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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
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
Source of Nutrition
? Enteral nutrition
? Parenteral nutrition
- Central parenteral nutrition (CPN=TPN)
- Peripheral parenteral nutrition (PPN)
- Long-term home parenteral nutrition (HPN)
Clinical decision algorithm route of nutrition support
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
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
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
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)
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
Dextrose-content Solution
? 1 g glucose = 3.4 Kcal
? 1 g glucose = 5 mOsm/L
Amino acid solution
Lipid emulsions
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
TPN Order
Vascular Access for TPN
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
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
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
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
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
Intestinal complication
? Villous atrophy: decreases in gut weight and mucosal height
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
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
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
* 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)
* 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
Sequence of events
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
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)
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
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
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
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
Source of Nutrition
? Enteral nutrition
? Parenteral nutrition
- Central parenteral nutrition (CPN=TPN)
- Peripheral parenteral nutrition (PPN)
- Long-term home parenteral nutrition (HPN)
Clinical decision algorithm route of nutrition support
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
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
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
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)
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
Dextrose-content Solution
? 1 g glucose = 3.4 Kcal
? 1 g glucose = 5 mOsm/L
Amino acid solution
Lipid emulsions
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
TPN Order
Vascular Access for TPN
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
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
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
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
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
Intestinal complication
? Villous atrophy: decreases in gut weight and mucosal height
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
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
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
* 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)
* 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
Sequence of events
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
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)
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
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
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