Introduction to TPN

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Introduction to TPN

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Nutrition Support Team

• Physicians
• Clinical pharmacists
• Nurse-Clinicians
• Dietitians
• Laboratory research technician
• Ward nursing staff
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Source of Nutrition

• Enteral nutrition
• Parenteral nutrition
• Central parenteral nutrition (CPNTPN)
• Peripheral parenteral nutrition (PPN)
• Long-term home parenteral nutrition (HPN)

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Clinical decision algorithm route of nutrition
support
Nutrition Assessment
Decision to institute special nutrition support
YES
NO
Functional GI Tract
Enteral Nutrition
Parenteral Nutrition
Short-term NG, ND,NJ
Long-term Gastrostomy Jejunostomy
GI function
TPN
PPN
GI function return
Intact Nutrients
Defined Formula
Adequate
Inadequate
Adequate
NO
YES
PN
Oral Feeding
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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

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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

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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

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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 gt 400 md/dl)

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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

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Dextrose-content Solution

• 1 g glucose 3.4 Kcal
• 1 g glucose 5 mOsm/L

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Amino acid solution
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Lipid emulsions
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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

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TPN Order
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Vascular Access for TPN
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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

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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

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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

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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 gt 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

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Biliary complication

• Acalculous cholecystitis, GB sludge,
  cholelithiasis in TPN for gt 3 weeks
• Decrease of bile salt reabsorption leads to
  formation of GB stone
• Encouraging enteral intake to stimulate GB
  contraction

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Intestinal complication

• Villous atrophy decreases in gut weight and
  mucosal height

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Metabolic bone disease

• Present in TPN for gt 3 months
• Bone pain, bone fracture or asymptomatic but
  demineralization in CxR
• Possible mechanisms
• Aluminum toxicity
• Vitamin D toxicity
• Negative calcium balance

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Refeeding syndrome

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

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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

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• 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 lt
  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)

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• 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

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Sequence of events
Within 48 hrs of starting TPN
After correction of hypophosphatemia
P, Sugar, K, Meta. acidosis
GI bleeding, Sepsis
Tachycardia, Hypotension
Persistent Cardiopulmonary Instability
Apnea, MV support
Death
ARDS, Pneumonia
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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 days
  resting ER)
• Protein, 12kg, 2 weeks worth of calories but is
  for nonfuel function

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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)

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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

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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