全靜脈營養治療
--- 護理人員應備的基本認識
徐中平 醫師
國立陽明大學 外科教授 台中榮民總醫院 臨床營養醫療組召集人 腔外科主治醫師 急診外科主任
Malnutrition
Kwashiorkor - Acute
Inadequate protein intake
Hypoalbuminemia
Fatty liver
Marasmus – Chronic
Inadequate energy intake
Subcutaneous fat loss
Muscle wasting
Marasmic-kwashiorkor
Combination of Kwashiorkor and Marasmus
Historical Attempts at Correcting Malnutrition
BC - Ancient Egyptians rectal feedings
1596 - Tube feeding via esophagus
1790 - Tube feeding into stomach
1881 - Long-term rectal feedings administered
1910 - Duodenal feeding with weighted tube
1918 - Immediate post gastrostomy jejunal feeding, with milk, dextrose, whisky
1940 - duodenal-lumen tube for jejunal feeding, and gastric aspiration
1944 - Early post-op feeding, casein hydrolysate
1952 - Feeding with fine polyethylene tubes milk, liver protein, eggs, hydrolyzed starch
Landmark Hospital Malnutrition Study
Body height not recorded in 56%
Body weight not recorded in 23%
61% of those with recorded weight lost
> 6 Kg
37% had albumin < 3.0 g/dL
Butterworth CE, Nutr Today, 1974
Prevalence of Malnutrition in Hospitals
Numerous studies on hospital
malnutrition have been published
Prevalence of malnutrition in U.S. hospital today ranges from 30% to 50%
Patients’ nutritional status declines with extended hospital stay
Cost KG et al, J Am Diet Assoc, 1993
Malnutrition Among Hospitalized Patient: A Problem with Physician Awareness
Up to 50% of patients admitted may be malnourished
Prior to specific nutritional assessment training
Only 12.5% of malnourished patients identified
After training (4 hours training)
100% of malnourished patient can be identified
Roubenoff R et al, Arch Intern Med, 1987
Prevalence of Malnutrition in Hospitalized Patients
0%
10%
20%
30%
40%
50%
60%
70%
Distribution of Patients
Severely Malnourished Moderately Nourished Well Nourished
Detsky AS et al, JPEN, 1987 Mobarhan S et al, JPEN, 1987
10% 21% 69%
Prevalence of Malnutrition in Hospitalized Patients
46% of general medical patients
45% of respiratory patients
27% of surgical patients
43% of elderly patients
McWhirter JP et al., Br Med J, 1994
Consequences of Malnutrition in Metabolically Stressed Patients
Muscle wasting
Severe weight loss
Delay wound healing
Impaired immunity
Multi-organ dysfunction
Increased length of stay
Higher costs
Increased morbidity/mortality
Malnutrition Is Associated
with Increased Complications
42% of patients with severe malnutrition experience major complications
9% of patients with moderate malnutrition experience major complications
Severely malnourished patients are four times as likely to have post-operative complications as well-nourished patients
Detsky AS et al., JPEN, 1987 Detsky AS et al., JAMA, 1994
Summary
Malnutrition
Widely prevalent
Associated with
Increased morbidity/mortality
Increased length of hospital stay
Higher costs
Nutritional therapy must become an integral part of patient care
Metabolic Response to Starvation and Injury
Metabolism of substrates and micro-nutrients is altered in starvation and injury.
During starvation, metabolic processes slow down to conserve energy and adapt to caloric deprivation.
Following injury, the hormonal milieu of the body is altered increasing the demand for energy, protein, and micronutrients.
Failure to recognize and provide nutritional needs during starvation or injury can result in loss of body mass, loss of body protein, and impairment or loss of body function.
Metabolic Response to Starvation
↑Production and utilization of ketone bodies
↑Release and use of free fatty acids
↓Metabolic rate
Conservation of visceral protein
Metabolic Response to Starvation
Hormone Source Secretion
change Norepinephrine Sympathetic nerve
system
↓↓↓
Norepinephrine Adrenal gland ↑ Epinephrine Adrenal gland ↑ Thyroid hormone
T4 Thyroid gland
(changed to T3 peripherally)
↓↓↓
Landsberg L et al., N Engl J Med, 1978
Metabolic Response to Injury
Ebb Phase
Flow Phase
Time
Energy Expenditure
Cuthbertson D et al., Adv Clin Chem, 1969
Metabolic Response to Injury --- Ebb Phase
Often characterized by hypovolemic shock
Priority is life maintenance/homeostasis
↓Cardiac output
↓ Oxygen consumption
↓ Blood pressure
↓ Tissue perfusion
↓ Body temperature
↓ Metabolic rate
Cuthbertson D et al., Adv Clin Chem, 1969
Metabolic Response to Injury --- Flow Phase
↑Catecholamines
↑ Glucocoticoids
↑ Glucagon
Release of cytokines, lipid mediators
Production of acute phase proteins
Cuthbertson D et al., Adv Clin Chem, 1969
Metabolic Response to Starvation and Injury
Starvation Injury /Illness
Metabolic Rate ↓ ↑↑
Body Fuel conserved wasted
Body Protein conserved wasted
Urinary Nitrogen ↓ ↑↑
Weight Loss slow rapid
The body adapts to starvation but not when accompanied by critical injury or illness.
Popp MB et al., In: Fischer JF, ed. Surgical Nutrition, 1983.
Methods for Determining Caloric Needs
Indirect calorimetry
Most reliable
Harris-Benedict (BEE) x activity factor x stress factor
Most popular
Rapid method
25-30 kcal/kg body weight
Metabolic Response to Overfeeding
Hyperglycemia
Hypertriglyceridemia
Hypercapnia
Fatty liver
Macronutrients During Stress
Carbohydrate
Minimum of 100 g/day is required to prevent ketosis
Carbohydrate level in diet should provide 60-70% of non-protein calories during
stress
Glucose intake should not exceed 5 mg/kg/min
Macronutrients During Stress
Fat
Fat should provide approximately 20-55% of total calories
Maximum recommended rate of intravenous fat infusion is 1.0-1.5 g/kg/day
Serum triglyceride level should be monitored to ensure proper fat
clearance
Macronutrients During Stress
Protein
Requirements range from 1.2-2.0 g/kg/day in stress
Protein should comprise approximately 20% of total calories during stress
Determining Protein Needs of the Hospital Patient
Stress level Non-stressed Mildly stressed Severely stressed
Kcal/N Ratio ≧150:1 150-100:1 ﹤100:1
% Protein/Kcal ﹤15% protein 15-20% protein ﹥20% protein Protein/kg BW 0.8 g/kg/day 1.0-1.2 g/kg/day 1.5-2.0 g/kg/day
Role of Glutamine in Metabolic Injury
Is considered “conditionally essential” for critically ill patient
Is depleted following injury
Provides fuel for the cells of the immune system and GI tract
Helps maintain or restore mucosal integrity
Lacey et al., Nutr Rev, 1990 Smith et al., JPEN, 1990 Pastores et al., Nutr, 1994 Calder, Clin Nutr, 1994
Role of Arginine in Metabolic Injury
Supports cells of the immune system
Enhances nitrogen retention after metabolic stress
Improves wound healing in animal models
Secretagogue and precursor for polyamines and nitric oxide
Barbul A, JPEN,1986
Key Vitamin and Mineral Functions
Vitamin A
Wound healing and tissue repair
Vitamin C
Collagen synthesis, wound repair
B Vitamins
Metabolism, carbohydrate utilization
Pyridoxine
Essential for protein synthesis
Zinc
Wound repair, immune function, protein synthesis
Vitamin E
Antioxidation
Folic Acid, Iron, B12
Necessary for synthesis and turnover of red blood cells
Definition of PNT
Parenteral nutritional therapy is intravenous nutrition
Partial
Complete
Routes of access
Peripheral vein
Central vein
Indication for PNT
The American Society for Parenteral and Enteral Nutrition (ASPEN) states that parenteral nutrition should be
considered as an alternative only when enteral access cannot be obtained or when feeding into the GI tract is
contracted, such as:
Non-functioning GI tract
Inability to use GI tract
“Bowel reset” necessary ASPEN, 1993
Benefits of Enteral Feeding for GI Physiology and Functioin
↓Hypermetabolic response to stress
Helps prevent stress ulcers
Maintains the secretion of gut peptides, secretory IgA and mucin
↓ Loss of nitrogen and protein associated with disuse atrophy
↑Synthesis of digestive enzymes
Maintains the absorptive, immune, endocrine functions of the GI tract
Maintains the barrier functions of the GI tract to prevent bacterial translocation
Clinical Conditions for PNT
Nonfunctioning GI tract
Inability to use the GI tract
Complete intestinal obstruction
Peritonitis
Intractable vomiting
Severe diarrhea of small bowel origin (>1500 mL/day)
Severe small-bowel ileus
High-output (>500 mL/day) entero-
cutaneous fistula (unless able to feed via GI tract distal to the fistula)
Short-bowel syndrome
Severe malabsorption
Contraindication for PNT
Ability to consume and absorb adequate nutrients orally or by enteral tube feeding
Hemodynamic instability
Undefined therapy goals
To prolong life in terminal illness
Central Venous PNT
Therapy > 10 days
Amino acids > 5%
Dextrose 50-70%
Vitamins, minerals, and trace elements
Osmolality > 700 mOsm/L
PNT formula
Amino acids
Standard concentrations range from 5% to 15%
Kcal from amino acids 4 kcal/g
N2 = grams of protein/6.25
PNT Protein Sources
Standard formulation
Crystalline amino acids
Renal formulation
Essential amino acids and histidine
1 g/hour is removed by PD or HD
Hepatic formulation
Branched chain amino acids
PNT Formula
Lipids
use to prevent
essential fatty acid deficiency
Used as a source of non-protein kcal
Available in 10%, 20%, or 30%
concentrations
May be added daily to the base PN
solution or given separately
Fatty acid composition
Chain length
Short chain (≦6 carbons)
Medium-chain (7-12 carbons)
Long-chain (13-27 carbons)
C-bond saturation
Saturated
Unsaturated
MUFA
PUFA (ω-3, and ω-6)
PNT Formula
Electrolytes
Calcium, magnesium, phosphate, chloride, potassium, sodium
Forms and amounts are titrated based on metabolic status and fluid and electrolyte balance
PNT Formula
Vitamins and Minerals
Generally added in amounts lower than RDA for stable patients
Added to the PNT solution daily just before infusion
Acute illness, infection, pre-
existing malnutrition or excessive fluid losses may increase vitamin needs
PNT Formula
Trace Elements
Includes zinc, copper, chromium, manganese daily
Needs may vary among patients and disease status
Long-term PNT patients require the addition of selenium and iron
PNT Monitoring
Parameters
Body weight
N2 balance
Visceral protein parameters
Creatinine-height index
Metabolic
Glucose
Fluid and electrolyte balance
Liver and renal function
Cholesterol and triglycerides
PNT Complications
Catheter related
Insertion
Pneumothorax
Chylothorax
Hemothorax
Air embolism
Arterial puncture
Nerve injury
PNT Complications
Catheter related
Mechanical
Malpositioned catheter
Phlebitis
Thrombosis
Catheter occlusion
Rupture
Embolus
PNT Complications
Catheter related
Infection
Exit site
Tunnel
Colonization
Bacteremia
Systemic sepsis
PNT Complications
Metabolic
Hyper-or hypoglycemia
Electrolyte imbalance
Parenteral azotemia
Acid/base abnormality
PNT Complications
Gastrointestinal
Gastritis and ulceration
Hepatic dysfunction
Gastrointestinal atrophy
PNT Complications
Overfeeding
More than 35 kcal/kg may lead to
Hepatic steatosis
Hyperglycemia
Increased BUN
Hypertriglyceridemia
Respiratory distress syndrome
Increased CO2 production
ENT Complications
Mechanical
Irritation or infection
Use appropriate tubes and devices
Tube displacement
Proper tube secure
Aspiration
30-45% head or bed elevation
Monitoring gastric residuals
Tube clogging
Flush q3-4 hours
ENT Complications
Gastrointestinal
Non-tube feeding factors
Medical condition
GI function
Medications
Failure to feed
Tube feeding factors
Formula composition
Delivery method
Contamination
Formula Composition
Osmolality
Slow infusion rate of hypertonic formula or change to isotonic formula
Lactose
Use lactose free formula
Fiber content
Use fiber-containing formula
Complexity
Change to oligomeric formulas for patients with malabsorption/maldigestion
Continuous Feeding Method of Delivery
In continuous feeding, advance full strength formula slowly
Starts with rate of 25 mL/hour,
then changes to 50 mL/hour, then
changes to 75 mL/hour
Intermittent Feeding Method of Delivery
Initiate at full strength
Initiate at small volumes and slow rates (≦ 250 mL/20 min)
Progress up to no more than 500 mL/30 min
Avoid bolus feeding
Administer jejunal feeding
continuously
Prevention of Tube Feeding Contamination
Recommended formula hang time
Decanted 8-12 hours
Commercially pre-filled containers 24 hours
Practice clean technique when preparing feeding
Criteria for Determining Patient Eligibility for HNT
Willingness to accept therapy
Medical suitability
Rehabilitation potential
Adequate social and economic issues
Acceptable home environment
Acceptable education, psychological and emotional factors