1. Introduction to TPN 新光吳火獅紀念醫院 內科部 胃腸肝膽科 柯威旭 醫師

2. Nutrition Support Team Physicians Clinical pharmacists Nurse-Clinicians Dietitians Laboratory research technician Ward nursing staff In SKH: 主任, 執行秘書, 各科醫師, 藥劑師, 營養 師

3. Source of Nutrition Enteral nutrition Parenteral nutrition –Central parenteral nutrition (CPN=TPN) –Peripheral parenteral nutrition (PPN) –Long-term home parenteral nutrition (HPN)

4. Clinical decision algorithm route of nutrition support Decision to institute special nutrition support Oral Feeding Nutrition Assessment Functional GI Tract Enteral NutritionParenteral Nutrition GI function PPN TPN GI function return Intact Nutrients Defined Formula Adequate Inadequate PN Short-term: NG, ND,NJ Long-term: Gastrostomy Jejunostomy YESNO YES Adequate

5. PPN High risk of thrombophlebitis Osmolarity: less than 800-900 mOsm/kg Short-term: up to 2 weeks Not the optimal choice for –significant malnutrition –severe metabolic stress –large nutrient or electrolyte needs (especially potassium, a strong vascular irritant) –fluid restriction –the need for prolonged intravenous nutrition support

6. Indications of TPN Impossibility for enteral nutrition Inadequacy for enteral nutrition Increment of the severity of disease by enteral nutrition PLUS Anticipated to have PN for more than 7 days

7. TPN in Internal Medicine Acute pancreatitis Intestinal disease (IBD, NEC, radiation colitis, ileus, intractable diarrhea / vomiting) Cancer Hepatic failure Renal failure Short bowel syndrome Enterocutaneous fistula AIDS Perioperative support

8. TPN should not be used in Malignancy: poor response to R/T or C/T Active stage of IBD Relative preserved GI function Hypertriglyceridemia (TG > 400 md/dl)

9. Components of TPN Carbohydrate, Amino acid, Fat, Electrolyte, Water, Vitamin, Trace element Standard solution –Dextrose, Amino acid –Electrolyte (Na, K, Cl, Mg, Ca, P) –Vitamin (A, B1, B2, Niacin, B6, Panthothenic acid, C, D, E, Zn, Cu, Mn, Cr) Lipid emulsion

10. Dextrose-content Solution 1 g glucose = 3.4 Kcal 1 g glucose = 5 mOsm/L

11. Amino acid solution 7% A.A. 含 essential A.A. 較高, 適用於腎衰竭病患 8% A.A. 含高濃度 branch chain A.A., 低濃度 aromatic A.A., 可使肝衰竭病患之 HE 改善 12% A.A. 成人 Standard Solution 之 A.A. 來源

12. Lipid emulsions 10% intralipid 20% intralipid 10% lipofundin Volume500 ml/B250 ml/B100 ml/B Calorie550 Kcal/B500 Kcal/B110 Kcal/B

13. TPN formula B: standard solution D: 8% A.A., high BCAA, low AAA; for hepatic disease E: 35% Dextrose, 12% A.A.; for HD and water restriction F: 29% Dextrose, 12% & 7% A.A.; for ARF with HD G: 29% Dextrose, 7% A.A.; for ESRD

14. TPN Order

15. Vascular Access for TPN CareComplicationInfection Subclavian veinEasyHighLow Internal jugular veinHardLowHigh Femoral veinHardLowHighest Antecubital veinEasyLowHigh

16. Mechanical complication Insertion-of-catheter related: –pneumothorax, brachial plexus injury, subclavian and carotid artery puncture, hemothorax, thoracic duct injury and chylothorax, cardiac perforation, catheter malposition Air embolism Catheter fragment embolism

17. Metabolic complication Fluid overload / Dehydration from osmotic diuresis Hypertriglyceridemia Hypocalcemia Hypomagnesemia Hypophosphatemia Hyperglycemia / Rebound hypoglycemia on sudden cessation of TPN Hyperammonemia Hyperchloremic metabolic acidosis NKHS

18. Infectious complication Catheter-related sepsis: Staph. epidermidis and aureus; solution contamination GNB for immunocompromise Direct evidence: tip culture or blood culture Indirect evidence: fever (up to 38  C, 2 times, every 4 hours), chills, abrupt increase of blood sugar, hypotension, tachycardia, leukocytosis

19. Hepatic complication Biochemical: elevated serum aminotransferase and alkaline phosphatase Histological: steatosis, steatohepatitis, cholestasis, fibrosis and cirrhosis Usually benign and transient, but severe in TPN for > 16 weeks Additive use of Choline, Glutamine and Carnitine may be helpful If cholestasis is present, Cu and Mg should be deleted to prevent acculumation in liver and BG

20. Biliary complication Acalculous cholecystitis, GB sludge, cholelithiasis in TPN for > 3 weeks Decrease of bile salt reabsorption leads to formation of GB stone; Encouraging enteral intake to stimulate GB contraction

21. Intestinal complication Villous atrophy: decreases in gut weight and mucosal height

22. Metabolic bone disease Present in TPN for > 3 months Bone pain, bone fracture or asymptomatic but demineralization in CxR Possible mechanisms –Aluminum toxicity –Vitamin D toxicity –Negative calcium balance

23. Refeeding syndrome The metabolic and physiologic consequences of the depletion, repletion, compartmental shifts and interrelationships of the followings –Phosphorus (< 1mg/dl, death within hours) –Potassium –Magnesium –Glucose metabolism –Vitamin deficiency –Fluid resuscitation

24. Case History 66 y/o female, abdominal pain and anorexia for 6 weeks persistent profuse, yellow, watery diarrhea after construction an ileal conduit for ureteral obstruction lasting for 3 months PE: BW 36 kg, 70% of IBW; afebrile, 108, 14, 98/70  anasarca, cachectic with generalized muscle wastage

25.  Hct 38%, WBC 17000, BUN/Cr 22/1.0, K 3.4, P 3.4, HCO3 17, Sugar 48, Alb. 1.59 Hospital Course  TPN was started with 750g dextrose, 120g AA, 60 mEq Na, 20 mEq K, 15 mmol P in 3L fluid  24 hrs after start of TPN, HR 180, SBP 50, CVP < 3 cmH2O  P 0.7, Na 142, K 1.4, HCO3 19, Mg 1.8,  Sugar 1010, BUN/Cr 27/1.3  pH 7.31, O2 59, CO2 24 (O2 2L)

26.  Apnea and respiratory failure developed within one hour  With stopping TPN and fluid replacement, P 6.9, K 3.5 and Sugar 45 were obtained.  In the following hospitalization, bilateral pneumonia and ARDS were complicated.  Died on the 6th day Autopsy: ischemic enterocolitis, pneumonia, ARDS and peritonitis and the heart was unremarkable

28. Sequence of events P, Sugar, K, Meta. acidosis GI bleeding, Sepsis Tachycardia, Hypotension Apnea, MV support ARDS, Pneumonia Persistent Cardiopulmonary Instability Death Within 48 hrs of starting TPN After correction of hypophosphatemia

29. Physiology of Starvation When BMR = energy output to the limited intake, endogenous fuels must be used Major storage fuel is fat in form of TG (60-75 days) Carbohydrate, in contrast, is quantitatively insignificant storage fuel (1200 kcal, 1 day’s resting ER) Protein, 12kg, 2 weeks’ worth of calories; but is for nonfuel function

30. Metabolic Response to Refeeding A shift from body fat to CHO as major fuel source Insulin Glycogenolysis, gluconeogenesis and FA mobilization from adipose tissue is inhibited Cellular uptake of glucose, K, P, and Mg is enhanced by insulin Antinatriuretic effect (Na retention and ECF expansion)

31. Patient of risk for refeeding syndrome Chronic alcoholism Anorexia nervosa Classic marasmus Classic kwashiorkor Chronic undernourishment Morbid obesity with massive weight loss Prolonged hypocaloric intravenous hydration NPO for greater than 7-10 days Cardiac and cancer cachexia

32. Recommendations to avoid refeeding syndrome Be aware of the syndrome Recognize the patient at risk Correct electrolyte imbalance before initiating nutritional support whether by the oral, enteral or parenteral route Judiciously restore circulatory volume, monitor HR, and I/O Increase caloric delivery slowly Administer vitamins routinely Closely monitor electrolyte over the 1st week: Serum P, K, Mg, Sugar and urine electrolytes A little nutrition support is good, too much is lethal