GI Nutrition: GI Nutrition: Parenteral Nutrition and Short Gut

0:00Welcome to Board Pearls. This is episode two of four of the GI Nutrition chapter, in the Special Populations and Acute or Supportive Care module. This episode is feeding when the gut can't be used, and the gut that's been made too short. The first patient is a woman with Crohn fistulas, and her case shows who needs parenteral nutrition, how its calories are counted and why dextrose isn't four kilocalories per gram, why calcium and phosphate can't share a bag freely, why long-term feeding is cycled and which lipid is used, and what parenteral nutrition does to the line, the gallbladder, and the liver. A man with metastatic cancer shows who is harmed by it. The third patient is a man left with a short gut after mesenteric ischemia, and his case shows why the remaining anatomy matters more than the length lost, why plain water makes him worse, when cholestyramine helps or hurts, what teduglutide does and why it needs colonoscopies, and why a retained colon brings kidney stones and confusion.

0:58Here's the first patient. A thirty-nine-year-old woman has Crohn disease complicated by several small bowel enterocutaneous fistulas despite medical therapy, and her surgeons plan to operate in some months, once her inflammation and nutrition improve. Oral and tube feeds pour out of her fistulas. She weighs sixty kilograms, has lost eight kilograms in three months, and is starting parenteral nutrition through a tunneled central catheter, to continue at home.

1:23She has intestinal failure: her fistulas let feeds leave before they can be absorbed, so her gut can't meet her needs and she needs parenteral nutrition. Parenteral nutrition delivers dextrose, amino acids, lipid emulsion, electrolytes, vitamins, and trace elements through a central venous catheter when the gut is non-functional, inaccessible, or insufficient. The governing principle is that a functional gut wins, so it's reserved for patients who can't use the gut at all or whose gut supplies only a fraction of their needs. The indications are intestinal failure, which includes short bowel syndrome, motility failure, and multiple enterocutaneous fistulas like hers; severe acute pancreatitis that won't tolerate enteral feeding, though enteral feeding is favored whenever it's tolerated; ileus lasting more than seven days; bone marrow transplant mucositis that prevents any intake; and high-output stomas with dehydration that persists despite oral rehydration. In inflammatory bowel disease in general, enteral and parenteral feeding give equivalent outcomes, so the lower-risk enteral option is preferred. Her Crohn disease alone wouldn't justify a central line, but her fistulas do.

2:33Her prescription starts with how much to give and how to count it. Standard adult dosing is twenty-five to thirty kilocalories per kilogram per day, with one to one point two grams per kilogram of amino acids, and intravenous lipid twice weekly, typically five hundred milliliters of ten percent emulsion or an equivalent dose of a mixed emulsion, which is enough to prevent essential fatty acid deficiency. Dextrose provides three point four kilocalories per gram, not four, because pharmaceutical dextrose is a monohydrate, so part of each gram is water. Amino acids provide four kilocalories per gram and are counted in the total, because their carbon enters the same metabolic pool as carbohydrate. At sixty kilograms she needs one thousand five hundred to one thousand eight hundred kilocalories a day, and sixty to seventy-two grams of amino acids supply about two hundred forty to two hundred ninety of them. Counting her dextrose at four would leave her short. Because she's lost weight and eaten little, she starts slowly with her electrolytes watched for refeeding, as in episode one.

3:36Her bag also has chemistry limits, because some components precipitate together. Calcium and phosphate can't be combined freely without forming calcium-phosphate crystals, so compounding uses validated solubility tables or splits the two across separate bags or lines. Bicarbonate isn't added for the same reason, because it precipitates as calcium carbonate. When she needs alkali, acetate is the buffer, because it's converted to bicarbonate after it's infused.

4:02Her course may be long, so the lipid she gets is chosen to protect her liver. Older pure soybean emulsions are high in pro-inflammatory omega-six fatty acids and phytosterols, and they contribute to intestinal failure-associated liver disease in long-term use. Modern mixed emulsions of soybean oil, medium-chain triglycerides, olive oil, and fish oil slow that liver disease, because the omega-three fatty acids in fish oil compete with omega-six in eicosanoid synthesis and damp hepatic inflammation. Pure fish-oil emulsion is approved for intestinal failure-associated liver disease in children and used off-label as rescue therapy in adults. She starts a mixed emulsion from the beginning.

4:46The timing of her feeding is the second liver protection. Continuous parenteral nutrition runs over twenty-four hours. Cycled parenteral nutrition delivers the same daily load over twelve to eighteen hours, which reduces the liver's exposure to the lipid load, lowers insulin requirements, and is associated with less cholestasis, so long-term home patients are typically cycled. Once she's stable, hers runs overnight over about fourteen hours, written into her home plan from the start.

5:12Her line brings her first complication. Six weeks later she has fever and rigors after connecting her bag. She has a catheter-related bloodstream infection, which occurs at about one to two episodes per thousand catheter-days in experienced home programs and is the leading cause of hospitalization in these patients. Skin and oral flora introduced when the catheter is accessed form a biofilm on its lumen, and coagulase-negative staphylococci, Staphylococcus aureus, and Candida predominate. Saving the catheter rather than replacing it is attempted with systemic antibiotics plus catheter-lock therapy when the organism allows. Her cultures grow coagulase-negative staphylococcus, so she gets systemic antibiotics and an antibiotic lock and keeps her line, which is her only way to be fed. If she went on to have several infections, ethanol or taurolidine locks would be added to reduce recurrence: ethanol disrupts the biofilm matrix, and taurolidine is both antimicrobial and antibiofilm.

6:10The same fasting that makes her depend on the line also stills her gallbladder. Parenteral nutrition-associated cholelithiasis develops in about half of long-term patients, because without food in the duodenum, cholecystokinin isn't released, the gallbladder doesn't contract, and stagnant bile forms sludge and stones. That's the stasis pathway to gallstones covered in chapter twenty-seven. Even twenty to thirty percent of her needs given by mouth or tube reduces the stasis dramatically, because nutrient reaching the duodenum triggers cholecystokinin release. So any oral intake she can absorb before it leaves through her fistulas is worth giving.

6:49Her liver is threatened by several of the same factors, which is why her protections were built in from the start. Intestinal failure-associated liver disease progresses from steatosis to cholestasis to fibrosis and can reach end-stage liver disease. Its drivers are the lipid emulsion type, septic episodes, the lack of enteral stimulation, manganese accumulation, and choline deficiency. Management is switching to a mixed lipid at the lowest effective dose, treating sepsis aggressively, advancing enteral feeding wherever tolerated, cycling, and referral for intestinal transplantation when liver failure is established. She's had three protections from the start: a mixed lipid, a cycled regimen, and a promptly treated line infection. Manganese is one driver worth naming, because it's excreted in bile, so once cholestasis develops it builds up in the brain, and it's removed from the bag, as episode four covers.

7:46Her other long-term risks come from the formula itself. Parenteral nutrition can cause hyperglycemia, refeeding electrolyte shifts, and metabolic bone disease from chronic acidosis and from aluminum in older formulations. Aluminum bone disease is now largely historical with current formulations.

8:06Parenteral nutrition is for a gut that can't absorb, and the second patient shows what happens when it's offered for the wrong reason. A seventy-seven-year-old man with metastatic pancreatic cancer has lost fifteen kilograms and eats little, and his family asks whether parenteral nutrition would help him regain weight. It's contraindicated or harmful in metastatic cancer cachexia, because the weight loss is driven by catabolism that calories don't reverse, and the central line adds infection without adding survival. It's also the wrong choice in mild to moderate acute pancreatitis, where enteral nutrition is superior in randomized trials, with fewer infections and lower mortality, and it isn't a treatment for a low albumin. His family is told, gently, that his weight loss comes from his cancer rather than a gut that can't absorb, and that parenteral nutrition would add a line and its infections without adding time.

8:57The third patient has intestinal failure for a different reason, a gut that's been made too short. A forty-seven-year-old man had an emergency resection for mesenteric ischemia six months ago, leaving about one hundred twenty centimeters of jejunum joined to an intact colon, with his ileum and ileocecal valve removed. He's on parenteral nutrition five nights a week, has large-volume diarrhea, and drinks several liters of water a day because he's always thirsty.

9:22He has short bowel syndrome, which follows a resection that leaves less than two hundred centimeters of small bowel. It's classified by the anatomy that remains, rather than by the length removed, because the chance of coming off parenteral nutrition and the complications differ sharply by type. An end-jejunostomy, with no colon in continuity, has the worst prognosis. Stomal output is roughly one hundred milliliters per centimeter of remaining bowel per day, low magnesium and dehydration are chronic because the colon's fluid and electrolyte salvage is gone, and with less than one hundred centimeters of jejunum, parenteral nutrition is almost always permanent. Jejunocolic anatomy, with colon but no ileocecal valve, gains colonic salvage of fluid, sodium, and short-chain fatty acids made by fermenting unabsorbed carbohydrate, and with at least sixty to ninety centimeters of small bowel plus colon, patients often reach enteral autonomy. Jejunoileocolic anatomy, with the valve and colon intact, adapts best, because the valve slows transit and keeps colonic bacteria out of the small bowel. He's jejunocolic with more than ninety centimeters, so he has a real chance of autonomy.

10:33His type also predicts his complications. An end-jejunostomy with seventy centimeters would have meant high output, chronic dehydration and low magnesium, and almost certainly permanent parenteral nutrition, but no oxalate stones or D-lactic acidosis, because both need a colon. His retained colon gives him a chance at autonomy and makes both of those possible.

10:55Losing his ileum has its own cost, separate from the length lost. The terminal ileum is the only site of bile acid and B12 absorption, so his ileal loss causes bile acid malabsorption, diarrhea, and B12 deficiency that the bowel above it can't make up for. He needs B12 for life, as episode three covers.

11:15His thirst-driven water drinking is making his output worse, because of how the small bowel absorbs water. Oral rehydration solutions matched to small bowel sodium-glucose cotransport, with sodium at ninety milliequivalents per liter and glucose at ninety to one hundred ten millimoles per liter, drive net water absorption through sodium-glucose cotransporter one, SGLT1, which carries water across the membrane with each sodium-glucose pair. Plain water and most sports drinks fall below that ratio, so water moves into the lumen instead of out of it. Telling him to drink more for his thirst deepens the problem. He's switched to an oral rehydration solution with plain water limited, and his output and thirst fall.

11:58Once his fluid is right, drugs and diet reduce his output further. Antimotility agents, loperamide, diphenoxylate with atropine, and codeine in selected patients, slow small bowel transit. High-dose proton pump inhibitors reduce the gastric hypersecretion that follows extensive resection, which comes from losing jejunal cholecystokinin and other hormones that normally restrain gastrin. Adaptive hyperphagia, eating one and a half to two times calculated needs, compensates for malabsorption and is encouraged. He takes loperamide before meals and a high-dose proton pump inhibitor, PPI, and eats more than seems normal.

12:36Whether cholestyramine helps him depends on how much ileum was lost, so his operation note is read before it's prescribed. Cholestyramine is reserved for thirty to one hundred centimeters of ileal resection, where unabsorbed bile acids cause a colonic secretory diarrhea. Beyond one hundred centimeters, the bile acid pool itself is depleted, and binding what's left worsens steatorrhea, the difference between bile acid diarrhea and fatty diarrhea covered in chapter twelve. His whole ileum is gone, so he doesn't get it. Had he lost fifty centimeters of ileum, his diarrhea would have been bile acid diarrhea, and cholestyramine would have helped. If he also had pancreatic insufficiency, pancreatic enzyme replacement would be added.

13:21He's still dependent on parenteral nutrition, so the next step is a drug that grows his remaining bowel. Teduglutide is a glucagon-like peptide-two analog that increases villus height, slows gastric and intestinal transit, and reduces parenteral nutrition requirements in dependent adults with short bowel syndrome. In randomized trials, about sixty percent of treated patients cut their weekly parenteral volume by at least twenty percent, and a meaningful subset came off it entirely. Because its trophic effect raises a theoretical concern about colorectal polyp growth, colonoscopy with polyp removal is required within six months before starting, again at the end of the first year, and then every five years. That surveillance is precautionary, since colorectal cancer incidence in trial patients wasn't raised. Teduglutide is contraindicated in active gastrointestinal malignancy, because its trophic effect could speed tumor growth. His colonoscopy is normal, he starts teduglutide, and over a year his parenteral nutrition falls to two nights a week.

14:23His retained colon then brings kidney stones. Six months later he passes a calcium oxalate stone. He has enteric hyperoxaluria, which develops in short bowel patients who still have a colon. Normally, dietary calcium binds oxalate in the gut lumen, and the complex leaves in stool. With fat malabsorption, unabsorbed long-chain fatty acids bind calcium as soaps, leaving oxalate free for the colon to absorb and the kidney to precipitate. Prevention is a low-oxalate diet, avoiding spinach, rhubarb, beets, nuts, and chocolate, plus oral calcium taken with meals to bind dietary oxalate before it reaches the colon. While he's still on parenteral nutrition, he also carries the same gallstone risk as the first patient, by the same stasis mechanism.

15:09His colon can also make him confused. After a large pasta meal he becomes confused, with slurred speech and an unsteady gait, a normal standard lactate, and a high anion gap metabolic acidosis. He has D-lactic acidosis, which occurs only in short bowel syndrome with a retained colon. Carbohydrate that escapes small bowel absorption reaches the colon, where lactobacilli ferment it into both L-lactate and D-lactate. The body clears D-lactate slowly, so it accumulates, causing neurologic symptoms and a high anion gap. The standard assay measures only L-lactate, so D-lactate has to be requested specifically, and his is high. Treatment is carbohydrate restriction and oral metronidazole or neomycin to suppress the lactobacilli.

15:58If his rehabilitation had failed, surgery would be the remaining option. Lengthening procedures, serial transverse enteroplasty and longitudinal intestinal lengthening and tailoring, can double the functional length of dilated residual bowel in selected patients. Intestinal transplantation is reserved for irreversible failure of intestinal rehabilitation, typically defined by recurrent catheter infections, loss of central venous access, or intestinal failure-associated liver disease with end-stage liver disease.

16:29Here are the traps the boards set in parenteral nutrition. It isn't started when the gut works, or for a low albumin, cancer cachexia, or mild pancreatitis. Dextrose counts as three point four kilocalories per gram, not four. Lipid is given twice weekly to prevent essential fatty acid deficiency. Calcium and phosphate can't be mixed freely, and acetate, not bicarbonate, is the buffer. Long-term patients get a mixed lipid rather than pure soybean, and their feeding is cycled rather than continuous. An infected line is salvaged with antibiotics and a lock when the organism allows, rather than always pulled. A little enteral feeding protects the gallbladder and liver. And a patient whose liver failure is established, whose line infections keep recurring, or who is losing central venous access is referred for intestinal transplantation.

17:19For short bowel syndrome, the traps are these. Prognosis comes from the remaining anatomy, not the length alone. An end-jejunostomy with less than one hundred centimeters almost never reaches autonomy. Plain water and sports drinks increase output. High-dose PPI is needed after extensive resection. Cholestyramine worsens steatorrhea after more than one hundred centimeters of ileal loss. Ileal loss means lifelong B12. Teduglutide needs colonoscopy before it starts and is avoided with active gastrointestinal cancer. A retained colon needs a low-oxalate diet and calcium with meals. A normal standard lactate doesn't exclude D-lactic acidosis. And a patient without a colon doesn't get oxalate stones.

18:05So, start to finish. Use parenteral nutrition only when the gut can't be used: intestinal failure, prolonged ileus, severe pancreatitis that won't tolerate enteral feeding, transplant mucositis, or refractory high-output stomas. Give twenty-five to thirty kilocalories per kilogram with one to one point two grams of amino acids per kilogram, count dextrose at three point four, give lipid twice weekly, respect calcium-phosphate solubility, and use acetate rather than bicarbonate. Cycle long-term feeding over twelve to eighteen hours with a mixed or fish-oil lipid. Line infection, at one to two per thousand catheter-days, is salvaged with antibiotics and locks, and even a little enteral feeding reduces gallstones and liver injury.

18:53Predict short bowel outcome from anatomy: an end-jejunostomy under one hundred centimeters usually needs permanent parenteral nutrition, while a retained colon with sixty to ninety centimeters of small bowel, especially with an ileocecal valve, allows adaptation. Ileal loss means bile acid malabsorption and B12 deficiency. Use a sodium-glucose oral rehydration solution, antimotility drugs, high-dose PPI, and hyperphagia, and give cholestyramine for thirty to one hundred centimeters of ileal resection, not beyond. Teduglutide needs colonoscopy within six months before, at one year, and every five years. With a colon, prevent oxalate stones with a low-oxalate diet and calcium with meals, and treat D-lactic acidosis with carbohydrate restriction and antibiotics.

19:47Episode three is the vitamins, fat-soluble and water-soluble, and the essential fatty acids.

19:50For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode two of four of chapter thirty-two, and I'll see you in the next one.