Download - Post Operative Nutrition Basic
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Metabolic responses to starvation
After 12 hrs Starvation
Plasma Insulin Levels drop Glucagon Rises
Hepatic glycogenolysis
Muscle glycogenolysis
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After 24 hrs
Hepatic gluconeogenesis from proteins,
muscles
75 gram protein/day to 300 g of protein per
day may be lost
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Longer fasting
Fat stores mobilized
- glycerol and fatty acids
- ketogenesis 2-3 wks brain adapts to use ketones instead of
glucose
This reduces muscle breakdown
ATP-dependent pathways are suppressed
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Indications for nutritional intervention
Compromise in
Physiology
Immunity
Wound healing
Malnutrition
Infections**
Malignancy
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Indices
Clinical History
Body Composition Analysis
Anthropometry
Respiratory function Triceps thickness, Mid-arm circumference
Biomarkers:
- Pre-albumin
TBP
Nitrogen balance
End-of-bed-ogram
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Nitrogen Balance
measuring 24-hour losses
24-hour urine collection
nitrogen loss is compared with nitrogen
intake, and nitrogen balance is thus obtained.
Nitrogen balance = Intake - Loss (urine 90%,
stool 5%, others 5%)
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Measurements of Immunologic
Function Delayed cutaneous hypersensitivity (anergy)
most commonly tested by delayed reaction to skin
antigens
trauma or infection, anergy to injected cutaneous
recall antigens is associated with high mortality andmorbidity
Neutrophil function
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Glucose
Glucose is the preferred carbohydrate sourcein traditional TPN
Infused glucose has nitrogen-sparing effect:
1. hepatic gluconeogenesis is suppressed.
2. glucose itself is an energy substrate, so fewer
amino acids need be oxidized for energy
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maximum suppression of gluconeogenesis isachieved @infusion rates of4 mg/kg/min
(400 g/day for a 70-kg man)
@infusions rates higher than 9 mg/kg/min
glucose is degraded by nonoxidative pathways,leading to net synthesis of lipid.
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Toxicity of Hyperglycemia and
Excessive Calorie Administration Excess carbohydrate is converted to fat in the liver
-de novo lipogenesis
increase in Vco2
-impaired ventilatory function
Immunosuppression
increased frequency of nosocomial infections.
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Hyperglycaemia
Impairs
chemotaxis
Adherence
Phagocytosis
bactericidal function
* immunosuppression*
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Hypocaloric feeding
diabetic patient with difficult-to-control
blood sugar
massively volume overloaded patient in renal
failure
patient with poor oxygenation who is being
maintained on high ventilatory support
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reasonable protein goal - 1.5 g/kg/day
total calories - 1000kcal/day
limit excessive volume administration
obese patients- have large fat stores
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IMUNONUTRITION
Glutamine free amino acid in the extra and
intracellular compartments
nitrogen transport
acid base homeostasis
fuel for rapidly dividing cells such as
enterocytes, lymphocytes and fibroblasts
antioxidant defence mechanisms by
influencing glutathione synthesis
severe stress or nutritional depletion the
demand < body's capacity to synthesise it.
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Bioelectrical Impedance
Accumulation of lean body mass is theprincipal objective of nutritional support
Bioelectrical Impedance
Exchange of Labeled Ions- Na , K
Neutron Activation Analysis
Computed Tomography
Indirect Calorimetry (RQ)
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creatinine-height index
triceps skinfold thickness
Mid arm circumference ideal body weight (IBW) -before and after
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Carbohydrate:
Gets used in 24hrs
Protein:
Daily 60gm is used,
75 to 300 gm/day in post op
Fat
Daily use 150g
Higher in long starvation
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Cachexia of Cancer
reduced food intake altered metabolic rate
endocrine abnormalities
anticancer treatments cytokines - TNF, IL-1, IL-6, and IFN-
deranged central nervous system satiety
mechanisms Proteolysis-inducing factor (PIF).
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Marked muscle wasting in advanced cancer.
increased rate of ATP-dependent proteolysis with
increased levels of mRNA for ubiquitin and subunits
of the proteolysis-inducing factor (PIF)activates the
ubiquitin-proteasome pathway in muscle
treatment with eicosapentaenoic acid (EPA), blocks
formation of 15-hydroxyeicosatetraenoic acid by PIFin muscle cells, inhibits weight loss even in those
with advanced disease
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Indications for Nutrition Support
1. The patient's premorbid state (healthy or otherwise)
2. Poor nutritional status (current oral intake meeting 7 days' inanition)
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5. An anticipated duration of artificial nutrition
(particularly total parenteral nutrition [TPN]) of
longer than 7 days
6. The degree of the anticipated insult, surgical or
otherwise
7. A serum albumin value less than 3.0 g/dL
measured in the absence of an inflammatory state
8. A transferrin level of less than 200 mg/dL
9. Anergy to injected antigens
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Additional variables
Infections- upto 60%
Thyrotoxicosis
Metabolic disorders
Short bowel
Cancer patient
Burns 110% Multi-organ failure
Obstuctive pathology like Ca- Esophagus,
Distal Stomach
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BMR variations
Patient condition
No post op complications,Fistula without infection
Mild peritonitis, long bonefracture, mild-mod injury
Severe injury, ICU infection,MOF
40- 100% Burns
BMR
Normal
25% above
50% above normal
100% above normal
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Nutrition
Calories- 25-35kcal/kg body wt
Proteins- 1.5 g/kg0.8 to 2 or 2.5g/kg body wt
1g nitrogen (6.25g protein) /150kcal/day
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Vitamins, Trace elements
short-bowel syndrome
extensive ileal resection
pancreatic insufficiency
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Entero-hepatic Circulation
Minerals-zinc, copper, manganese, selenium
Vitamins -cobalamin, folate
Fat-soluble vitamins A, D, E, and K
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DAILY DOSAGE
Vitamins: Water soluble
Thiamine 25 mg
Riboflavin 25 mg
Niacin 200 mg
Pantothenic acid 50 mg
Pyridoxine 50 mg
Folic acid 2.5 mg
Vitamin B12 5 mg
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Fat soluble Vitamins
A- 5000 g
D-
400 g
E 100 g
K 10 mg
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Trace Elements
Zinc 10-20 mg
Copper 0.5-2.0 mg
Chromium 20 g Selenium 70-150 g
Manganese 2-2.5 mg
Iron 25 mg
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Initiation ofNutrition Support
Poor nutritional status (oral intake 10%)
Anticipated duration of artificial nutrition
longer than 7 days
Nonfunctioning gastrointestinal tract
Serum albumin
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Enhanced recovery of patients after
surgery (ERAS)
avoidance of long periods of pre-operative fasting;
re-establishment of oral feeding as early as possibleafter surgery;
integration of nutrition into the overall managementof the patient;
metabolic control, e.g. of blood glucose; electrolytes
reduction of factors which exacerbate stress-related
catabolism or impair gastrointestinal function; early mobilisation
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EN advantages
Prevents intestinal mucosal atrophy
Supports gut associated immunological shield
principal defense against an enteral osmoticload
Cheaper than TPN and has fewer
complications
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Routes for Administration of
Enteral Feeding
Nasogastric tube
Dobhoff tube feeding tubes with indwelling removable
metal stylet
rigid plastic overtube
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Gastrostomy
Stamm gastrostomy- a small laparotomy incision, LUQ
PEG-
Necrosis of the gastric wall
Erythema, Induration
leak due to pull
granulation tissue with intermittent bleeding
continuous drainage.
Percutaneous techniques-
Adhesions, colon perforation, open revision
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Jejunostomy
open jejunostomy
percutaneous -G-J tube
percutaneous - fluoroscopic or CT guidance
continuous fashion feeding
watching for signs of intolerancehypo-osmolar or at most iso-osmolar solutions
Risk ofpneumatosis, necrosis, perforation, and
death
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Gastric feeding
Mortality
Propped up position
hypo-osmolar feeds first
Then, increase osmolality & then volume
? Gastric residual volume
Avoid hyperosmolar feeding:
Pneumatosis bowel necrosis
Perforation mortality
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Parenteral Feeding
>900 mOsm/L
CVL
peripheralTPN (dextrose < 5%) Costly
? Benefit over enteral nutrition
? Complications
Feed tailored??
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Indications
Gastrointestinal cutaneous fistulas
Renal failure (ATN)
Short-bowel syndrome Acute burns
Hepatic failure
?Crohn's disease, Anorexia nervosa ?
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Supportive Benefit
Acute radiation enteritis
Acute chemotherapy toxicity
Prolonged ileus
Weight loss preliminary to major surgery
? Prolonged ventilatory support
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TNA
Total nutrient admixture- 3 in 1
1. Limits the number of central venous
catheter violations and chance for
contamination 2. Produces a hyperosmolar environment in
the TNA solution that protects against
bacterial growth 3. Allows continuous infusion, thereby
ensuring lipid administration at a safe rate
(
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common stock solutions
70% dextrose, 10% to 20% amino acids, and
20% lipid
1 L of solution in the absence of fat, the
maximal achievable concentrations are
7% amino acids (70 g/L) and 21% dextrose (210 g/L).
Volume can be reduced with lipid
emulsification
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PARAMETER DAY 1 DAY 2 DAY 3
Volume
(mL/24 hr)
1000 1000-1500 1500-2000
Calories
(% of goal)
50% 75%, may add fat 100%
Dextrose
(g/24 hr)
100-150 150-200 200-350
Amino acids
(% of total)
50%-100% 100% 100%, check BUN
Fat No Perhaps Often (3%-5%,30-50 g/24 hr)
Insulin Give separately Add 50% to TPN Add 50% to TPN
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Mandatory Monitoring During
Intravenous Nutrition
Clinical:
Vitals
Daily fluid balance
body weight
Evidence of infection-
catheter infectionthrombophlebitis
CVP
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Laboratory:
Baseline & OD
- Electrolytes, BUN, creatinine, Ca, Mg,PO4
Glucose Q6H
Weekly- liver function, coagulation
BASELINE:
LFT, COAGULATION, ELECTROLYTES
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BMR
Male BMR = 66 + (13.7wt in kg) + (5ht in
cm) - (6.8age in yr)
Female BMR = 65.5 + (9.6wt in kg) + (1.7ht
in cm) - (4.7age in yr)
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25 to 35 kcal/kg/day
patient is underweight ABW
patient is obese (ABW is >120%
of IBW)add 25% of the difference between ABW and
IBW to the IBW as the feeding weight.
If no reliable weight is available, use IBW
alone.
IBW [Ht-152
..]*0.91+50
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TPN Formulation
STANDARD
Non-STAND
ARD
(P
rescription)
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Hickmans Cath
Hickman, Broviac, Groshong
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Port A Cath
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Complications- CVL
Catheter Sepsis- Fungemia, S. epidermidis
Catheter Thrombosis
Pneumothorax
vascular injuries (arterial or venous lacerations, delayedarteriovenous fistulas)
brachial plexus injury
chronic pain
thoracic duct injury
air embolism
Erosion of the catheter into the bronchus/ right atrium
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Hepatic dysfunction
Hyperbilirubinemia
Hepatic steatosis, cholestasis
cirrhosis and death in infants
Metabolic Bone Disease
decreased bone mineral density
increased urinary calcium or phosphate excretion
decreased PTH levels
vitamin D deficiency
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Pancreatitis
severe hypertriglyceridemia
glucose intolerance
particularly if sepsis
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Is preoperative metabolic preparation
ofthe elective patient using carbohydrate
treatment useful?
Reduces insulin tolerance
Reduces PONV
But no diff b/w CHO drink and placebo
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Is postoperative interruption of oral
nutritional intake necessary after
surgery?
Inadequate oral intake for more than 14 days
Anticipated -unable to eat for 710 days
intestinal obstructions or ileus
severe shock
intestinal ischemia
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Trends
-3 fatty acids
neutralizing antibodies to TNF
glucocorticoid receptor antagonist RU-486
glucagon-like peptide-2 (GLP-2)
Insulin-like Growth Factors
Growth Hormone
? testosterone
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