Surgical Nutrition, TPN & Enterocutaneous Fistula
Feed the gut when you can, the vein when you must, and the fistula patiently
Assessing nutritional status and needs
Recognizing malnutrition. Unintentional loss of more than 10% of body weight over about 6 months, poor intake for more than a week, BMI below 18.5, and visible muscle and fat wasting identify patients at risk of infection, poor wound healing, and anastomotic failure. Severely malnourished patients benefit from 7–14 days of nutrition support before major elective surgery.
Serum proteins. Albumin (half-life about 20 days) reflects chronic status, and a level below 3 g/dL predicts complications. Transferrin (about 8–10 days) is intermediate, and prealbumin (transthyretin, about 2 days) tracks recent intake and the response to feeding. All three are negative acute-phase proteins that also fall with inflammation, liver disease, or protein loss, so read them alongside CRP.
Measuring balance. Indirect calorimetry is the most accurate measure of energy expenditure. Nitrogen balance equals protein intake in grams divided by 6.25, minus the 24-hour urine urea nitrogen plus 4 g; a positive balance means anabolism.
Enteral vs parenteral nutrition
If the gut works, use it. Enteral feeding preserves villi, gut IgA, and the mucosal barrier, limits bacterial translocation, and causes fewer infections at lower cost. Start within 24–48 hours of surgery, even after a bowel anastomosis; waiting for flatus is outdated. Obstruction, bowel ischemia, uncontrolled shock, and a high-output fistula are the contraindications.
Choosing the route. Nasogastric tubes suit short-term feeding. High gastric residuals, gastroparesis, recurrent vomiting, or aspiration call for post-pyloric (nasojejunal) feeding, and needs beyond about 4–6 weeks call for a percutaneous gastrostomy or surgical jejunostomy. Keep the head of the bed at 30–45°.
| Feature | Enteral | Parenteral (TPN) |
|---|---|---|
| Use when | The gut works and can be reached | Prolonged ileus, obstruction, high-output fistula, short bowel, severe malabsorption |
| Access | Nasogastric, nasojejunal, gastrostomy, jejunostomy | Central line (PICC or CVC) for hypertonic full-strength TPN |
| Gut mucosa | Barrier and immunity maintained | Villous atrophy, bacterial translocation |
| Timing | Within 24–48 h of surgery | After about 7 days if well nourished; early if malnourished |
TPN complications and refeeding syndrome
Line and metabolic problems. Catheter bloodstream infection (staphylococci, Candida), pneumothorax at insertion, and venous thrombosis. Hyperglycemia is the most common metabolic complication, followed by hypertriglyceridemia and electrolyte shifts.
Liver and gallbladder. Excess dextrose causes hepatic steatosis early, and prolonged TPN causes cholestasis. Without food in the duodenum, CCK is not released, the gallbladder does not empty, and sludge, stones, and acalculous cholecystitis follow.
Refeeding syndrome. In starved patients (alcohol use disorder, anorexia nervosa, little intake for more than 5–10 days, BMI below 16), a carbohydrate load triggers insulin release that drives phosphate, potassium, and magnesium into cells and consumes thiamine. Hypophosphatemia, the hallmark, depletes ATP and causes weakness, respiratory and heart failure, arrhythmias, rhabdomyolysis, hemolysis, and seizures; thiamine loss can precipitate Wernicke encephalopathy. Start at about 10–20 kcal/kg/day and advance over several days, replete electrolytes, give thiamine before the first calories, and check levels daily. If it develops, slow the feeding and replace electrolytes IV rather than adding dextrose or insulin.
Enterocutaneous fistula
Cause and output. Most fistulas follow an anastomotic leak or inadvertent enterotomy. Output below 200 mL/day is low, 200–500 moderate, and above 500 high. High-output fistulas, usually from the proximal small bowel, close less often and cause dehydration, hypokalemia, hypomagnesemia, and non-anion-gap acidosis.
- Resuscitate, control sepsisCT-guided abscess drainage and antibiotics; early laparotomy in a hostile abdomen risks new enterotomies.
- Protect skin, replace lossesPouching against caustic effluent; fluids and electrolytes.
- Nutrition, reduce outputNPO with TPN for high-output or proximal fistulas; octreotide and PPIs cut output, though octreotide has not reliably raised closure rates.
- Define the anatomyCT or fistulography.
- Wait, then repairMost fistulas that will close do so within 4–6 weeks of sepsis control; definitive resection waits at least 3–6 months.
| Factor | Example |
|---|---|
| Foreign body | Mesh or suture in the tract |
| Radiation | Irradiated bowel heals poorly |
| Inflammation or infection | Crohn disease, undrained abscess |
| Epithelialization | Mucosa lines the tract |
| Neoplasm | Tumor in the tract |
| Distal obstruction | Contents take the easier path out |
| Steroids | Impaired healing |
Short bowel syndrome
Definition and consequences. Short bowel syndrome follows resection leaving less than about 200 cm of functional small bowel, typically for mesenteric ischemia, Crohn disease, volvulus, or necrotizing enterocolitis. Diarrhea, dehydration, and malabsorption result. Loss of the terminal ileum adds B12 deficiency and bile-acid diarrhea; with the colon in continuity, calcium oxalate stones and D-lactic acidosis appear.
Management. Parenteral fluids and nutrition come first while the remnant adapts over 1–2 years, followed by small frequent meals, loperamide, and PPIs for gastric hypersecretion. Teduglutide, a GLP-2 analog, promotes mucosal growth and reduces parenteral dependence; colonoscopy precedes it because it can accelerate polyp growth. Intestinal transplantation is reserved for intestinal failure.