{"type":"rich","version":"1.0","provider_name":"Transistor","provider_url":"https://transistor.fm","author_name":"Board Pearls","title":"Chapter 32, Ep 2 of 4: Parenteral Nutrition and Short Bowel Syndrome","html":"","width":"100%","height":180,"duration":1050,"description":"Episode two takes the patient whose gut cannot do the work. Parenteral nutrition is a tool for a non-functional gut, with composition rules that follow from chemistry rather than biology and indication discipline that follows from trial data. Its long-term complications are driven by the loss of enteral stimulation, from gallbladder stasis and IFALD to manganese parkinsonism and catheter biofilm infection. Short bowel syndrome then turns on residual anatomy, where the colon's presence or absence determines both the rehabilitation trajectory and the complication pattern, and teduglutide's trophic effect explains both its efficacy and its surveillance burden.\n \nTopics covered\n\nWhen parenteral nutrition is the answer\nComposition rules from chemistry\nLipid emulsions and IFALD\nIndication discipline versus cachexia\nCholelithiasis and manganese parkinsonism\nCatheter-related bloodstream infection\nShort bowel anatomic phenotypes\nTeduglutide and surveillance\nEnteric hyperoxaluria and D-lactic acidosis\n \nKey decisions\n\nDextrose in parenteral nutrition provides three and four-tenths kilocalories per gram, not four, because pharmaceutical dextrose is a monohydrate whose water contributes no calories, so calculating at four per gram overshoots.\nCalcium and phosphate cannot be co-administered freely because they precipitate, so compounding uses solubility tables or split bags, and acetate is the buffer of choice because it is metabolized to bicarbonate.\nParenteral nutrition is reserved for a non-functional gut and is contraindicated or harmful in metastatic cancer cachexia and inferior to enteral feeding in mild-to-moderate acute pancreatitis.\nEven enteral feeding at twenty to thirty percent of caloric needs restores CCK-driven gallbladder contraction and reduces parenteral-nutrition-associated cholelithiasis.\nManganese is removed from parenteral nutrition formulations once cholestasis develops or once globus pallidus T1 hyperintensity appears, since impaired biliary excretion...","thumbnail_url":"https://img.transistorcdn.com/-FuAdDBcPDLhEoUmroZKtOBRvuBn_FHPpYlh41hOnU4/rs:fill:0:0:1/w:400/h:400/q:60/mb:500000/aHR0cHM6Ly9pbWct/dXBsb2FkLXByb2R1/Y3Rpb24udHJhbnNp/c3Rvci5mbS9iNzlh/ZTU4Y2MzNWExMjQ5/MjA5OWMwMmI3ZTk5/NGFiZS5wbmc.webp","thumbnail_width":300,"thumbnail_height":300}