Nutrition Support Decision Making - The A.S.P.E.N. Nutrition Support Practice Manual, 2nd Editi

Acknowledgements

A. History

IV. Nutrition Support Decision Making

Increased morbidity and mortality are associated with malnutrition.^80–82 Malnutrition results in loss of lean body mass and subsequent loss of structure or function. Impaired respiratory function, reduced cardiac contractility, impaired renal function, altered immune function, and poor wound healing are known consequences of malnutrition.^58,80,81Based on data gathered from the comprehensive nutritional assessment, a nutrition diagnosis is made and a plan of care set forth. Nutritional intervention decisions include timing, nutrient needs, route of therapy, and whether specialized nutritional formulations are needed. See Figure 1-3 for a decision-making algorithm.

A. Nutrition diagnosis

1. Malnutrition is often diagnosed as mild, moderate, or severe, as seen in Table 1-8. This model is based on weight loss, while other models are a combination of nutritional assessment parameters.

An example of the latter is the Nutrition Risk Index, which strat- ifies nutritional status based on serum albumin and percentage of usual body weight.⁸³

2. Marasmus and kwashiorkor are other diagnostic terms used to describe malnutrition. While these terms traditionally labeled Age Weight Height Circumference

(yrs) gain (cm/yr) (cm/yr)

Preschool 1–2 3.5 kg/yr 12 5

4 2–4 kg/yr 6–8 <1

Middle 7 2 kg/yr 5–6

childhood 10 4 kg/yr 5–6

Adolescent 14–18 13 kg over 4 yrs 9.5–10.3 boys

Adolescent 13–16 11 kg over 3 yrs 8.4–9.0 girls

TABLE 1-11. General Growth Guidelines for Children and Adolescents⁵⁵

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

marasmus malnutrition as depleted fat and muscle stores and the kwashiorkor type as pure protein malnutrition, these terms are con- troversial. Both refer to states of uncomplicated malnutrition, which is a rare occurrence in acute care settings. Further, kwashiorkor, first described in malnourished children in the 1930s, may actually be a condition of undernutrition and inflammation rather than uncomplicated protein deficiency.⁸⁴

3. Coding for malnutrition diagnoses can be found in Chapter 33.

B. Timing of nutritional intervention

1. A well-nourished adult patient without excessive metabolic stress can be expected to tolerate little or no nutrition for up to 7 days.² In adults, it is reasonable to initiate specialized nutrition support (provision of nutrients orally, enterally, or parenterally with therapeutic intent) within 7 to 14 days of inadequate oral intake or if inadequate oral intake is expected over a period of at least 7 to 14 days.^2,8

2. Pediatric patients have increased metabolic rate nutrient needs for growth, and lower nutrient reserves. Surgery or a short-term illness can alter a child’s nutritional status rapidly.⁸⁵Early intro- duction of nutrition support is thought to be indicated for children at high risk of malnutrition or those who are malnourished.

For example, initiation of parenteral nutrition on the first or sec- ond day of life in premature infants has been shown to be bene- ficial for improving early growth^86,87and establishing positive nitrogen balance.⁸⁸For those under 2 years with malnutrition prior to admission, initiation of trophic feedings within 8 hours has been suggested, along with advancing to the nutrition goal within 48 hours if tolerated.⁸⁹For older children, it is suggested that nutrition support start within the first 18 hours and be advanced as tolerated within 24 to 36 hours to goal.

C. Mode of nutrition intervention. Integral to the process of nutrition care and the administration of specialized nutrition support is the decision on route of administration (Figure 1-3).²

1. Indications for enteral nutrition. Enteral nutrition should generally be given in preference to parenteral nutrition when nutritional requirements are not met by oral intake and there is a functional gastrointestinal tract of sufficient length and condition to allow adequate nutrient absorption.²See Chapter 5 for further indications and enteral nutrition management.

2. Indications for parenteral nutrition. Parenteral nutrition should be used when the gastrointestinal tract is not functional or cannot be accessed and in patients who cannot be adequately nourished by oral diets or enteral nutrition.²See Chapter 8 for parenteral nutrition indications and management.

3. Specialized nutrition support may be needed for management of specific conditions such as renal failure, liver failure, or critical illness.

D. Nutrition monitoring and evaluation

1. Once the nutrition assessment is complete and nutrition intervention begins, continuous reassessment (otherwise known as monitoring) is needed. Many of the assessment parameters used initially are repeated serially to assess the efficacy of therapy related to desired outcomes and for potential complications associated with the therapy.

2. The data collected also determine the need for continued nutrition care or discharge from nutrition care.^1,2

(Nutrition assessment chapters from the 1st edition were con- tributed by Eva Politzer Shronts, Judith Fish, Kathy Pesce- Hammond, Kimberly A. Klotz, Jacqueline Wessel, and Geraldine A. Hennies.)

Positive Negative Function

Fibrinogen Clotting process

Prothrombin Clotting process

Antihemophilic Clotting process

Plasminogen Clotting process

Complement proteins Complement cascade, in- (C1s, C1, C2, B, C3, cluding cell lysis, opsonic C4, C5, C56, 1NH) action, and target roles in

immune response Pancreatic secretory Protease enzyme inhibitor trypsin inhibitor that prevents damage to

a1-Antitrypsin healthy tissue

a-Antichymotrypsin

Haptoglobulin Binding of free hemoglobin, inhibition of prostaglandin synthesis

Ceruloplasmin Binding of copper,

antioxidant

C-reactive protein Complement activation, opsonization of DNA and cell membrane debris for subsequent scavenging Albumin Binding of multiple mole-

cules, antioxidant, plasma oncotic pressure

Prealbumin Thyroxine transport and for- mation of a complex with retinol binding protein Retinol-binding Retinol transport

protein

Transferrin Iron absorption and transport Fibronectin Opsonization of noxious

agents, enhancing immune clearance

Insulin-like Promotion of protein syn- growth factor thesis in liver and muscle

and inhibition of lipolysis Reprinted with permission from Mueller C. True or false: serum hepatic protein concentrations measure nutritional status. Support Line.

2004;26(1):8–16.

TABLE 1-12. Acute-Phase Protein Classification and Function

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Vitamin Laboratory assay Normal vvalues Signs of deficiency Signs of toxicity Niacin (B5) Urinary niacin >1.6 mg per g of Pellegra, dermatitis, dementia, death, Liver damage, vascular dilation,

Metabolites creatinine loss of memory, headaches, glossitis flushing, and irritation Folate (B9) Serum folate >6.0 ng/mL Macrocytic anemia, diarrhea, glossitis, None known

lethargy, and stomatitis

Cyanoco- Serum B12 >150 pg/mL Pernicious anemia, glossitis, spinal None known

balamin (B12) cord degeneration, and peripheral

neuropathy

Thiamine (B1) Urinary thiamine >60 mcg per g of Beriberi, paresthesias, nystagmus, (Rare) irritability, headache, insomnia, creatinine impaired memory, congestive heart and interference with B2and B6

failure, lactic acidosis, and Wernicke- Korsakoff syndrome

Riboflavin (B2) Urinary riboflavin >80 mcg per g of Mucositis, dermatitis, cheilosis, None known

creatinine vascularization of cornea, photophobia,

lacrimation, decreased vision, impaired wound healing, and normocytic anemia

Pyridoxine (B6) Plasma B6 >50 ng/mL Dermatitis, neuritis, convulsions, and None known microcytic anemia

Pantothenic Urinary >1 mg/d Fatigue, malaise, headache, insomnia, Diarrhea

acid (B3) pantothenic acid vomiting, and abdominal cramps

Biotin Serum biotin 0.5–2.7 ng/mL Dermatitis, depression, alopecia, None known lassitude, somnolence, anorexia, and

paresthesias

Ascorbic acid Serum ascorbic acid >0.30 mg/dL Enlargement and keratosis of hair Osmotic diarrhea, oxalate kidney stones,

anemia, lethargy, depression, bleed- therapy ing, and ecchymosis

A Plasma vitamin A >20 mcg/dL Dermatitis, night blindness, kera- Acute: nausea, vomiting, headache, tomalacia, and xerophthalmia dizziness; chronic: peeling skin, gingivitis,

and alopecia

D Plasma 25- 29.4 ± 15.7 ng/mL Rickets, osteomalacia, and muscle Excess bone and soft tissue calcification, hydroxyvitamin D weakness kidney stones, and hypercalcemia

E Plasma alpha- >0.5 mg/dL Hemolysis, anemia, neuronal axonopa, Prolonged clotting time tocopherol thy, and myopathy

K Prothrombin time Clotting with 1 s of Bleeding, purpura, and bruising Jaundice laboratory control

TABLE 1-13. Assessment of Vitamin Status^64,72

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

Nutrition assessment

Functional GI Tract Yes

Enteral nutrition Long-term

gastrostomy jejunostomy

Short-term nasogastric nasoduodenal nasojejunal

Diffuse peritonitis, intestinal abstruction, intractable vomiting, ileus, intractable diarrhea, gastrointestinal schemia

GI function

No Yes

Parenteral nutrition

GI function returns

Short-term Long-term or fluid restrition

Peripheral PN Compromised

Normal

Speciality formulas Standard nutrients

Nutrient tolerance

Inadequate PN supplementation

Progress to total enteral feedings

Adequate progress to more complex diet and oral feedings as tolerated Adequate

progress to oral feedings

Central PN

FIGURE 1-3. Routes to Deliver Nutrition Support to Adults: Clinical Decision Algorithm

Reprinted with permission from American Society for Parenteral and Enteral Nutrition.²

Trace Laboratory Normal

Mineral Assay Serum Values Signs of Deficiency Signs of Toxicity

Zinc Serum value 50–150 mcg/dL Dermatitis, hypogeusia, diarrhea, apathy, depression, Nausea, vomiting, metallic taste, impaired wound healing, immunosuppression chills, headache

Copper Serum value 70–150 mcg/dL Neutropenia, microcytic anemia, osteoporosis, decreased Nausea, vomiting, epigastric hair and skin pigmentation, dermatitis, hypotonia pain, diarrhea

Chromium Serum value 1–3 mg/mL Glucose intolerance, peripheral neuropathy, increased None known serum cholesterol and triglyceride, insulin resistance

Manganese Serum value 2–3 mcg/dL Nausea, vomiting, dermatitis, color changes in hair, Extrapyramidal symptoms, hypocholesterolemia, growth retardation encephalitis like symptoms Selenium Serum value 0.01–0.34 mcg/dL Muscle weakness and pain, cardiomyopathy Hair loss, dermatitis, garlic odor,

brittle nails

Molybdenum Neutron 0.4–0.5 mg/mL Tachycardia, tachypnea, altered mental status, vision Increased copper excretion changes, headache, nausea, vomiting

TABLE 1-14. Assessment of Trace Mineral Status^64,72

S E C T I O N I Fundamentals of Nutrition Support Practice and Management

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Dalam dokumen The A.S.P.E.N. Nutrition Support Practice Manual, 2nd Edition (Halaman 41-48)