Parenteral nutrition Intolerance to enteral nutrition Gastroduodenal, pancreatic, or jejuno-ileal

fistulae Proximal fistulas if distal enteral access is not

possible Reinfusion into the distal bowel

Infection control Intraabdominal abscess Intravenous antibiotics Infected wounds

Fistula drainage Wound management

Dressings Intubation Suction or sump drainage system

Pharmacotherapy Octreotide H2-receptor antagonists

Skin protection Barrier device Powder Examined and cleansed frequently

Surgical treatment Fistulas fail to heal with

nonoperative measures Sepsis cannot be controlled

Spontaneous closure unlikely.. FRIEND

Foreign body Radiation injury Inflammatory bowel disease Epithelialization of fistular tract Neoplasia Distal obstruction

Unfavourable Favourable

Lateral fistula End fistula

Large adjacent abscess No associated abscess

Adjacent bowel diseased Adjacent bowel healthy

Distal obstruction Free distal flow

Fistula tract <2 cm — epithelialisation

Fistula tract >2 cm — non-epithelialised

Enteral defect >1 cm Enteral defect <1 cm

Fistula site:• Gastric• Lateral duodenal• Ligament of Treitz• Ileal 

Fistula site:• Oropharyngeal• Esophageal• Duodenal stump• Pancreatobiliary• Jejunal

High output fistula High morbidity and mortality Strategy to reduce both output

volume and the content of corrosive enzymes in the exudate would be likely to decrease the healing time, greatly improving prognosis

Somatostatin-14 in combination with TPN Accelerated spontaneous closure of postoperative

gastrointestinal fistulae, significantly reducing the required period of TPN treatment (time to healing 13.9±1.84 days somatostatin-14+tpn v 20.4±2.98 days TPN alone; N=20, respectively; Ph0.05) with a consequent reduction in morbidity (35% somatostatin-14+tpn v 68.85% TPN alone; Ph0.05).

Inhibit both basal and stimulated digestive secretion, as well as reducing fluid loss, electrolyte imbalance, and malnutrition, leading to potential reductions in fistula output and time to closure.

Mechanisms of octreotide Inhibits the release of gastrin,

cholecystokinin, secretin, motilin, and other GI hormones. Decreases secretion of bicarbonate, water, and

pancreatic enzymes into the intestine, subsequently decreasing intestinal volume.

Relaxes intestinal smooth muscle, thereby allowing for a greater intestinal capacity.

Increases intestinal water and electrolyte absorption

Reasons for pharmacotherapy Rapidly reduce fistula output

Improvement in nutritional and electrolyte status Reduction of the concentration of caustic enzymes

in the discharge will convey beneficial effects on both wound healing and nutritional losses

Significantly shorten healing time Shortening hospitalisation Improvements in quality of life Reductions in overall treatment costs

However, lacking data from large scale, double blind, randomised, controlled studies

Guideline:Somatostatin use

Guideline:GI fistulamanagement

Summary:high output GI fistula management Early detection Stabilize the patient

Aggressive fluid resuscitation Electrolyte and acid-base balance Nutrition support and bowel rest Control infection Drainage and skin protection

Evaluation the status and prognosis factor Try pharmacotherapy Surgical treatment if needed

Reference The Washington Manual of Surgery, 2nd ed. Feldman: Sleisenger & Fordtran's

Gastrointestinal and Liver Disease, 7th ed Optimising the treatment of upper

gastrointestinal fistulae, I González-Pinto and E Moreno GonzálezGut 2001; 49 (Suppl 4): iv21-iv28

The relevance of gastrointestinal fistulae in clinical practice: a reviewM Falconi and P PederzoliGut 2001; 49 (Suppl 4): iv2-iv10

End