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
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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
Nutrition Assessment
Decision to institute special nutrition support
YES
Functional GI Tract
Enteral Nutrition
Short-term:
NG, ND,NJ
Parenteral Nutrition
Long-term:
Gastrostomy Jejunostomy
GI function
Intact
Nutrients
Adequate
NO
PPN
Defined
Formula
Inadequate
PN
Oral Feeding
Adequate
TPN
GI function return
YES
NO
PPN
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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
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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
7% A.A. 含 essential A.A. 較高, 適用於腎衰竭病患
含高濃度 branch chain A.A., 低濃度
8% A.A.
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
Lipid emulsions
Volume
Calorie
10%
intralipid
20%
intralipid
10%
lipofundin
500 ml/B
250 ml/B
100 ml/B
550 Kcal/B 500 Kcal/B 110 Kcal/B
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
Care
Complication
Infection
Subclavian vein
Easy
High
Low
Internal jugular vein
Hard
Low
High
Femoral vein
Hard
Low
Highest
Antecubital vein
Easy
Low
High
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
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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
Within 48 hrs of starting TPN
P, Sugar, K, Meta. acidosis
After correction of hypophosphatemia
GI bleeding, Sepsis
Tachycardia, Hypotension
Persistent Cardiopulmonary
Instability
Apnea, MV support
ARDS, Pneumonia
Death
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
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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