nutri Flashcards
Triglyceride (TG) present in adipose tissue is the body’s major fuel reserve and is critical for survival during periods of starvation
The high energy density and hydrophobic nature of
TGs make them a five-fold better fuel per unit mass than glycogen.
TGs liberate 9.3 kcal/g when oxidized and are stored compactly as oil inside the fat cell
comparison, glycogen produces only 4.1 kcal/g on oxidation and is stored intracellularly as a gel
During endurance exercise, glycogen and TGs in muscle tissue provide an important source of fuel for working muscles
Daily total energy expenditure (TEE) has three components:
resting energy expenditure (REE) (≈70% of TEE);
the energy expenditure of physical activity (≈20% of TEE)
the thermic effect of feeding (≈10% of TEE), which is thetemporary increase in energy expenditure that accompanies enteral ingestion or parenteral administration of nutrients
REE represents energy expenditure while a person lies quietly awake in an interprandial state; under these conditions, about 1 kcal/kg body weight is consumed per hour in healthy adults.
The liver, intestine, brain, kidneys, and heart constitute roughly 10% of total body weight but account for about 75% of REE.
In contrast, skeletal muscle at rest consumes some 20% of REE, but represents approximately 40% of body weight
Adipose tissue consumes less than 5% of REE but usually accounts for greater than 20% of body weight.
accurate assessment of REE is best obtained by indirect calorimetry, in which in vivo energy expenditure is estimated by measuring carbon dioxide production and oxygen consumption
while the subject is at rest.
Although indirect calorimetry is considered a gold standard for determining REE, obtaining such a measurement is not always practical
Harris-Benedict and Mifflin equations are designed for use in adults, whereas the WHO formulas includes equations for both children and adults.
Protein energy malnutrition (PEM) and hypocaloric feeding without superimposed illness each decrease REE to values 10% to 15% below those expected for actual body size, whereas acute illness or trauma predictably increases energy expenditure
Highly trained athletes can increase their TEE 10- to 20-fold during athletic events
The energy expended during a particular physical activity is equal to (REE per hour) × (activity factor) × (duration of activity in hours).
TEE represents the summation of energy expended during all daily activities, including rest periods
Eating or infusing nutrients increases metabolic rate.
Dietary protein causes the greatest stimulation of metabolic rate, followed by carbohydrate
and then fat.
A meal containing all these nutrients usually increases metabolic rate by 5% to 10% of ingested or infused calories
In arriving at a nutritional plan for hospitalized patients, it is usually not necessary to obtain actual measurements of energy expenditure with a bedside indirect calorimeter
The increase in energy expenditure is roughly proportional to the magnitude of the stress
Thus, the total daily energy requirement of an acutely ill patient can be estimated by multiplying the predicted REE (as determined by the Harris-Benedict or WHO equations) by a stress factor:
In acutely ill hospitalized patients, it is not usually necessary to include an activity factor
An alternative and simple formula for adult inpatients,
although accompanied by some further loss in accuracy, is
20 to 25 kcal/kg of actual body weight (ABW)/day for unstressed or mildly stressed patients
25 to 30 kcal/ABW/day for moderately stressed patients
30 to 35 kcal/ABW/day for severely stressed patients
In using this formula, adjustments are necessary when the ABW is a misleading reflection of lean body mass.
An adjusted ideal body weight (IBW) should be substituted for ABW in obese individuals who are more than 30% heavier than their IBW (desirable body weights
Using an adjusted IBW helps prevent an overestimation of energy requirements and is calculated as:
Adjusted IBW = IBW + 0.5 (ABW − IBW)
Relative Thermic Effect of Various Levels of Physical Activity
Resting 1.0
Very light Standing, driving, typing 1.1-2.0
Light Walking 2-3 miles/hr, shopping, light housekeeping 2.1-4.0
Moderate Walking 3-4 miles/hr, biking, gardening, scrubbing floors
4.1-6.0
Heavy Running, swimming, climbing, basketball
6.1-10.0
In patients with large artifactual increases in weight due to extracellular fluid retention (e.g., ascites), the IBW should be used to estimate energy requirements rather than the ABW
The most accurate and extensively validated equation for predicting daily energy expenditure in ill patients is one that does not incorporate a stress factor; it does, however, require knowledge of the minute ventilation, so its use is restricted to patients on mechanical ventilation.
This formula (often referred to as the “Penn State Equation”)
Injury or Illness Relative Stress Factor*
Second- or third-degree burns, >40% BSA
1.6-2.0
Multiple trauma 1.5-1.7
Second- or third-degree burns, 20%-40% BSA
1.4-1.5
Severe infections 1.3-1.4
Acute pancreatitis 1.1-1.2
Second- or third-degree burns, 10%-20% BSA
1.2-1.4
Long bone fracture 1.2
Peritonitis 1.2
Uncomplicated postoperative state 1.1
*A stress factor of 1.0 is assumed for healthy controls.
significantly reduced in those randomized to intensive insulin therapy who maintained serum glucose levels below 111 mg/dL, compared with those whose glucose values were maintained below 215 mg/dL.
popular nutritional approach to such patients is
so-called hypocaloric feeding, in which only 60% to 70% of the estimated energy requirement (or 11 to 14 kcal/kg of ABW) is delivered in conjunction with 2 to 2.5 grams of protein/kg of IBW per day,
the latter minimizing the risk of producing net protein catabolism and loss of lean body mass purported advantages of hypocaloric feeding include improved glycemic control and prevention of metabolic complications like hypercapnia and hypertriglyceridemia.
Estimated Energy Requirements for Hospitalized Patients Based on Body Mass Index
Energy Requirements (kcal/kg/ day)*
<15 =35-40
15-19 =30-35
20-29 =20-25
≥30 =15-20
These values are recommended for critically ill patients and all obese patients; add 20% of the total calories when estimating energy requirements in non–critically ill patients.
Twenty different amino acids (AAs) are commonly found in human proteins.
Some AAs (histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, valine, and possibly arginine) are considered essential because their carbon skeletons cannot be synthesized by the body
The body of an average 75-kg man contains about 12 kg of protein. In contrast to fat and carbohydrate, there is no storage depot for protein, so excess intake is catabolized and the nitrogen component is excreted
The U.S. Recommended Daily Allowance (RDA) of protein has been established at 0.8 g/kg/day, which reflects a mean calculated requirement of 0.6 g/kg/day plus an added factor to take into account the biological
variance in requirement observed in a healthy population
Clinical Condition Daily Protein Requirement (g/kg IBW)
Normal 0.80
Metabolic stress 1.0-1.6
Hemodialysis 1.2-1.4
Peritoneal dialysis 1.3-1.5
As metabolic stress (and with it, metabolic rate) increases, nitrogen excretion increases proportionately; quantitatively, the relationship is approximately 2 mg nitrogen (N)/kcal of REE.
in metabolic stress, a larger proportion of the total substrate oxidized for energy is from protein.
The first is that illness, by increasing catabolism and metabolic rate, increases the absolute requirement
for protein and does so in a manner that is
roughly proportional to the degree of stress.
Second, because a greater proportion of energy substrate in acute illness comes from protein, nitrogen balance is more readily achieved if a larger proportion
of the total calories are from protein
Most patients with hepatic encephalopathy respond
to simple pharmacologic measures and, therefore, do not require protein restriction; those who do not respond may benefit from a modest protein restriction (≈0.6 g/kg/day)
Nitrogen (N) balance is commonly used as a proxy measure of protein balance
Every 6.25 g of administered protein (or AAs) contains approximately 1 g of N.
The additional 4 g of N loss incorporated into
the equation is intended to account for the insensible losses from the other sources listed and because urinary urea N only accounts for approximately 80% of total urinary nitrogen.
N balance is a suitable surrogate for protein balance, because roughly 98% of total body N is in protein, regardless of one’s health.
A positive N balance (i.e., intake > loss) represents anabolism and a net increase in total body protein, whereas a negative N balance represents net protein catabolism.
For example, a negative N balance of 1 g/day represents a 6.25 g/day loss of body protein, which is equivalent to a 30 g/day loss of hydrated lean tissue
Complete digestion of the principal dietary digestible carbohydrates— starch, sucrose, and lactose—generate monosaccharides (glucose, fructose, and galactose).
In addition, 5 to 20 g of indigestible carbohydrates (soluble and insoluble fibers) are typically
consumed daily.
glucose is the required or preferred fuel for red and white blood cells, the renal medulla, eye tissues, peripheral nerves, and the brain.
However, once glucose requirements for these tissues are met (≈150 g/day), the protein-sparing effects of carbohydrate and fat are similar
Dietary lipids are composed mainly of TGs,
which contain saturated and unsaturated long-chain fatty acids (FAs) of 16 to 18 carbons.
Use of fat as a fuel requires hydrolysis
of endogenous or exogenous TGs and cellular uptake of released FAs (see Chapter 102).
Long-chain FAs are delivered across the outer and inner mitochondrial membranes by a carnitine- dependent transport system.
Humans lack the desaturase enzyme needed to produce the n-3 (double bond between carbons 3 and 4) and n-6 (double bond between carbons 6 and 7) FA series.
Linoleic acid (C18:2, n-6) and linolenic acid (C18:3, n-3) are essential FAs and, therefore, should constitute at least 2% and 0.5%,
Adults who have moderate-to-severe fat malabsorption
(fractional fat excretion >20%) from other causes and
who are not TPN-dependent also frequently display a biochemical profile of EFAD
The biochemical diagnosis of EFAD is defined as an absolute and relative deficiency in the 2 EFAs in the plasma FA profile.
The full clinical EFAD syndrome includes alopecia, scaly dermatitis, capillary fragility, poor wound healing, increased susceptibility to infection, fatty liver, and growth retardation in infants and children
Major minerals are inorganic nutrients that are required in large (>100 mg/day) quantities and are important for ionic equilibrium, water balance, and normal cell function
Micronutrients (vitamins and trace minerals) are a diverse array of dietary components that are necessary to sustain health
none of the fat-soluble vitamins appear to serve as coenzymes, whereas almost all of the watersoluble
vitamins appear to function in that role
Calcium 1000-1200 mg
5-15
Metabolic bone disease, tetany, arrhythmias
24-hr urinary calcium = Reflects recent intake
Dual energy radiation absorptiometry= Reflects bone calcium content
Magnesium 300-400 mg
5-15
Weakness, twitching, tetany,
arrhythmias, hypocalcemia
Serum magnesium = May not reflect body stores
Urinary magnesium= May not reflect body stores
Phosphorus 800-1200 mg
20-60
Weakness, fatigue, leukocyte and platelet dysfunction, hemolytic anemia, cardiac failure, decreased oxygenation
Plasma phosphorus = May not reflect body stores
Potassium 2-5 g
60-100
Weakness, paresthesias, arrhythmias
Serum potassium =May not reflect body stores
Sodium 0.5-5 g
60-150
Hypovolemia, weakness
Urinary sodium May not reflect body stores
clinical evaluation is best
Vit A
Follicular hyperkeratosis and night blindness are early indicators.
Conjunctival xerosis, degeneration of the cornea (keratomalacia), and dedifferentiation of rapidly proliferating epithelia are later indications of deficiency.
Bitot spots (focal areas of the conjunctiva or cornea with foamy appearance) are an indication of xerosis.
Blindness caused by corneal destruction and retinal dysfunction may ensue.
Increased susceptibility to infection is also a consequence (1 μg of retinol is equivalent to 3.33 IU of
vitamin A; F, 700 μg; M, 900 μg)
Vit A
In adults, >150,000 μg may cause acute toxicity: fatal intracranial hypertension, skin exfoliation, and
hepatocellular injury. Chronic toxicity may occur with habitual daily intake of >10,000 μg: alopecia, ataxia, bone
and muscle pain, dermatitis, cheilitis, conjunctivitis, pseudotumor cerebri, hepatic fibrosis, hyperlipidemia, and hyperostosis are common. Single large doses of vitamin A (30,000 μg) or habitual intake of >4500 μg/ day during early pregnancy can be teratogenic. Excessive intake of carotenoids causes a benign
condition characterized by yellowish discoloration of the skin (3000 μg).
Retinol concentration in the plasma, as well as vitamin A concentrations in milk and tears, are reasonably accurate measures of status. Toxicity is best assessed by elevated levels of retinyl esters in plasma. A quantitative measure of dark adaptation for night vision and electroretinography are useful functional tests.
VitD D
Deficiency results in decreased mineralization of newly formed bone, a condition called rickets in childhood and osteomalacia in adults.
Deficiency also contributes to osteoporosis in later life and is common following gastric bypass procedures.
Expansion of epiphyseal growth plates and replacement of normal bone with unmineralized
bone matrix are the cardinal features of rickets;
the latter feature also characterizes osteomalacia.
Deformity of bone and pathologic fractures result.
Decreased serum concentrations of calcium and
phosphate may occur (1 μg is equivalent to 40 IU;
15 μg, ages 19-70; 20 μg, ages > 70).
Excess amounts result in abnormally high concentrations of calcium and phosphate in the serum; metastatic calcifications, renal damage, and altered mentation may occur (100 μg for ages >9).
Serum concentration of the major circulating metabolite, 25-hydroxyvitamin D, is an excellent indicator of systemic
status except in advanced kidney disease (stages 4-5), in which impairment of renal 1-hydroxylation results in dissociation of the mono- and dihydroxy vitamin concentrations; measuring the serum concentration of
1,25-dihydroxyvitamin D is then necessary.
Vitamin E
Deficiency caused by dietary inadequacy is rare in developed countries. Usually seen in premature
infants, individuals with fat malabsorption, and
individuals with abetalipoproteinemia.
RBC fragility occurs and can produce hemolytic
anemia. Neuronal degeneration produces
peripheral neuropathies, ophthalmoplegia, and
destruction of the posterior columns of the
spinal cord.
Neurologic disease is frequently
irreversible if deficiency is not corrected early
enough.
May contribute to hemolytic anemia and retrolental fibroplasia in premature infants. Has been reported to suppress cell-mediated immunity (15 mg).
Depressed levels of vitamin K-dependent procoagulants, potentiation of oral anticoagulants, and impaired leukocyte function have been reported. Doses of 800 mg/day have been reported to increase slightly the incidence of hemorrhagic stroke (1000 mg).
Plasma or serum concentration of alpha-tocopherol is used most commonly. Additional accuracy is obtained by expressing this value per mg of total plasma lipid. The RBC peroxide hemolysis test is not entirely specific but is a useful measure of the susceptibility of cell membranes to oxidation
Vit K
Deficiency syndrome is uncommon except in breast-fed newborns (in whom it may cause “hemorrhagic disease of the newborn”), adults who have fat malabsorption or are taking drugs that interfere with vitamin K metabolism (e.g., warfarin, phenytoin, broad-spectrum antibiotics), and individuals taking large doses of vitamin E and anticoagulant drugs. Excessive hemorrhage is the usual manifestation (F, 90 μg; M, 120 μg).
Rapid IV infusion of vitamin K1 has been associated with dyspnea, flushing, and cardiovascular
collapse; this is likely related to the dispersing agents in the dissolution solvent.
Supplementation may interfere with warfarin-based
anticoagulation.
Pregnant women taking large amounts of the
provitamin menadione may deliver infants with hemolytic anemia, hyperbilirubinemia, and kernicterus
(TUL not established).
Prothrombin time is typically used as a measure of functional vitamin K status; it is neither sensitive nor specific for vitamin K deficiency.
Determination of fasting plasma vitamin K is an accurate indicator.
Undercarboxylated plasma prothrombin is also an accurate metric, but only for detecting the deficient state, and is less widely available.
Thiamine (vitamin B1)
Classic deficiency syndrome (beriberi) remains
endemic in Asian populations consuming polished
rice diet.
Globally, alcoholism, chronic renal dialysis, and persistent nausea and vomiting after bariatric surgery are common precipitants.
High carbohydrate intake increases the need for B1. Mild deficiency commonly produces irritability, fatigue,
and headaches.
More pronounced deficiency can produce peripheral neuropathy, cardiovascular and cerebral dysfunction.
Cardiovascular involvement (wet beriberi) includes heart failure and low peripheral vascular resistance.
Cerebral disease includes nystagmus, ophthalmoplegia, and ataxia (Wernicke encephalopathy), as well as hallucinations, impaired short-term memory, and confabulation (Korsakoff psychosis).
Deficiency syndrome responds within 24 hr to parenteral thiamine but is partially or wholly irreversible after a certain stage (F, 1.1 mg; M, 1.2 mg).
Excess intake is largely excreted in the urine, although parenteral doses of >400 mg/day are reported to cause
lethargy, ataxia, and reduced tone of the GI tract (TUL not established).
The most effective measure of vitamin B1 status is the RBC transketolase activity coefficient, which measures enzyme activity before and after addition of exogenous
TPP;
RBCs from a deficient individual express a substantial
increase in enzyme activity with addition of TPP. Thiamine concentrations in the blood or urine are also measured
Riboflavin
(vitamin B2)
Deficiency is usually seen in conjunction with deficiencies of other B vitamins.
Isolated deficiency of riboflavin produces hyperemia
and edema of nasopharyngeal mucosa, cheilosis, angular stomatitis, glossitis, seborrheic
dermatitis, and normochromic, normocytic
anemia (F, 1.1 mg; M, 1.3 mg).
Toxicity has not been reported in humans (TUL not established).
Most common method of assessment is determining the activity coefficient of glutathione
reductase in RBCs (the test is invalid for individuals with glucose- 6-phosphate dehydrogenase
deficiency).
Measurements of blood and urine concentrations are less desirable methods.
Niacin (vitamin B3)
Pellagra is the classic deficiency syndrome and is
often seen in populations in which corn is the major
source of energy.
Still endemic in parts of China, Africa, and India. Diarrhea, dementia (or associated symptoms of anxiety or insomnia), and a pigmented dermatitis that develops in sun-exposed areas are typical features. Glossitis, stomatitis, vaginitis, vertigo, and burning dysesthesias are early signs.
Occasionally occurs in carcinoid syndrome, because tryptophan is diverted to other synthetic pathways (F, 14 mg; M, 16 mg).
Human toxicity is known largely through studies examining hypolipidemic effects; includes flushing,
hyperglycemia, hepatocellular injury, and hyperuricemia (35 mg).
Assessment of status is problematic; blood levels of the vitamin are not reliable.
Measurement of urinary excretion of the niacin
metabolites N-methylnicotinamide and 2-pyridone are thought to be the most effective means of assessment.
Pantothenic acid (vitamin B5)
Deficiency is rare; reported only as a result of
feeding semisynthetic diets or consumption
of an antagonist such as calcium homopantothenate, which has been used to treat Alzheimer disease.
Experimental isolated deficiency in humans produces fatigue, abdominal pain and vomiting, insomnia, and
paresthesias of the extremities (5 mg).
Diarrhea is reported to occur with doses exceeding 10 g/day (TUL not established).
Whole blood and urine concentrations of pantothenic
acid are indicators of status; serum levels are not thought to be accurate.
Pyridoxine
(vitamin B6)
Deficiency is usually seen in conjunction with other
water-soluble vitamin deficiencies. Stomatitis,
angular cheilosis, glossitis, irritability, depression,
and confusion occur in moderate to severe
depletion; normochromic, normocytic anemia
has been reported in severe deficiency.
Abnormal EEGs and, in infants, convulsions also have been reported.
Isoniazid, cycloserine, penicillamine, ethanol, and theophylline are drugs that can inhibit B6 metabolism (ages 19-50, 1.3 mg; >50 yr, 1.5 mg for women, 1.7 mg for men)
Chronic use with doses exceeding 200 mg/day (in adults) may cause peripheral neuropathies and photosensitivity (100 mg).
Many useful laboratory methods of assessment exist. Plasma or erythrocyte PLP levels are most common.
Urinary excretion of xanthurenic acid after an oral
tryptophan load or activity indices of RBC aminotransferases (ALT and AST) all are functional measures of B6-dependent enzyme activity
Biotin (vitamin B7)
Isolated deficiency is rare.
Deficiency in humans has been produced experimentally by dietary inadequacy, prolonged administration of TPN that lacks the vitamin, and ingestion of large quantities of raw egg white, which contains avidin, a protein that binds biotin with such high affinity that it renders it bio-unavailable.
Alterations in mental status, myalgias, hyperesthesias, and anorexia occur. Later, seborrheic dermatitis and alopecia develop. Biotin deficiency is usually accompanied by lactic acidosis and organic aciduria (30 μg).
Toxicity has not been reported in humans, with doses as high as 60 mg/day in children (TUL not established).
Plasma and urine concentrations of biotin are diminished in the deficient state. Elevated urine concentrations of methyl citrate, 3-methylcrotonylglycine, and 3-hydroxyisovalerate are also observed in deficiency
Folate (Vitamin B9)
Women of childbearing age are the most likely
to develop deficiency.
The classic deficiency syndrome is a megaloblastic anemia.
Hematopoietic cells in the bone marrow become
enlarged and have immature nuclei, reflecting
ineffective DNA synthesis.
The peripheral blood smear demonstrates macro-ovalocytes and polymorphonuclear leukocytes with an average of more than 3.5 nuclear lobes.
Megaloblastic changes in other rapidly proliferating epithelia (e.g., oral mucosa, GI tract) produce glossitis
and diarrhea, respectively.
Sulfasalazine and diphenytoin inhibit absorption, predisposing to deficiency.
Habitually low intake may increase the risk of colorectal cancer. (400 μg of dietary folate equivalent [DFE]; 1 μg folic acid = 1 μg DFE; 1 μg food folate = 0.6 μg DFE)
Daily dosage >1000 μg may partially correct the anemia of B12 deficiency and therefore mask
(and perhaps exacerbate) the
associated neuropathy.
Large doses are reported to lower seizure
threshold in individuals prone to
seizures.
Parenteral administration is rarely reported to cause allergic phenomena from dispersion agents
(1000 μg).
Serum folate levels reflect short-term folate balance, whereas RBC folate is a better reflection of tissue
status.
Serum homocysteine levels rise early in deficiency but
are nonspecific because B12 or B6 deficiency, renal insufficiency, and older age may also cause elevations.
Cobalamin (vitamin B12)
Dietary inadequacy is a rare cause of deficiency,
except in strict vegetarians.
The vast majority of cases of deficiency arise from loss of intestinal absorption—a result of pernicious anemia,
pancreatic insufficiency, atrophic gastritis, SIBO,
or ileal disease.
Megaloblastic anemia and megaloblastic changes in other epithelia (see “Folate”) are the result of sustained depletion.
Demyelination of peripheral nerves, the posterior
and lateral columns of the spinal cord, and
nerves within the brain may occur. Altered
mentation, depression, and psychoses occur.
Hematologic and neurologic complications may
occur independently.
Folate supplementation in doses exceeding 1000 μg/day may partly correct the anemia, thereby masking (or perhaps exacerbating) the neuropathic complications (2.4 μg
A few allergic reactions have been reported from crystalline B12 preparations and are probably due to impurities, not the vitamin (TUL not established).
Serum or plasma concentrations are generally accurate.
Subtle deficiency with neurologic complications is increasingly recognized among those ≥ 60 yr of
age, and can best be established by concurrently measuring the concentration of plasma B12 and (1) serum methylmalonic acid (MMA) or (2) holotranscobalamin II (holoTCII) because the latter are sensitive indicators of cellular deficiency.
A low-normal plasma B12 of 200-350 pg/mL (=148-258
pmol/L) with an elevated MMA or decreased holoTCII should be considered a state of deficiency
Ascorbic and dehydroascorbic acid (vitamin C)
Overt deficiency is uncommonly observed in
developed countries.
The classic deficiency syndrome is scurvy, characterized by fatigue, depression, and widespread abnormalities in connective tissues (e.g., inflamed gingivae, petechiae, perifollicular hemorrhages, impaired wound healing, coiled hairs, hyperkeratosis, and bleeding into body cavities).
In infants, defects in ossification and bone growth may occur. Tobacco smoking lowers plasma and leukocyte
vitamin C levels (F, 75 mg; M, 90 mg; the requirement for cigarette smokers is increased by 35 mg/day).
Quantities exceeding 500 mg/day (in
adults) sometimes cause nausea and
diarrhea.
Acidification of the urine with vitamin C supplementation, and the potential for enhanced
oxalate synthesis, have raised concerns regarding nephrolithiasis, but this has yet to be demonstrated.
Supplementation with vitamin C may interfere with laboratory tests based on redox potential (e.g., fecal occult blood testing, serum cholesterol,
serum glucose).
Withdrawal from chronic ingestion of high doses of vitamin C supplements should occur gradually over 1 month because accommodation does seem to occur, raising a concern for rebound scurvy (2000 mg).
Plasma ascorbic acid concentration reflects recent dietary intake, whereas leukocyte levels more
closely reflect tissue stores.
Plasma levels in women are ≈20% higher than in men for any given dietary intake.
Chromium Deficiency in humans is only described for patients on long-term TPN containing inadequate
chromium
Hyperglycemia or impaired glucose tolerance is uniformly observed
Copper Dietary deficiency is rare
it has been observed in premature and low-birth-weight infants exclusively fed a cow’s milk diet and in
individuals on long-term TPN without copper.
Clinical manifestations include depigmentation
of skin and hair, neurologic disturbances, leukopenia and hypochromic, microcytic anemia, skeletal abnormalities, and poor wound healing
The deficiency syndrome, except the anemia and leukopenia, is also observed in Menkes disease, a rare inherited condition associated with impaired copper uptake (900 μg).
Acute copper toxicity has been described after excessive oral intake and with absorption of copper salts applied to burned skin.
Toxicity may be seen with doses as low as 70 μg/kg/day.
Chronic toxicity is also described.
Wilson disease is a rare inherited disease associated with abnormally low ceruloplasmin levels and accumulation of copper particularly in the liver and brain,
Fluoride
Intake of <0.1 mg/day in infants and 0.5 mg/ day in children is associated with an increased incidence of dental caries.
Optimal intake in adults is between 1.5 and 4.0 mg/day (F, 3 mg; M, 4.0 mg).
Acute ingestion of >30 mg/kg body weight of fluoride is likely to cause death.
Excessive chronic intake (0.1 mg/kg/ day) leads to mottling of the teeth (dental fluorosis), calcification of tendons and ligaments, and exostoses, and may
increase brittleness of bones (10 mg).
Maternal iodine deficiency leads to fetal deficiency, which produces spontaneous abortions, stillbirths, hypothyroidism, cretinism, and dwarfism.
Rapid brain development continues through the second year, and permanent cognitive deficits may be induced by iodine deficiency during that period. In adults, compensatory hypertrophy of the thyroid
(goiter) occurs, along with varying degrees of
hypothyroidism (150 μg).
Large doses (>2 mg/day in adults) may induce hypothyroidism by blocking thyroid hormone synthesis.
Supplementation with >100 μg/day to an individual who was formerly deficient occasionally induces hyperthyroidism (1.1 mg).
Iron
Most common micronutrient deficiency in the
world.
Women of childbearing age constitute
the highest risk group because of menstrual
blood losses, pregnancy, and lactation.
Hookworm infection is the most common
cause worldwide.
The classic deficiency syndrome is hypochromic microcytic anemia.
Glossitis and koilonychia (spoon nails) are also
observed.
Easy fatigability often develops as an
early symptom before appearance of anemia.
In children, mild deficiency of insufficient severity to cause anemia is associated with behavioral disturbances and poor school performance (postmenopausal F, 8 mg; M, 8 mg; premenopausal F, 18 mg).
Iron overload typically occurs when habitual dietary intake is extremely high, intestinal absorption is excessive, repeated parenteral administration of iron occurs, or a combination of these factors exists.
Excessive iron stores usually accumulate in reticuloendothelial tissues and cause little damage (hemosiderosis).
If overload continues, iron will eventually begin to accumulate in tissues such as hepatic parenchyma, pancreas, heart, and synovium, damaging these
tissues (hemochromatosis).
Hereditary hemochromatosis arises as a result of homozygosity of a common recessive trait.
Excessive intestinal absorption of iron is observed in homozygotes (45 mg).
Negative iron balance initially leads to depletion of iron stores in the bone marrow; bone marrow biopsy and
the concentration of serum ferritin are accurate and early indicators of such depletion.
As deficiency becomes more severe, serum iron (SI) decreases and total iron binding capacity (TIBC) increases; an iron saturation (= SI/TIBC) of <16%
suggests iron deficiency.
Microcytosis, hypochromia, and anemia ensue in
latter stages of the deficient state.
Elevated levels of serum ferritin or an iron saturation >60% raises suspicion of iron overload, although systemic inflammation elevates serum ferritin level regardless of iron status.
Manganese
It is said to cause hypocholesterolemia, weight loss, hair and nail changes, dermatitis, and impaired synthesis of vitamin K–dependent proteins
Toxicity by oral ingestion is unknown in humans.
Toxic inhalation causes hallucinations, other alterations in mentation, and extrapyramidal movement disorders (11 mg).
Selenium
Such individuals have myalgias and/or cardiomyopathy.
Populations in some regions of the world, most notably some parts of China, have marginal intake of selenium.
It is in these regions of China that Keshan disease is endemic,
Toxicity is associated with nausea, diarrhea, alterations in mental status, peripheral neuropathy, and loss of hair and nails; such symptoms were observed in adults who inadvertently consumed between 27 and 2400 mg (400 μg
Zinc
Deficiency of zinc has its most profound effect
on rapidly proliferating tissues.
Mild deficiency causes growth retardation in children.
More severe deficiency is associated with growth
arrest, teratogenicity, hypogonadism and infertility,
dysgeusia, poor wound healing, diarrhea,
dermatitis on the extremities and around orifices,
glossitis, alopecia, corneal clouding, loss of dark
adaptation, and behavioral changes.
Impaired cellular immunity also is observed. Excessive loss of GI secretions (e.g., through chronic diarrhea or
fistulas) may precipitate deficiency.
Acrodermatitis
enteropathica is a rare recessively inherited
disease in which intestinal absorption of zinc is
impaired
Alkaline phosphatase is a zinc-dependent protein,
and therefore serum activity of the enzyme has sometimes been
proposed as a functional measure of zinc status.
Some reports have indicated that TPN solutions that deliver several-fold more manganese than what is recommended in
may lead to deposition of the mineral in the basal ganglia, with resulting extrapyramidal symptoms, seizures, or both.
The mean vitamin B12 status of most populations,
for example, declines significantly with older age, in large part because of the high prevalence of atrophic gastritis and its resultant impairment of protein-bound vitamin B12 absorption
Guidelines for Daily Administration of Parenteral
Micronutrients in Adults
A 1000 μg (= 3300 IU)
D 5 μg (= 200 IU)
E 10 mg (= 10 IU)
K 1 mg
Both fat- and water-soluble micronutrients are absorbed predominantly in the proximal small intestine, the only exception being vitamin B12, which is absorbed in the ileum.
The polyethylene glycol succinate form of vitamin E
(Nutr-E-Sol) is very effective in patients with severe fat malabsorption who cannot absorb conventional alpha-tocopherol
Maldigestion usually results from chronic pancreatic insufficiency, which, if untreated, frequently causes fat malabsorption and deficiencies of fat-soluble vitamins.
Vitamin B12 malabsorption also can be demonstrated in this setting, but clinical vitamin B12 deficiency is rare unless other conditions known to diminish its absorption are also present (e.g., atrophic gastritis or chronic administration of PPIs
Whether long-term administration of PPIs alone warrants occasional checks of vitamin B12 status is a matter of debate
Regardless, malabsorption of vitamin B12 from atrophic gastritis or with PPIs is confined to dietary sources of vitamin B12.
Monitoring of serum calcium levels is indicated in
the first few weeks of therapy with hydroxylated forms of vitamin D, because they are considerably more potent than vitamin D2 or D3, and risk of vitamin D toxicity exists
Regardless, malabsorption of vitamin B12 from atrophic gastritis or with PPIs is confined to dietary sources of vitamin B12.
Small supplemental doses of crystalline vitamin B12 are absorbed readily in both cases. Histamine-2 receptor antagonists also inhibit protein-bound vitamin B12 absorption, although the effect generally is believed to be less potent than with the PPIs.
Cholestyramine
Vitamin D, folate
Adsorbs nutrient, decreases absorption
Dextroamphetamine, fenfluramine, levodopa
Potentially all micronutrients
Induces anorexia
Isoniazid Pyridoxine Impairs uptake of vitamin B6
NSAIDs Iron GI blood loss
Penicillamine Zinc Increases renal excretion
PPIs Vitamin B12 Modest bacterial overgrowth, decreases gastric acid/ pepsin, impairs absorption
Sulfasalazine
Folate Impairs absorption and inhibits folate-dependent enzymes
During the first 24 hours of fasting, the most readily available energy substrates (i.e., circulating glucose, FAs and TGs, and liver and muscle glycogen) are used as fuel sources.
The sum of energy provided by these stores in a 70-kg man, however, is only about 5000 kJ (1200 kcal) and therefore is less than a full day’s requirements
Oxidation of FAs released from adipose tissue TGs accounts for about 65% of the energy consumed during the first 24 hours of fasting.
Approximately 15% of the REE is provided by oxidation
of protein
The relative contribution of gluconeogenesis to hepatic glucose production increases as the rate of hepatic glycogenolysis declines because the latter process becomes redundant; after 24 hours of fasting, only 15% of liver glycogen stores remain.
During short-term starvation (1 to 14 days), several adaptive responses appear that lessen the loss of lean mass.
A decline in levels of plasma insulin, an increase in plasma epinephrine levels, and an increase in lipolytic sensitivity to catecholamines stimulate adipose tissue lipolysis
A maximal rate of ketogenesis is reached by 3 days of starvation, and plasma ketone body concentration is increased 75-fold by 7 days
In contrast to FAs, ketone bodies can cross the blood-brain barrier and provide most of the brain’s energy needs by 7 days of starvation
Whole-body glucose production decreases by greater than 50% during the first few days of fasting because of a marked reduction in hepatic glucose output
During long-term starvation (14 to 60 days), maximal adaptation is reflected by a plateau in lipid, carbohydrate, and protein metabolism. The body relies almost entirely on adipose tissue for its fuel, providing greater than 90% of daily energy requirements
Muscle protein breakdown decreases to less
than 30 g/day, causing a marked decrease in urea nitrogen production and excretion.
The decrease in osmotic load diminishes urine volume to 200 mL/day, thereby reducing fluid requirements.
Total glucose production decreases to approximately 75 g/day, providing fuel for glycolytic tissues (40 g/day) and the brain (35 g/day) while maintaining a constant plasma glucose concentration.
Energy expenditure decreases by 20% to 25% at 30 days of fasting and remains relatively constant thereafter despite continued starvation
In humans, it has been proposed that there are certain
thresholds beyond which lethality is inevitable:
depletion of total body protein between 30% and 50% and of fat stores between 70% and 95%,
or reduction of BMI below 13 kg/m2 for men and 11 kg/m2 for women
Primary PEM is caused by inadequate intake of protein, calories, or both, or, less commonly, when the protein ingested is of such poor quality that one or more essential AAs becomes a limiting factor
in the maintenance of normal protein metabolism.
Secondary PEM is caused by illness or injury
Illness and injury also commonly induce anorexia (see later for mechanisms), so primary and secondary factors often act in concert to create PEM in the setting of illness.
Illness or injury may directly interfere with nutrient assimilation; for example, extensive ileal disease or resection may directly produce fat malabsorption and a caloric deficit.
The most common causes of secondary PEM, however, are the remarkable increases in protein catabolism and energy expenditure that occur as a result of a systemic inflammatory response
A healthy adult typically loses about 12 g N/day in urine, and excretion may increase to as much
as 30 g/day during critical illness.
Because 1 g of urinary N represents the catabolism of approximately 30 g of lean mass, it follows that severe illness may produce a daily loss of up to about 0.5 kg of lean mass as a result of excess protein catabolism
Most of this loss comes from skeletal muscle, where the efflux of AAs increases two- to six-fold in critically ill patients.
Over 95% of energy expenditure resides in the lean body mass, which, therefore, contains the bulk of metabolism that sustains homeostasis
kwashiorkor
“disease of the displaced child” because it was commonly seen after weaning
The presence of peripheral edema distinguishes
children with kwashiorkor from those with marasmus
and nutritional dwarfism. Children with kwashiorkor also have characteristic skin and hair changes
The abdomen is protuberant because of weakened abdominal muscles, intestinal distention, and hepatomegaly, but ascites is rare
Children with kwashiorkor are typically lethargic and apathetic, but become very irritable when held. Kwashiorkor most often occurs when a physiologic stress (e.g., infection) is superimposed on an already malnourished child.
Kwashiorkor is characterized by leaky cell membranes
that permit movement of potassium and other intracellular ions into the extracellular space, causing water movement and edema.
Kwashiorkor Appetite Poor Edema Present Mood Irritable when picked up, apathetic when alone Weight for age (% expected) 60-80 Weight for height Normal or decreased
Marasmus Appetite Good Edema Absent Alert Weight for age (% expected) <60 Weight for height Markedly decreased
Nutritional Dwarfism Appetite Good Edema Absent Alert Weight for age (% expected) <60 Weight for height Normal
Marasmus
Weight loss and marked depletion of subcutaneous fat and muscle mass are characteristic features of children with marasmus.
Ribs, joints, and facial bones are prominent, and the skin
is thin, loose, and lies in folds.
In contrast, the visceral protein compartment is relatively spared, a fact that often is reflected by a normal serum albumin level, which in turn sustains normal oncotic pressure in the vascular compartment, thus minimizing edema and helping to distinguish these children from those with kwashiorkor.
Nutritional Dwarfism
The child with failure to thrive may be of normal weight for height but have short stature and delayed sexual development.
Providing appropriate feeding can stimulate catch-up growth and sexual maturation.
The diagnosis of PEM is different in adults than in children, because adults do not grow in height. Therefore, undernutrition in adults causes wasting rather than stunting.
In addition, although pure forms of kwashiorkor and marasmus can occur in adults, contemporary studies of adult PEM in high-income societies typically focus on hospitalized patients with secondary PEM, coexisting illness or injury, and overlapping features of kwashiorkor and marasmus.
functional atrophy of the small intestinal mucosa, as evidenced by a loss of brush border enzymes and diminished integrity of the epithelial barrier.
Villus atrophy may also be observed with lack
of intestinal stimulation, but in the absence of PEM, the degree of structural atrophy is minor
The immune system is the most vulnerable to PEM, which explains why several functions of immunity are used diagnostically as indicators of malnutrition
Primary gonadal dysfunction is common in adults with
moderate-to-severe PEM and results in impaired reproductive potential.
Decreased circulating levels of testosterone in men
and estrogen in women is evident, and amenorrhea is common.
Delayed puberty or loss of menstrual periods most often occurs when lean body mass drops below a critical threshold.
chronically ill, PEM is usually defined by comparing an anthropometric measurement to established normative standards
In contrast, there is no gold standard to define and measure PEM in the acutely ill patient, because most parameters used to assess PEM in otherwise healthy persons are altered by illness; weight and the concentration of serum proteins are prime examples
<16.0 Severely malnourished
- 0-16.9 Moderately malnourished
- 0-18.4 Mildly malnourished
- 5-24.9 Normal
- 0-29.9 Overweight
30.0-34.9 Obese (class I)
35.0-39.9 Obese (class II)
≥40 Obese (class III)
Extremely underweight adult patients (BMI <14 kg/m2) are at high risk of death and should be strongly considered for admission to the hospital to initiate intensive nutritional support.
Abnormally low values for triceps skinfold and MAMC
are independent predictors of mortality in patients with cirrhosis, and their incorporation into a Cox regression model improves the prognostic value of the Child-Turcotte Score
FGD uses a hand-held dynamometer to measure the maximal fist-grip force that can be elicited. When examined as a surrogate measure of total body protein in patients awaiting GI surgery, FGD correlated
strongly with in vivo neutron activation analysis and with MAMC
In patients undergoing surgery for GI cancers, FGD had superior sensitivity and specificity in predicting perioperative morbidity and mortality than a widely used discriminant analysis called the prognostic nutritional index.
The serum concentrations of several proteins synthesized in the liver are used as indicators of protein-calorie status: albumin, prealbumin (transthyretin), transferrin, and retinol-binding protein
(RBP)
In the absence of concurrent illness or injury,
a low concentration of any of these proteins strongly suggests the presence of PEM
Because the half-lives of prealbumin, transferrin,
and RBP are considerably shorter than that of albumin, it follows that changes in nutritional status will be reflected more promptly in levels of these three proteins than in albumin
Prealbumin levels are often elevated in chronic kidney disease or by glucocorticoid or oral contraceptive administration
their serum concentrations drop in response to systemic inflammation, roughly proportional to the magnitude of the inflammatory response. This effect diminishes their reliability as indicators of PEM in the acutely ill patient, particularly when used as a sole metric of nutritional status
Creatinine-Height Index
The amount of creatinine excreted in the urine over a 24-hour period, corrected for the patient’s height, is an excellent means of assessing total skeletal muscle mass.
The relationship holds because a relatively constant percentage (≈2%) of muscle creatine is converted to creatinine each day.
In patients receiving prolonged mechanical ventilation, CHI is a strong independent risk factor concurring with the likelihood of successful weaning and survival
Albumin
4.5
Maintains plasma oncotic pressure; carrier for small molecules
Subjective Global Assessment
SGA was initially intended for use in surgical inpatients as a means of assessing nutritional status and predicting postoperative infections for the latter, it was found to be a better predictor
than serum albumin concentration, delayed skin hypersensitivity, MAMC, CHI, and the prognostic nutritional index
In practice, any acutely ill patient who has moderate-to-severe malnutrition and is unlikely to be able to meet his or her own nutritional needs within 48 hours is a strong candidate for aggressive nutritional support
Aggressive nutritional support for 7 or more days before surgery reduces perioperative complications and sometimes mortality in malnourished patients
The prevalence of moderate-to-severe PEM is so high in patients admitted for acute alcoholic hepatitis and other forms of decompensated alcoholic liver disease that it is best to assume all such patients are malnourished
In patients with head and neck cancers, supplemental PEG feedings have also
been shown to improve quality of life. Although improvements in survival or decreased morbidity have not yet been demonstrated, improved quality of life alone may warrant its use in
this setting
Intestinal failure (IF) describes a state of insufficient intestinal capacity to fulfill nutritional demands, resulting in dependency on the use of PN
In the ESPEN definition, 2 criteria must be present: a “decreased absorption of macronutrients
and/or water and electrolytes due to a loss of gut function” and the “need for parenteral support.”
IF is further classified into Types I, II, and III.
Type I IF is acute, short-term, and due to a self-limiting condition such as ileus following abdominal surgery, which may require a brief period of nutritional support
Type I IF is acute, short-term, and due to a self-limiting condition such as ileus following abdominal surgery,
which may require a brief period of nutritional support.
Type II IF results from a prolonged acute condition, often in metabolically unstable patients who require IV supplementation over periods of weeks or months, and may be reversible or irreversible.
Type II IF patients may recover fully or progress to
type III intestinal failure, which is a chronic state of IF requiring long-term nutritional support, typically in the form of home PN
Short bowel syndrome (SBS) due to intestinal malabsorption associated with a functional small intestine length of less than 200 cm is a common cause of IF
After extensive intestinal resection, 3 clinical stages have been described.
The first stage occurs during the first few weeks after resection and is characterized by significant fluid and electrolyte shifts that require copious amounts of IV fluids to prevent dehydration.
During the second stage, which may last for up to 2 years, there is both structural adaptation (increase in size and absorptive surface as a result of cellular hyperplasia) and functional adaptation (slowing of bowel transit to allow increased time for absorption)
The third stage is a stable phase during which no further improvement or adaptive changes occur.
Nutritional management of SBS depends on the amount and location of small intestine removed, because the intestine has the ability to adapt and increase its absorptive function over time
During stage 2, oral feedings are gradually started, and the volume of PN is reduced as oral feedings are increasingly tolerated.
Patients should eat small, frequent meals—avoiding simple sugars, fiber, and nutrient-poor foods
Dietary intake should be increased by at least 50% because most stable adult SBS patients absorb only half to two thirds as many calories as normal.
Such a hyperphagic diet is best tolerated when consumed as 5 to 6 meals throughout the day.
Diarrhea may result from oral feedings and
may limit weaning from PN. While percutaneous endoscopic gastrostomy (PEG) placement in the management of SBS is controversial, enteral tube feeding administered continuously over 12 to 24 hours is usually better tolerated than intermittent bolus
feeding because of greater nutrient absorption and less osmotic
diarrhea.
EN is usually slowly advanced while PN is isocalorically
decreased over several months, with frequent monitoring of tolerance as determined by the development of symptoms, amounts of food and fluid intake, stool and urine output, body weight,
hydration status, and micronutrient levels
type I SBS, patients have only jejunum remaining with an end jejunostomy and no colon.
These patients experience massive fluid shifts, show little signs of adaptation over time, and are more likely to be PN dependent.
In type II SBS, patients have variable length of jejunum connected in series with some portion of colon.
Clinically they show greater signs of adaptation but demonstrate slow deterioration of nutritional
status over time without parenteral support.
Type III SBS, intestinal rehabilitation of the remaining small intestine is most likely to be successful (meaning the patient can resume intake of adequate oral nutrition) because the colon has been preserved and is in continuity with the small intestine and the ileocecal valve is maintained
glucagon-like peptide (GLP)-1 by the remnant of terminal ileum has a trophic effect and stimulates SB adaptation, as a result of which these patients rarely need EN or PN
Intestinal autonomy is defined by the ability of a SBS patient to live without PN and may be expected if a patient has
70 to 90 cm of small bowel and an intact
colon,
or 130 to 150 cm of small bowel with no colon
Citrulline, a non-protein amino acid produced by intestinal mucosa, has been proposed as a predictor of permanent versus transient IF
plasma citrulline level of below 20 μmol/L identified
patients destined to have permanent IF,
Patients with severe SBS (<200 cm small bowel remaining) usually require a glucose-electrolyte oral rehydration solution (ORS).
Ingestion of an ORS containing glucose with a sodium
concentration of at least 90 mmol/L aids in water absorption by making use of sodium-glucose co-transporters in the jejunum
Between 2 and 3 L of an ORS solution should
be sipped throughout the day. Hypo-osmolar fluids should be avoided, as their absorption is dependent mostly on passive diffusion.
Hyperosmolar fluids also should be avoided in patients
with SBS, because they lead to fluid shifts into the bowel lumen, worsening diarrhea.
If a patient has had a partial ileal resection (resection of <100 cm) and has an intact colon, the bile-binding resin cholestyramine can be used to reduce bile salt-induced diarrhea.
In patients with a limited amount of ileum remaining (>100 cm of ileum resected) and an intact colon, however, cholestyramine can increase diarrhea by depleting the bile salt pool.
In general, fat restriction should not be used for SBS type I patients who do not have a colon, but it may be beneficial in reducing diarrhea for SBS types II and III, in which some length of colon remains
Vitamin B12 injections should be administered monthly if more than 50 to 60 cm of terminal ileum has been resected.
The somatostatin analog octreotide has been shown to prolong small intestinal transit time and decrease GI secretions, but its use remains controversial because it is also associated with gallstone formation and decreased splanchnic protein synthesis, and has not been shown to eliminate the need for PN
Data on early feeding (initiated within 24 to 36
hours of admission) in AP have demonstrated lower risk of multiorgan failure (MOF), operative interventions, systemic infections, septic complications, and even mortality compared with what had been standard therapy (no EN/PN) or delayed EN
significant 2-fold reduction in the risk of total and pancreatic infectious complications, and a 2.5-fold reduction in the risk of death in patients receiving EN
Patients with CP should consume small, frequent meals and avoid foods that are difficult to digest
Fat restriction is no longer recommended. In
patients with weight loss, medium-chain triglycerides (MCTs) may be useful to provide extra calories without causing steatorrhea
MCTs, however, may be poorly tolerated because they are foul-tasting and can cause cramps, nausea, and diarrhea
Fat soluble vitamins, vitamin B12, and calcium should be replaced as clinically indicated
Vitamin D deficiency is seen in about 50% of patients with CD.
Besides a role in osteoporosis, vitamin D has also been implicated in the pathogenesis of CD, as it may down-regulate TNF-α–related genes.
An enteral formula with transforming growth factor-β
is marketed specifically for IBD, but there is no robust evidence to recommend its use at this time.
Malnutrition is an independent risk factor for postoperative complications
Malnutrition is common in advanced liver disease patients, with a prevalence of 50% to 90% in those with cirrhosis, depending on the methods used for nutritional assessment
Malnutrition leads to more complications (e.g., ascites, hepatorenal syndrome) and has been shown to be an independent predictor of survival.
Patients with cirrhosis have been found to have dysgeusia, which can result from magnesium deficiency
Restriction of dietary sodium and protein to manage ascites and hepatic encephalopathy
The branchedchain amino acids (BCAAs) valine, leucine, and isoleucine are used preferentially as a protein source by patients in liver failure because they are metabolized by the muscle, kidney, adipose, and brain tissue
In contrast, the aromatic amino acids (AAAs)
tyrosine, phenylalanine, and methionine are metabolized and deaminated solely by the liver. Normal serum AA concentrations are altered in cirrhosis, with a rise in AAAs and a fall in BCAAs
Outpatient RCTs suggest that long-term nutrition supplementation with oral BCAA granules may be useful in slowing progression of hepatic disease and prolonging event-free survival.
Patients with hepatic encephalopathy already receiving antibiotics and lactulose derive no further improvement in outcome (mental status or coma grade) by adding BCAAs to their therapy.
Water-soluble vitamin (vitamin B complex and C)
deficiencies can occur in both alcohol-associated and nonalcohol- associated liver disease. Thiamine deficiency can lead to Wernicke encephalopathy and Korsakoff dementia, not only in alcoholics, but also in patients with HCV-related cirrhosis.
As a result, thiamine supplementation is recommended in all patients with cirrhosis
Decreased levels of folate and vitamin B6 have been reported in HCV infection, and it is noted that
pegylated interferon and ribavirin therapy further decrease levels of thiamine, riboflavin, and vitamin B6.
Fat-soluble vitamin deficiencies occur more frequently with cholestatic than parenchymal
liver disease.
Vitamin A deficiency has been reported in cirrhosis and is considered a risk factor for cancer, including HCC.
Vitamin D levels are low in patients with liver disease
and fall as liver disease progresses
Vitamin E deficiency has been reported
in both cholestatic and alcohol-associated liver disease, and low levels may facilitate progression of fatty liver to steatohepatitis.
Zinc deficiency is also associated with liver disease, especially alcohol-associated liver disease, and may lead to anorexia, altered taste and smell, immune dysfunction, altered protein metabolism, hepatic encephalopathy, and impaired glucose tolerance
EN is preferred over PN in patients with cirrhosis who
require nutritional support, because liver function can worsen, and patients with ascites may not be able to tolerate the large fluid volumes associated with PN
Excess dextrose and glucose can lead to steatosis, and patients receiving long-term PN can develop cholestasis, fibrosis, and cirrhosis
Lack of liver glycogen stores and reduced capacity for gluconeogenesis can lead to hypoglycemia and reductions in lean body mass during prolonged NPO periods.
For these reasons, cirrhotic patients should not go more than 3 hours without eating, and a bedtime snack should be ingested
benefit from fiber in preventing symptomatic diverticular
disease, but no well-designed RCTs support this practice
Fiber intake should be at least 25 g/day and provided as insoluble fiber, such as that contained in wheat bran, bran muffins, and fiber-based cereals.
The use of probiotics has had some success
in treating and preventing diverticulitis
However, high-quality data on prevention of complications and recurrence are scant and currently the AGA guidelines recommend against the use of probiotics after uncomplicated diverticulitis.
Obesity and physical inactivity have been shown to
increase risk of symptomatic diverticular disease in both men and women
Dumping syndrome, which occurs when food passes too rapidly into the small intestine, can occur after gastrectomy, vagotomy, or esophageal surgery, and is increasingly being seen with the growing popularity of bariatric surgery
Early dumping syndrome occurs within 30 minutes of a meal and is characterized by abdominal pain, diarrhea, borborygmi, bloating, nausea, and vasomotor symptoms including flushing, sweating, tachycardia,
hypotension, and syncope.
This syndrome results from shifting of fluids out of the intravascular space and into the hyperosmolar
environment of the duodenal lumen, as well as from
enhanced release of GI hormones caused by a high carbohydrate load entering the small intestine
Late dumping syndrome occurs 1 to 3 hours after a meal and is characterized by hypoglycemia, sweating,
hunger, fatigue, and syncope and is thought to be related to hypoglycemia from the rapid (earlier) increase in insulin via
GLP-1 in response to the excessive carbohydrate load in the jejunum
Dumping syndrome is diagnosed by clinical assessment and a modified oral glucose tolerance test.
31% to 40% in patients with sarcomas, breast, and hematologic cancers;
54% to 64% in patients with colon, prostate, and lung cancers; and over 80% in patients with pancreatic and gastric cancers
Malnutrition is not only affected by the type of cancer, but also by the specific antitumor therapy regimen and patient characteristics (age, gender, and comorbidities such as diabetes and GI disorders
Appetite stimulation with glucocorticoids and megestrol
acetate has been used successfully in cancer patients with mild malnutrition
Although both agents lead to improved appetite
and weight gain, use of megestrol acetate is associated with a higher risk of DVT
EN has been used successfully in patients with head and neck cancer to prevent weight loss, reduce hospitalizations, and reduce interruptions in
chemotherapy and radiotherapy, although dependence on PEG feedings may delay return of swallowing function and PO intake
Use of PN support in the cancer patient should be restricted to those patients with a reasonable life expectancy and a sufficient quality of life (Karnofsky
Score >50), who are not expected to maintain their nutritional needs for a prolonged period
Obesity is the second leading cause of preventable death
indirect calorimetry remains the
gold standard
In an obese patient with glucose intolerance or diabetes, the concentrated glucose solution in PN
can lead to hyperglycemia, which in critically ill patients has beenshown to increase the risk for nosocomial infection, weaken the immune response, delay wound healing, and increase overall mortality.
During metabolic stress, protein breakdown leads to
gluconeogenesis.
Several studies have suggested that protein-rich hypocaloric feeding (2 g protein/kg ideal body weight [IBW]/day and 65% to 70% of caloric requirements), also known as permissive underfeeding, is advantageous over standard nutritional regimens because oxidation of endogenous lipid stores supplies the energy source while protein supplementation is used to promote protein anabolism;
In critically ill obese patients, the American Society for Parenteral and Enteral Nutrition recommends
11 to 14 kcal/kg actual body weight per day for BMI 30 to 50 and
22 to 25 kcal/kg IBW/day for BMI greater than 50
The recommended dose of protein is
2 g/kg IBW for BMI of 30 to 40, and
2.5 g/kg IBW for BMI ≥40
all adults be screened for obesity, and those with
a BMI of 30 kg/m2 or higher be offered a referral to intensive multicomponent behavioral interventions
Bariatric surgery is recommended for individuals with a BMI greater than 40 kg/m2 and for those with a BMI greater than 35 kg/m2 who have obesity- related comorbidities
Micronutrient deficiencies, particularly iron and vitamin D, are commonly present in obese patients and should be corrected preoperatively
In patients with Roux-en-Y gastric bypass, limitation in oral intake is necessary because of the small size of the gastric pouch.
The shorter the length of the common channel in the Roux-en-Y gastric bypass, the more likely there will be micronutrient and macronutrient deficiencies
The laparoscopic adjustable gastric
band, which is least likely to cause nutritional problems, is gradually being phased out because of its high rate of complications requiring removal in greater than 40% of cases
The vertical sleeve gastrectomy is being increasingly utilized because of its less disruptive effect on GI physiology and its effective impact on weight reduction and decreased risk of diabetes
Post-bariatric surgery nutritional deficiencies can be divided into 3 types: protein-calorie malnutrition, vitamin and mineral deficiencies, and dehydration.
Iron, folate, calcium, and vitamin B12 deficiencies can occur after Roux-en-Y gastric bypass.
Dehydration is common after bariatric surgery, especially in warm weather and after vigorous exercise.
The patient’s ability to drink large amounts of fluid is restricted because of the reduced size of the stomach
Approximately 2 L of fluid intake is usually
recommended per day, though the amount can vary depending on the specific patient and his or her daily activity
Approximately 2 L of fluid intake is usually
recommended per day, though the amount can vary depending on the specific patient and his or her daily activity
pharmacotherapy for obesity should be considered if patients have a BMI of ≥30 kg/m2 or a BMI of ≥27 kg/m2 with weight-related comorbidities, such as hypertension, dyslipidemia, type 2 diabetes, or obstructive sleep apnea
Phentermine is the most commonly prescribed medication for obesity in the USA. It is a schedule IV controlled substance and classified as an adrenergic agonist that functions to increase resting energy expenditure and suppress appetite
As monotherapy, it is indicated for short-term use (3 months)
Orlistat promotes weight loss via inhibition of pancreatic and gastric lipases, thus preventing
the absorption of fat.
Orlistat also has the added benefit of lowering serum glucose and improving insulin sensitivity
Lorcaserin is a selective serotonin-2C receptor agonist for long-term treatment of obesity
The 5-hydroxytryptamine 2C receptor has
a role in the regulation of the dopamine system, and is postulated to affect food-related behaviors
Two agents—bupropion (a dopamine and norepinephrine re-uptake inhibitor) and naltrexone (an opioid antagonist
Liraglutide was approved by the FDA for chronic weight management and treatment of type 2 diabetes.
It mimics GLP-1, which is released in response to food intake, and acts to reduce hunger, decrease food intake, and delay gastric emptying
Patients determined to be at high nutritional risk (NRS-2002 >5 or NUTRIC score ≥5) should have EN started early within 24 to 36 hours of admission to the ICU.
Advancement to goal should take 3 to 4 days in order to minimize the chance for overfeeding, as exogenous
feeds are additive to endogenous gluconeogenesis by the liver
Getting to the protein goal sooner (up to 2.0 g/kg/
day) is more important than getting to the caloric goal (20 to 25 kcal/kg/day)
Appropriate adjustments to protocol should be made
in the setting of hemodynamic compromise or instability.
In this scenario, EN should be withheld if vasopressive therapy is being initiated.
Initiation or re-initiation of EN may be considered
with caution once the patient is fully resuscitated and stable for 24 to 36 hours and pressor support has begun to be withdrawn.
In patients at low nutritional risk, PN should not be used until after the first 7 days following ICU admission if the patient cannot maintain volitional intake and early EN is not feasible
In any critically ill patient, regardless of risk, who is already on EN tube feeding but receiving less than 60% of the prescribed goal regimen, addition of supplemental PN should be withheld until after 7 to 10 days from admission.
As tolerance to EN improves, the amount of PN energy should be reduced and finally discontinued when the patient is receiving more than 60% of target energy requirements from EN
In all ICU patients who require PN, high protein hypocaloric PN should be considered initially over the first week, with provision of 80% of energy requirements (20 kcal/kg actual body weight/day).
Compared with eucaloric PN, permissive underfeeding
has been shown to reduce the incidence of hyperglycemia, infections, ICU and hospital lengths of stay, and duration of mechanical ventilation
EN supports both the structural and functional integrity of the GI tract.
EN sustains structural integrity by maintaining mucosal
mass and villus height, stimulating epithelial cell proliferation, promoting the production of brush border enzymes, and maintaining the secretory immunoglobulin (Ig)A-producing immunocytes, which make up the gut-associated lymphoid tissue (GALT)
Small bowel feeding is recommended for critically ill patients determined to be at high risk of aspiration or those shown to be intolerant to gastric feeding
Bedside nasoenteric tube (NET) placement is the most common enteral access technique used in the hospital and long-term care environments
Alternatively, the endoscopic over-the-guidewire NET (ENET) technique can be used when placement under direct visualization is desired
A bridle can be used to secure the ENET once it is placed
For bedside NET placement, typically, an 8 to 12 Fr NG tube is lubricated and passed into the stomach with the patient’s head flexed; the patient ingests sips of water to assist in passage of the tube.
NJ feeding tubes can be placed endoscopically at the bedside with the patient moderately sedated. In the “drag-and-pull” method, a suture is attached to the end of an NJ tube and used to drag the tube into position in the small intestine with a grasping
forceps
Percutaneous access devices, such as a PEG, are indicated for patients who will be unable to maintain sufficient nutritional intake for more than 1 month, despite a functional GI tract.
In high-risk patients, a high mortality after PEG is usually not a result of the procedure itself, but a reflection of the patient’s comorbidities and moribund status
Patients with head and neck cancer (HNC) are at high risk for malnutrition stemming from dysphagia from the tumor itself or from required anti-tumor therapies
Approximately 50% of patients with HNC require alternative means of nutritional support
EN support via PEG has been shown to reduce the number of hospitalizations required from dehydration and malnutrition, prevent weight loss, and avoid treatment interruptions
In patients with malignant bowel obstruction, a PEG tube can also be safely and effectively used for intestinal decompression.
Such a “venting” PEG obviates the need for an NG tube, relieves symptoms of nausea and vomiting, and can allow end-of-life patients to be discharged from the hospital tolerating some degree of an oral soft diet
Use of EN or PN in advanced unresectable cancer is controversial.
The Karnofsky Performance Scale Index can be used to
assess quality of life in individual patients
Data support the use of PEG tubes in patients with
stroke-related dysphagia, as a bridge to return of swallowing function and oral intake.
Compared with NG feeding, early PEG placement was found to be associated with a lower incidence of
ventilator-associated pneumonia
PEG feeding compared with NG tube feeding was associated with a reduction in treatment failures, and a higher overall rate of delivery of feeds
The most common reasons for PEG placement in patients with dementia include reduction in risk of aspiration, maintenance of skin integrity with prevention of pressure sores, improvement in quality of life, and prolongation of survival
Risk of developing pressure ulcers in nursing
home residents with PEG tube placement may actually increase because of decreased mobility and the need to be restrained
PEG tube placement may do little to reduce aspiration pneumonia, as patients are still capable of aspirating oropharyngeal secretions
The traditional PEG site is marked by the x in the left upper quadrant.
Better placement is above the umbilicus, close to the midline, or slightly to the patient’s right of the midline position (circles).
The PEG then is in the gastric antrum, which is ideal should conversion to a PEGJ be required later.
X with circles show the tremendous variability in the site for DPEJ placement, which can occur anywhere from the left costal margin down to the left iliac crest.
Traditional sites in the LUQ have a longer, more tangential tract into the midbody or even lower fundus. C, Placing a coin in the umbilicus (dark circle) and injecting 500 mL of air through the NG tube before PEG placement helps identify the gastric antrum, easing selection of the PEG site.
The use of prophylactic IV antibiotics before the procedure is important to prevent peristomal infections after the procedure
An antibiotic with optimal skin coverage, such as IV cefazolin (1 g), should be administered 30 minutes prior to the procedure.
Placement of a PEG tube can be accomplished by either the Ponsky (Pull) or Sachs-Vine (Push) technique, depending on physician preference, as both are equally effective.
A third technique (Russell [Introducer]) may be indicated in cases of an exophytic oropharyngeal or esophageal cancer, recent oropharyngeal
incisions from a head and neck surgical procedure, or a tight esophageal stricture that impedes passage of the scope or PEG tube
The most common PEG tubes for adult patients range in size from 16 to 20 Fr, and are made of silicone.
A larger diameter PEG tube is associated
with a greater likelihood of side torsion and enlargement of the stomal tract diameter.
Replacement PEG tubes are broadly divided into 2 categories, replacement gastrostomy tubes and low-profile devices
Replacement gastrostomy tubes usually have a balloon-type internal bolster These balloon tubes can be inserted blindly through the gastrostomy site into the gastric lumen.
The balloon is inflated to serve as the internal bolster
Because of balloon breakage, the tube often requires replacement within 3 to 6 months. There also are replacement PEG tubes with a distensible internal bumper
The internal bumper is stretched with a stylet
and pushed blindly through the gastrostomy site; the stylet is then removed, allowing the internal bolster to assume its previous shape.
Low-profile gastrostomy devices provide skin level access to the gastric lumen and may be particularly useful for disoriented patients who may habitually tug at their bedclothes and pull out their tube connections
Three common techniques are used for PEGJ placement.
With the Kirby technique, a guidewire passed through
the PEG is grabbed by an extra-long 320 cm biopsy forceps and dragged down into the proximal jejunum.
The average longevity of this tube system is about 120 days
With the Johlin technique a wire polypectomy snare is inserted through the gastrostomy tube into the stomach and the endoscope is then passed through the open snare and advanced as far as possible down into the proximal jejunum.
A standard 0.035-in flexible-tip guidewire is passed through the endoscopic channel and passed out further into the small bowel.
DPEJ involves the direct placement of a small diameter 14 to 16 Fr PEG tube into the small intestine using a modified Ponsky Pull technique and a pediatric colonoscope to reach a puncture position beyond the ligament of Treitz
Once the snare is transferred to the trocar, the rest of the procedure is virtually identical to the Ponsky Pull technique for PEG placement.
The Sachs-Vine Push and the Russel Introducer techniques should not be used for this procedure. Management of the DPEJ tube is likewise similar to that of PEG tubes
Most post-PEG complications arise from a patient’s comorbidities, such as poor wound healing, aspiration, or coagulopathy.
To reduce the risk of aspiration, caregivers should raise the head of the patient’s bed 30 to 45 degrees during feeding and for 1 hour afterward.
Risk factors for peristomal infection include diabetes, obesity, malnutrition, chronic glucocorticoid use, small incisions at the PEG insertion site, lack of antibiotic prophylaxis, and excessive pressure of the external bumper on the PEG site
Excessive tightening of the PEG tube external bolster against the abdominal wall can cause buried bumper syndrome (BBS) which in turn can lead to mucosal ulceration, bleeding, stomal leakage, peristomal
To minimize the chance for BBS, the external bolster of the PEG tube should be maintained up against the skin (without indentation) for 4 days post-placement, after which it should be carefully moved back 1 cm from the anterior abdominal wall.
Peristomal wound infections are often treated for 7 days with an oral antibiotic such as cephalexin to cover skin-related microorganisms The infected area should also have daily topical cleansing with mild soap and water
Clogged PEG tubes may be cleared by flushing with warm water, soft drinks, or a slurry of pancreatic enzymes mixed in a bicarbonate solution
Mechanical declogging with a wire, specimen
brush, endoscopic cleaning brush, or commercially available corkscrew declogging device
Leakage of gastric acid or bile around the PEG tube can cause erythema and skin breakdown that is often mistaken for infection
topical zinc oxide, maintaining the external bumper 1 cm from the skin, stabilizing the gastrostomy tube with a vertical clamping device, and the use of PPIs
Pneumoperitoneum is common after PEG placement and is of no concern in the absence of
peritoneal signs.
Any signs of peritoneal irritation should prompt
an investigation with a contrast study through the PEG tube to determine presence or absence of a leak.
Confirmation of a leak should lead to surgical exploration.
colocutaneous fistula results from inadvertent placement of a percutaneous feeding tube through the colon before it enters the stomach
If a PEG tube becomes dislodged within 7 days of placement, the patient should be brought back to the endoscopy suite and a new PEG placed through the same site on the anterior abdominal wall.
If the PEG tube becomes dislodged more than 4 weeks after placement, the tract should be mature enough to blindly replace the PEG tube at the bedside without fluoroscopic or endoscopic monitoring
Proper placement should be confirmed with a contrast radiologic study through the PEG tube prior to using the tube for feedings.
Bolus feeding delivery allows a relatively
large volume of tube feeding (200 to 400 mL) to be delivered over a short period of time by a syringe.
Intermittent feedings are delivered over a few hours by pump or by gravity drip using a bedside pole.
Continuous feedings are usually delivered over 12
to 24 hours by a mechanical pump
Patients who receive small bowel feedings are almost always fed using continuous feedings.
An intermittent or continuous feeding regimen, rather than the rapid bolus method, may be used to limit the risk of tube-feeding aspiration
Gastric residual volume (GRV) does not correlate well with the incidence of regurgitation, aspiration, or pneumonia, and are a poor measure of gastric emptying.
Checking routinely for GRV is no longer recommended
Measures to reduce the risk of aspiration
include keeping the head of the bed elevated 30 to 45 degrees in intubated ICU patients, changing from bolus to continuous infusion, using promotility drugs (e.g., metoclopramide or erythromycin) or narcotic antagonists (naloxone or alvimopan), and converting the level of infusion from gastric to post-pyloric.
Standard polymeric formulations are lactose-free and glutenfree, and are the basic feeding formulas designed for long-term EN use in hospitalized adult patients.
These formulations are denoted as polymeric because the macronutrient components are intact and not predigested.
Standard formulations contain
15% to 20% calories from proteins,
45% to 60% calories from carbohydrates, and
30% to 40% calories from fats.
formulations provide 1 kcal/mL, although they may be concentrated to 1.5 to 2.0 kcal/mL.
Most enteral formulas contain close to 80% free water
Elemental formulas contain protein in the form of free
amino acids and are nearly fat-free (i.e., less than 2% to 3% of the caloric content is fat).
Semi-elemental formulas contain protein in the form of small chain peptides, predominantly of 3 to 5 amino acids in length.
Protein absorption is more efficient, as
the small peptide chains can be transported across the intestinal wall intact by a single active transporter, rather than requiring a separate transporter for each amino acid
Fat is in the form of MCT, which can be absorbed directly into the portal vein without lipase, colipase, or bile salt transportation
The semi-elemental small peptide/MCT oil formulations have largely supplanted the original elemental formulas, and are designed for patients with limited digestive capacity
GI side effects of tube feedings are reported in 15% to 30% of patients, and include nausea, vomiting, abdominal distention, abdominal cramping, and diarrhea.
Diarrhea is most commonly due to medications and less often to Clostridioides difficile enterocolitis
Medications can be altered from tablet
to liquid form for easy instillation through the feeding tube, by dissolution in a sorbitol base (a known cathartic).
Magnesium containing medications, hypertonic medications, and promotility agents may also promote diarrhea.
High-osmolarity EN formulations, even with an osmolarity as high as 600 to 700 mOsm/L, are rarely a cause of diarrhea.
In a patient with new-onset diarrhea who
was previously tolerant to an enteral formula, the patient should be assessed for medication-induced and infectious etiologies prior
to changing the formula. There are no data to support dilution of the enteral formulation to improve GI tolerance.
For patients with compromised bowel function, use of the semi-elemental formulas may improve absorption and reduce diarrhea. Soluble fiber supplementation or use of a commercial mixed soluble/insoluble fiber formula may improve diarrhea as well
Phenytoin administration is affected, because the drug binds to the enteral formula and forms a phenytoin-tube feeding complex that adheres to the wall of the feeding tube
Ciprofloxacin has also been shown to bind with tube feedings, reducing its absorption.
Vitamin K, present in many enteral formulas, will make a patient more resistant to the effects of warfarin.
For patients with a nonfunctioning GI tract, nutrients can be delivered directly into the venous system via PN.
PN delivers a solution comprising macronutrients (carbohydrates, proteins, lipids), micronutrients (vitamins, minerals, trace elements), water, electrolytes,
and medications.
Carbohydrates are delivered as dextrose, proteins as amino acids, and lipids as IV fat emulsions (IVFEs).
When all 3 macronutrients are combined into a single solution, it is referred to as a total nutrient admixture or 3-in-1 solution.
PN is usually delivered over 12 to 24 hours.
A PN solution is 6 times more concentrated than blood (1800 to 2400 mOsm/L) and generally consists of approximately 30 to 50 g/L of protein and 1000 to 1200 kcal/L.
Each component of PN has a defined caloric content, with protein = 4 kcal/g
carbohydrate (dextrose) = 3.4 kcal/g
and IVFE = 10 kcal/g (9 kcal/g from fat, 1 kcal/g from emulsifier).
Protein needs vary in the range of 1.2 to 2.0 g/kg/day depending on the level of metabolic stress.
Protein should not be restricted, even in patients with severe hepatic encephalopathy or renal failure with
azotemia requiring imminent dialysis.
Fat is usually provided at 1 g/kg/day, but may need to be reduced or restricted for patients with hypertriglyceridemia (>400 mg/dL
Despite fat restriction, a minimal amount of fat is still given, usually 10% of estimated fat calories (or 500 mL of 20% Intralipid per week), to prevent essential fatty acid deficiency
To prevent hyperglycemia and refeeding syndrome (see later under Metabolic Complications), the amount of dextrose should initially not exceed 200 g
Overall water requirements are estimated at 25 to 35 mL/ kg/day
Stepwise Approach to Writing a Parenteral
Nutrition Order for a 70-kg Man
CALORIC CONTENTS OF NUTRIENT SUBSTANCES
Protein: 4 kcal/g
Fat: 10 kcal/g
Carbohydrates: 3.4 kcal/g
ESTIMATED DAILY NEEDS FOR THIS PATIENT
Calories: 25 kcal/kg = 1750 kcal
Protein: 1.2 g/kg = 84 g
Fluids: 30 mL/kg = 2100 mL
STEPS
1. Add protein (1.2 g/kg/day) to the PN mixture.
84 g of protein needed
1 g of protein = 4 kcal (total, 326 kcal)
1750 kcal-326 kcal = 1424 kcal still required
- Add lipids (1-1.5 g/kg/day).
70 g fat = 700 kcal
1424 residual calories-700 kcal = 724 kcal still required - Add carbohydrates (3-5 g/kg/day).
724 kcal/3.4 kcal/g carbohydrate = 212.9 g - Make total volume.
30 mL/kg = 2100 mL
ADDITIONAL ADDITIVES
Electrolytes, minerals, vitamins
Drug additives: H2RAs, insulin, heparin
At initiation, the PN formula should be infused over 24 hours.
Patients with glucose intolerance or those at risk for refeeding syndrome should have their PN infused at 25% of their daily caloric needs for the first 24 hours
This ratio may be increased to full caloric
needs over the following 48 to 72 hours, with monitoring of serum levels of glucose, magnesium, potassium, and phosphate, as well as fluid tolerance
Hyperglycemia is the most common complication and is directly related to PN dextrose content, the patient’s insulin sensitivity, and the rate of PN infusion.
Critically ill patients and those with pre-existing glucose intolerance require the most aggressive serum glucose monitoring.
Of the total amount of sliding scale insulin required over 24 hours, two thirds should be added to the next day’s PN formula.
Refeeding syndrome is a metabolic consequence of nutrition support resulting from sudden provision of a large amount of glucose calories to a patient who was previously malnourished
With nutrient infusion, the metabolism of these patients rapidly becomes anabolic. Insulin production is increased, pushing potassium, phosphorus, magnesium, and thiamine into the intracellular space, with resultant hypokalemia, hypophosphatemia, and hypomagnesemia.
Sudden shifts in serum electrolytes may precipitate cardiac dysrhythmias.
To prevent refeeding syndrome, the initial caloric content should be limited and the macronutrients gradually titrated (particularly dextrose) from 25% up to 80% to 100% of energy goals over 3 to 4 days, while
electrolytes are carefully monitored and corrected
as needed. While refeeding syndrome may be precipitated by EN or PN, risk is greater with provision of EN
Abnormal liver enzymes are common after initiation of PN and typically feature elevations of serum aminotransferase levels up to twice normal. Greater elevations in aminotransferase levels
and associated hyperbilirubinemia warrant investigation.
PN can lead to 3 types of PN-associated hepatobiliary disease: steatosis, cholestasis, and gallbladder sludge/stones.
Gallbladder stasis can lead to development of gallstones or gallbladder sludge, resulting in both calculus and acalculous cholecystitis.
PN-associated steatosis presents as a fatty infiltration
of the liver that is especially prominent in the periportal areas.
Patients with PN-associated steatosis have modest elevations of serum aminotransferases that usually occur within 2 weeks of starting PN and may return to normal with time.
SIBO is another risk factor for liver disease, most
likely caused by the production of alcohol through fermentation or hepatotoxins by anaerobic bacteria
Choline deficiency may play a role in the development of liver disease associated with long-term PN
cycling the PN regimen over 12 to 18 hours each day, performing indirect calorimetry to confirm energy requirements and readjusting to avoid overfeeding, and switching the soy-based intralipid IVFE to a mixture of lipids (SMOF containing soy, MCTs, olive, and fish oils
Addition of heparin (1000 units/L) to each bag of PN solution can prevent subclinical thrombus formation to which bacteria or fungi can attach, thereby potentially reducing the risk of catheter sepsis.
Routine use of anticoagulant therapy to reduce
the risk of catheter-related infection, however, is not recommended.
The use of catheter locks has been shown to reduce the risk of CRBSI.
Antibiotic lock therapy has been shown to decrease
the incidence of recurrent CRBSI. Ethanol has both bactericidal and fungicidal properties, and has a low risk for causing antimicrobial resistance
early EN feeding after abdominal or thoracic surgery may reduce postoperative complications, hospital length of stay, and mortality (although vomiting may be increased
Full liquid diets are indicated for patients who are unable to chew, swallow, or digest solids. They are largely milk-based and should not be used for lactose-intolerant patients.
They contain a large amount of simple carbohydrates and should be used with caution in diabetic patients.
low-fat diet for a prolonged period of time, fat-soluble vitamins (A, D, E, K) must be supplemented. MCT oil may be used to substitute for long-chain triglycerides.
MCTs have 6- to 12-carbon fatty acid chains, high aqueous solubility, and do not require bile salts for absorption in the small intestine
MCTs do not require chylomicron formation and are absorbed directly into the portal venous system.
Early bleeding usually occurs within 24 hours postoperatively at the staple lines of the GJA, gastric
remnant, or jejunojejunal anastomosis.
A significant proportion of early bleeding can be extraluminal and this should be considered if melena or hematemesis is not apparent; these patients may develop hemodynamic instability, oliguria, and abdominal distention without overt signs of GI blood loss.
Leaks often present without fever, leukocytosis, or pain.
The most common reported sign of a leak is tachycardia
Medications have also been used to treat weight regain, however, in a retrospective analysis only 1 medication used off-label (topiramate) demonstrated significant weight loss, and only 56% of the entire cohort with inadequate weight loss or weight regain achieved 5% or more of their post-surgical total weight loss
Endoscopic bariatric therapy (EBT
patients are eligible only if they have obesity class III (BMI 40 kg/m2) or obesity class II (BMI 35 to 39.9 kg/m2) with significant associated comorbid illness
IGBs are space-occupying devices
which are inflated in the stomach with either saline or nitrogen mixed gas and removed endoscopically after 6 months.
These devices promote weight loss through both taking up space in the stomach and, in the case of the fluid-filled balloons, also result in slowing of gastric emptying
Serotonin has long been a focus of attention for its possible role in disrupted satiety. There is substantial evidence that altered 5-hydroxytryptamine (5-HT, serotonin) functioning contributes to dysregulated appetite, mood, and impulse control in EDs and that such alteration persists after recovery from AN and BN, possibly reflecting premorbid vulnerability
Findings for AN are inconsistent. Although there is some evidence that young women with AN have high levels of pre- and postprandial CCK that may impede treatment progress by contributing to postprandial nausea and vomiting other reports have shown decreased CCK compared with controls
BN, there is consistent evidence for an impaired
satiety response, characterized by a blunted postprandial CCK response as well as delayed gastric emptying
Peptide tyrosine (PYY), the intestinally derived anorexigen that elicits satiety, appears to be dysregulated in individuals with AN and BN, but not in those with BED.
The orexigenic peptide ghrelin is of interest in EDs because it is the only known GI hormone that stimulates appetite and promotes food intake.
Ghrelin influences secretion of growth
hormone, induces adiposity, and is implicated in signaling the hypothalamic nuclei involved in energy homeostasis
AN have shown that
(1) circulating basal levels of ghrelin are elevated,
a likely consequence of prolonged starvation40, 42,
2) growth hormone and appetite responses to ghrelin are blunted, suggesting ghrelin resistance or altered ghrelin sensitivity
(3) ghrelin levels return to normal after partial weight
recovery, suggesting a physiologic effect to compensate for lack of nutritional intake and energy stores
Plasma levels of ghrelin are normal or elevated in individuals with BN, which suggests that abnormal eating behaviors, including binge eating and purging, may influence ghrelin secretion
Leptin and adiponectin are hormonal signals associated with longer-term regulation of body fat stores.
Leptin is also directly implicated in satiety through its binding to the ventral medial nucleus of the hypothalamus, an area termed the satiety center.
AN and BN most commonly have their onset in adolescence,
BED usually manifests in the early 20s
but EDs can occur throughout most of the life span and appear to be increasing in frequency in middle-aged and older women
ARFID most commonly has its onset in the early years but can continue into adulthood.
Pica has been described in both children and adults, but little is known about the courses of pica and rumination disorder
AN is characterized by a significantly low weight (the weight that is less than minimally normal), fear of gaining weight (despite being thin), and a disturbance in the way body shape or weight is perceived
Behaviors Used to Compensate for Excessive
Food Intake or to Prevent Weight Gain
PURGING BEHAVIORS
Diuretic abuse
Laxative and/or enema abuse
Self-induced vomiting (including syrup of ipecac abuse)
NON-PURGING BEHAVIORS
Excessive physical activity
Fasting, skipping meals, restrictive-eating pattern
Inappropriate withholding or under-dosing of insulin (among individuals with diabetes mellitus)
Stimulant abuse (e.g., caffeine, ephedra, methylphenidate, cocaine)
AN is further divided into 2 subtypes: restricting type (those who primarily control their weight through dieting, fasting, or exercising) and binge-eating/purging type (those who routinely purge calories to control weight and/or routinely binge eat
clinical hallmark of BN is recurrent binge eating accompanied by inappropriate compensatory behaviors to control weight or to purge calories consumed during a binge
On average, these behaviors must occur once each week for at least 3 months to meet diagnostic criteria
Also intrinsic to the diagnosis of BN is the excessive influence of weight and/or shape on self-image.
Individuals with BN have poor self-image that is often
anchored to their weight. It is not unusual for individuals with AN or BN to weigh themselves daily, even several times each day, and to experience fluctuations in self-esteem and mood based on
the result
binge eating is consumption of an unusually
large amount of food during a “discrete period of time” accompanied by the feeling that the eating cannot be controlled
BED is characterized by recurrent and persistent binge eating.
To meet diagnostic criteria, binge episodes should occur at least weekly, on average, over a duration of 3 or more months.
Unlike BN, BED is not associated with recurrent inappropriate compensatory behaviors to prevent weight gain.
