Nutrition and Metabolism Flashcards
1
Q
TGs liberate ____ when oxidized and are stored compactly as oil inside the fat cell.
A
9.3 kcal/g
2
Q
glycogen produces only ___ on oxidation and is stored intracellularly as a gel, containing approximately 2 g of water per gram of glycogen.
A
4.1 kcal/g
3
Q
Daily total energy expenditure (TEE) has three components:
A
resting energy expenditure (REE) (≈70% of TEE); the energy expenditure of physical activity (≈20% of TEE);
and the thermic effect of feeding (≈10% of TEE), which is the temporary increase in energy expenditure that accompanies enteral ingestion or parenteral administration of nutrients.
4
Q
Resting Energy Expenditure
A
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.
5
Q
liver, intestine, brain, kidneys, and heart
A
constitute roughly 10% of total body weight but account for about 75% of REE.
6
Q
skeletal muscle at rest consumes
A
some 20% of REE, but represents approximately 40% of body weight.
7
Q
Adipose tissue
A
consumes less than 5% of REE but usually accounts for greater than 20% of body weight.
8
Q
An accurate assessment of REE
A
best obtained by indirect calorimetry, in vivo energy expenditure is estimated by measuring carbon dioxide production and oxygen consumption while the subject is at rest.
9
Q
The energy expended during a particular physical activity
A
is equal to (REE per hour) × (activity factor) × (duration of activity in hours)
10
Q
Thermic Effect of Feeding
A
A meal containing all these nutrients usually increases metabolic rate by 5% to 10% of ingested or infused calories.
11
Q
stress factor
A
TEE = REE × Stress factor
12
Q
An alternative and simple formula for adult inpatients, although accompanied by some further loss in accuracy, is:
A
20 to 25 kcal/kg of actual body weight (ABW)/day for un- stressed or mildly stressed patients
25 to 30 kcal/ABW/day for moderately stressed patients
30 to 35 kcal/ABW/day for severely stressed patients
13
Q
Adjusted IBW
A
Adjusted IBW = IBW + 0.5 (ABW−IBW)
14
Q
Relative
Thermic Effect of Various Levels Physical activity
A
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: basketball
6.1-10.0
15
Q
In patients with large artifactual increases in weight due to extracellular fluid retention (e.g., ascites)
A
IBW should be used to estimate energy requirements
16
Q
“Penn State Equation”) is:
A
TEE = (REE calculated by Mifflin equation × 0.96) + (Tmax × 167) + (Ve × 31) − 6212
17
Q
Metabolic Stress Factors for Estimating Total Energy Expenditure in Hospitalized Patients
A
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
18
Q
One reason for this conservatism is that acute illness and its management often exacerbate preexisting diabetes or produce de novo glucose intolerance.
A
hyperglycemia is a frequent consequence of enteral, and especially parenteral, nutrition.
19
Q
Extremely tight control, with target range
A
a target range of 81 to 108 mg/dL
A panel of experts recently recommended instituting protocols to keep blood sugar levels at 150 mg/dL or lower in ICU patients, preferably by use of a continuous infusion of insulin, with monitoring every 1 to 2 hours so that appropriate adjustments can be made and blood sugar values less than 70 mg/ dL are avoided
20
Q
Estimated Energy Requirements for Hospitalized Patients Based on Body Mass Index
A
<15 kg/m2: 35-40 kcal/kg/day
15-19kg/m2: 30-35kcal/kg/day
20-29 kg/m2: 20-25 kcal/kg/day
≥30 kg/m2: 15-20 kcal/kg/day
21
Q
hypocaloric feeding,
A
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.
22
Q
considered essential because their carbon skeletons cannot be synthesized by the body.
A
histidine, isoleucine, leucine, lysine, methio- nine, phenylalanine, threonine, tryptophan, valine, and possibly arginine
23
Q
nonessential in most circumstances because they can be made from endogenous precursors or essential AAs
A
glycine, alanine, serine, cysteine, tyrosine, glutamine, glutamic acid, asparagine, and aspartic acid
24
Q
The U.S. Recommended Daily Allowance (RDA) of protein has been established at
A
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 bio- logical variance in requirement observed in a healthy population.
25
recommended Daily Protein Intake
Normal: 0.80g/kg IBW
Metabolic stress: 1.0-1.6g/kg IBW
Hemodialysis: 1.2-1.4g/kg/IBW
Peritoneal dialysis: 1.3-1.5g/kg/IBW
26
In normal adults, approximately _____ of total protein requirements should be in the form of essential AAs.
15-20%
27
Once adequate dialysis is available, protein delivery should be increased to the actual projected need,
including additional protein to compensate for losses resulting from dialysis
28
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
29
proxy measure of protein balance (i.e., whether the quantity of protein [or AAs] taken in is sufficient to prevent any net loss of protein).
Nitrogen Balance
N balance = (Grams of N administered as nutrition) − (Urinary urea N [g] + 4)
30
N balance (i.e., intake > loss) represents anabolism and a net increase in total body protein
positive N balance
31
represents net protein catabolism
negative N balance
32
Carbohydrates
Complete digestion of the principal dietary digestible carbohy- drates—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.
33
glucose is the required or preferred fuel for red and white blood cells, the renal medulla, eye tissues, peripheral nerves, and the brain.
once glucose requirements for these tissues are met (≈150 g/day), the protein-sparing effects of carbohydrate and fat are similar.
34
Lipids
consist of TGs, sterols, and phospholipids.
35
they are essential FAs and, therefore, should constitute at least 2% and 0.5%, respectively, of the daily caloric intake to prevent a deficiency state.
Linoleic acid (C18:2, n-6) and linolenic acid (C18:3, n-3)
36
inorganic nutrients that are required in large (>100 mg/day) quantities and are important for ionic equilibrium, water balance, and normal cell function.
Major Minerals
37
MICRONUTRIENTS
micronutrients are distinguished from macronutrients (carbohydrates, fats, and proteins) and macrominerals (calcium, magnesium, and phosphorus).
38
Compelling evidence exists for the essential nature of 10 trace elements in humans
ron, zinc, copper, chromium, selenium, iodine, fluorine, manganese, molybdenum, and cobalt
39
Deficiency:
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).
Vitamin A
40
Vitamin A Toxicity:
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.
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).
41
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).
Vitamin D
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.
42
Vitamin D toxicity
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).
43
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).
Vitamin E
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.
44
Vitamin E toxicity
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).
45
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).
Vitamin K
46
Vitamin K toxicity
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).
47
Vitamin K
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.
48
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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).
```
Thiamine (vitamin B1)
Deficiency (RDA)*
Classic deficiency syndrome (beriberi) remains endemic in Asian populations consuming polished
49
Thiamine (vitamin B1) toxicity
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.
50
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).
Riboflavin (vitamin B2)
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.
51
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).
Niacin (vitamin B3)
52
Niacin (vitamin B3) toxicity
Human toxicity is known largely through studies examining hypolipidemic effects; includes flushing, hyperglycemia, hepatocellular injury, and hyperuricemia (35 mg).
53
Niacin (vitamin B3) assessment
Measurement of urinary excretion of the niacin metabolites N-methylnicotinamide and 2-pyridone are thought to
be the most effective means of assessment.
54
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).
Pantothenic acid (vitamin B5)
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.
55
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).
Pyridoxine (vitamin B6)
Chronic use with doses exceeding 200 mg/day (in adults) may cause peripheral neuropathies and photosensitivity (100 mg).
56
Pyridoxine (vitamin B6) assessment
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.
57
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).
Biotin (vitamin B7)
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.
58
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).
Folate (Vitamin B9)
59
Folate (Vitamin B9) toxicity
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).
60
Folate assessment
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.
61
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 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).
Cobalamin (vitamin B12)
62
A few allergic reactions have been reported from crystalline B12 preparations and are probably due to impurities, not the vitamin (TUL not established).
Cobalamin (vitamin B12) toxicity
63
Cobalamin (vitamin B12) assessment
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.
64
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).
Ascorbic and dehydroascorbic acid (vitamin C)
65
Ascorbic and dehydroascorbic acid (vitamin C) toxicity
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).
66
Ascorbic and dehydroascorbic acid (vitamin C) assessment
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.
67
Deficiency in humans is only described for patients on long-term TPN containing inadequate chromium. Hyperglycemia or impaired
glucose tolerance is uniformly observed. Elevated plasma free fatty acid concentrations, neuropathy, encephalopathy, and abnormalities in nitrogen metabolism are also reported. Whether supplemental chromium may improve glucose tolerance in mildly glucose intolerant but otherwise healthy individuals remains controversial (F, 25 μg; M, 35 μg).
Chromium
Toxicity after oral ingestion is uncommon and seems confined to gastric irritation. Airborne exposure may cause contact dermatitis, eczema, skin ulcers, and bronchogenic carcinoma (No TUL established).
68
Chromium assessment
Plasma or serum concentration of chromium is a crude indicator of chromium status; it appears to
be meaningful when the value is markedly above or below the normal range.
69
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 anemia arises from impaired uptake of iron and is, therefore, a secondary form of iron deficiency anemia. 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).
copper
70
Acute copper toxicity
Acute copper toxicity has been described after excessive oral intake and with absorption of copper salts applied to burned skin. Milder manifestations include nausea, vomiting, epigastric pain, and diarrhea; coma and hepatocellular injury may ensue in severe cases. 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, eventually leading to damage of these 2 organs (10 mg).
71
Acute copper assessment
Practical methods for detecting marginal deficiency are not available. Marked deficiency is reliably detected by diminished serum copper and ceruloplasmin concentrations, as
well as low erythrocyte superoxide dismutase activity.
72
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).
fluoride
73
fluoride toxicity
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).
74
In the absence of supplementation, populations relying primarily on food from soils with low iodine content have endemic iodine deficiency. 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).
iodine
75
iodine toxicity
```
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).
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76
iodine measurement
Urinary excretion of iodine is an effective laboratory means of assessment. The thyroid-stimulating hormone (TSH) level in the blood is an
indirect, not entirely specific means of assessment. Iodine status of a population can be estimated by the prevalence of goiter.
77
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
78
iron toxicity
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)
79
Iron assessment
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.
80
has not been conclusively demonstrated in humans. It is said to cause hypocholesterolemia, weight loss, hair and nail changes, dermatitis, and impaired synthesis of vitamin K–dependent proteins (F, 1.8 mg; M, 2.3 mg).
Manganese deficiency
81
Manganese toxicity
toxicity by oral ingestion is unknown in humans. Toxic inhalation causes hallucinations, other alterations
in mentation, and extrapyramidal movement disorders (11 mg).
82
Cases of human deficiency are extremely rare; caused by TPN lacking the element or by parenteral administration of sulfite. Reported to result in hyperoxypurinemia, hypouricemia, low urinary sulfate excretion, and CNS disturbances (45 μg).
Molybdenum
Molybdenum has low toxicity; occupational exposures and high dietary intake are linked to hyperuricemia and gout in epidemiologic studies (2 mg).
83
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Deficiency is rare in North America but has been observed in individuals on long-term TPN lacking 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, a condition characterized by cardiomyopathy. Keshan disease can
be prevented (but not treated) by selenium supplementation (55 μg).
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selenium
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).
84
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 (F, 8 mg; M, 11 mg).
Deficiency of zinc
85
Acute zinc toxicity
can usually be induced by ingestion of >200 mg of zinc in a single day (in adults). It is manifested by epigastric pain, nausea, vomiting, and diarrhea. Hyperpnea, diaphoresis, and weakness may follow inhalation of zinc fumes. Copper and zinc compete for intestinal absorption: chronic ingestion of >25 mg zinc/day may lead to copper deficiency. Chronic ingestion of >150 mg/day has been reported to cause gastric erosions, low high-density lipoprotein cholesterol levels, and impaired cellular immunity (40 mg).
86
zinc deficiency
aside from iron, the trace mineral depletion clinicians are most likely to encounter is zinc deficiency.
Zinc depletion is a particularly germane issue to the gastroenterologist, because the GI tract is a major site for zinc excretion.
it is well recognized that in acute illness a shift in zinc occurs from the serum compartment into the liver, further obscuring the diagnostic value of serum zinc levels.
87
zinc-dependent protein, and therefore serum activity of the enzyme has sometimes been proposed as a functional measure of zinc status.
Alkaline phosphatase
88
Malabsorption and Maldigestion
both fat- and water-soluble micronutrients are absorbed pre- dominantly in the proximal small intestine, the only exception being vitamin B12, which is absorbed in the ileum.
89
Fat-soluble vitamin deficiencies
well-recognized complications of cystic fibrosis and congenital biliary atresia, in which fat malabsorp- tion often is overt, but monitoring is also necessary in conditions associated with more subtle fat malabsorption, such as the latter stages of chronic cholestatic liver disease.
90
During the first 24 hours of fasting, the most readily avail- able energy substrates
circulating glucose, FAs and TGs, and liver and muscle glycogen) are used as fuel sources.
91
During the first several days of starvation
obligate glucose- requiring tissues like the brain and blood cells, which collec- tively account for about 20% of total energy consumption, can use only glycolytic pathways to obtain energy.
92
major source of substrate for this purpose.
Glucogenic AAs derived from skeletal muscle (chiefly alanine and glutamine)
93
ketogenesis
A maximal rate of ketogenesis is reached by 3 days of starvation, and plasma ketone body concentration is increased 75-fold by 7 days.
ketone bodies can cross the blood-brain barrier and provide most of the brain’s energy needs by 7 days of starvation.
94
During long-term starvation
(14 to 60 days), maximal adaptation is reflected by a plateau in lipid, carbohydrate, and protein metabolism.
Muscle protein breakdown decreases to less than 30 g/day, causing a marked decrease in urea nitrogen pro- duction and excretion.
95
Obesity
Obesity is associated with a blunted increase in lipolysis and decrease in glucose production compared with that in lean persons
96
During the final phase of starvation
body fat stores reach a critical level, energy derived from body fat decreases, and muscle protein catabolism is accelerated.
97
Malnutrition
malnutrition is used to describe a state of inadequacy in protein, calories, or both and is more precisely called protein-energy malnutrition or protein-calorie malnutrition.
98
are the most important mediators of alterations
in energy and protein metabolism that accompany illness and
injury.
Cytokines
99
In a wide spectrum of systemic illnesses
increased secretion of interleukin (IL)-1β, tumor necrosis factor -α, IL-6, and
interferon-γ has been observed to be associated with increased
energy expenditure and protein catabolism, as well as the shift of
AAs into the visceral compartments
100
in the wasting syndrome associated with cancer
proteolysis-inducing factor and zinc-α-2-glycoprotein (‘lipid-mobilizing
factor’) are humoral mediators that appear to be unique to cancer
cachexia, contributing to protein catabolism and loss of adipose
tissue, respectively.
101
IFN-γ
Lymphocytes, pulmonary macrophages
| Increased monocyte respiratory burst
102
IL-1β
Monocytes/macrophages, neutrophils, lymphocytes, keratinocytes, Kupffer cells
Increased ACTH and cortisol levels
Increased acute-phase protein synthesis
Increased AA release from muscles
Decreased insulin secretion Fever
103
IL-6
Monocytes/macrophages, keratinocytes, endothelial cells, fibroblasts, T cells, epithelial cells
Increased acute-phase protein synthesis
Fever
Decreased appetite
104
TNF-α
Monocytes/macrophages, lymphocytes, Kupffer cells, glial cells, endothelial cells, natural killer cells, mast cells
```
Decreased FFA synthesis
Increased lipolysis
Increased AA release from muscles
Increased hepatic AA uptake
Fever
```
105
The abdomen is protuberant because of weakened abdominal muscles, intestinal distention, and hepatomegaly, but ascites is rare
kwashiorkor
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.
106
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.
107
Weight loss and marked depletion of subcutaneous fat and muscle mass
Ribs, joints, and facial bones are prominent, and the skin is thin, loose, and lies in folds.
characteristic features of children with marasmus.
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
108
Weight loss
it is useful to quantify such loss by determining whether the patient has sustained a mild (<5%), moderate (5% to 10%), or severe (>10%) degree of loss over the preceding 6 months.
109
BMI
A low BMI (<18.5 kg/m2) is interpreted as an indication of PEM, and a high BMI (>24.9 kg/ m2) is interpreted as excessive fat mass (overweight or obesity).
110
Weight measurements
The triceps and subscapular sites are used most commonly for this purpose, and it is best to use the sum of the triceps and subscapular folds because sizable inter-individual differences exist in fat distribution.
111
indicators of protein-calorie status:
albumin, pre- albumin (transthyretin), transferrin, and retinol-binding protein (RBP)
All these proteins behave as negative acute-phase reactants,
i.e., their serum concentrations drop in response to systemic
inflammation, roughly proportional to the magnitude of the
inflammatory response.
112
Prealbumin levels
are often elevated in chronic kidney dis- ease or by glucocorticoid or oral contraceptive administration.
113
In the ESPEN definition, 2 criteria must be present: a “decreased absorption of macronu- trients and/or water and electrolytes due to a loss of gut function” and the “need for parenteral support.”
Intestinal Failure
114
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
115
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 irre- versible
Type II IF
116
which is a chronic state of IF requir- ing long-term nutritional support, typically in the form of home PN.
Type III IF
117
intestinal malabsorption associated with a functional small intestine length of less than 200 cm is a common cause of IF
Short bowel syndrome (SBS)
118
After extensive intestinal resection, 3 clinical stages
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 absorp- tion).
The third stage is a stable phase during which no further improvement or adaptive changes occur.
PN is prescribed during stage 1 to meet nutritional needs.
119
During stage 2
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—and separate the times of fluid and solid food ingestion. Lactose is usually well tolerated, unless the proximal jejunum is resected.
120
In 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.
121
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.
122
in 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.
123
Production of glucagon-like peptide (GLP)-1
Production of 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.
124
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.
Intestinal autonomy
125
usually require a glucose-electrolyte oral rehydration solution (ORS).
Patients with severe SBS (<200 cm small bowel remaining)
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
126
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.
127
In addition
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.
128
Treatment
Vitamin B12 injections should be administered monthly if more than 50 to 60 cm of terminal ileum has been resected.
129
Treatment
The somatostatin analog octreotide has been shown to prolong small intes- tinal transit time and decrease GI secretions, but its use remains controversial because it is also associated with gallstone forma- tion and decreased splanchnic protein synthesis, and has not been shown to eliminate the need for PN.
130
Pancreatitis
data on early feeding (initiated within 24 to 36 hours of admission) in AP have demonstrated lower risk of multi- organ failure (MOF), operative interventions, systemic infections, septic complications, and even mortality compared with what had been standard therapy (no EN/PN) or delayed EN.
131
Severe pancreatitis
If the SIRS response is severe enough to require admission to the ICU (especially if the patient is placed on mechanical ventila- tion), a NG/NJ tube should be placed and EN initiated within 24 to 36 hours of admission.
132
If the SIRS response is minimal and the patient can be managed on the hospital wards
then oral diet should be offered as tolerated and EN considered only when there is failure to advance the diet after 4 days.
133
chronic pancreatitis (CP)
Jejunal feeding in such patients has been used to improve weight as well as to reduce abdominal pain, GI side effects, and narcotic use
Taken altogether, it would seem that elderly patients with alcohol as the etiology for their CP are less likely to benefit from antioxidant therapy than younger patients with a non-alcoholic etiology.
134
Patients with CP
should consume small, frequent meals and avoid foods that are difficult to digest (e.g., legumes). 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.
135
Crohn Disease (CD)
Deficiencies of magnesium, selenium, potassium, zinc, iron, and vitamin B12
136
Liver Disease
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
137
Cirrhosis
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, respectively, can further lead to reduced food variety and poor oral intake.
138
cholestatic liver disease.
Decreased bile salt production results in an intolerance to high-fat foods and the development of fat-soluble vitamin malabsorption
139
Cirrhosis
Gluconeogenesis and protein catabolism are up-regulated, glycogenolysis is down-regulated, and insulin resistance occurs, leading to a depletion of muscle mass and fat mass because of their use as energy sources.
140
Liver failure
the branched- chain 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.
the aromatic amino acids (AAAs) tyrosine, phenylalanine, and methionine are metabolized and deaminated solely by the liver.
141
BCAA
BCAAs by skeletal muscle supplies carbon skeletons for the formation of α-ketoglutarate, which combines with 2 ammonia molecules to become glutamine
142
deficiency in Liver disease
Micronutrient deficiencies can occur in patients with cirrhosis. Water-soluble vitamin (vitamin B complex and C) deficiencies can occur in both alcohol-associated and non- alcohol-associated liver disease.
thiamine supplementation is recommended in all patients with cirrhosis
143
HCV
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 lev- els of thiamine, riboflavin, and vitamin B6.
144
deficiency has been reported in cirrhosis and is considered a risk factor for cancer, including HCC.
Vitamin A
fat-soluble vitamin deficiencies occur more frequently with cholestatic
145
are low in patients with liver dis- ease and fall as liver disease progresses, as a result of which there is a high prevalence of osteoporosis in both cholestatic and non-cholestatic liver diseases.
vitamin D levels
146
feeding in liver cirrhosis
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.
147
diverticular disease nutrition
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.
148
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
Dumping syndrome
149
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 shift- ing 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.
These hormones, including enteroglucagon, pancreatic polypeptide, peptide YY, vasoactive intestinal polypeptide, and neurotensin, have been implicated in the etiology of the vasomotor symptoms by causing systemic and splanchnic vasodilation.
Early dumping syndrome
150
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.
Late dumping syndrome
151
Cancer
appetite stimulation with glucocorticoids and megestrol acetate has been used successfully in cancer patients with mild malnutrition
152
Water, ethyl alcohol, copper, iodide, fluoride, molybdenum
stomach
153
Calcium, iron, phosphorus, magnesium, copper, selenium, thiamin, riboflavin, niacin, biotin, folate; vitamins A, D, E, K
duodenum
154
Dipeptides, tripeptides, amino acids, calcium, phosphorus, magnesium, iron, zinc, chromium, manganese, molybdenum, thiamin, riboflavin, niacin, pantothenic acid, biotin, folate; vitamins B6, C, A, D, E, K
jejunum
155
Folate, magnesium; vitamins B12, C, D
ileum
156
obesity feeding
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
157
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
158
after bariatric surgery
patients are sequentially advanced from a clear liquid diet to a solid diet, and postoperative nutritional guidance by a dedicated bariatric dietician is highly encouraged.
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.
Iron, folate, calcium, and vitamin B12 deficiencies can occur after Roux-en-Y gastric bypass.
159
Post-bariatric surgery nutritional deficiencies can be divided into 3 types
protein-calorie malnutrition, vitamin and mineral deficiencies, and dehydration.
160
According to the 2013 joint guidelines from the American College of Cardiology, the American Heart Association, and the Obesity Society for the management of over- weight and obesity in adults, and the Endocrine Society’s clinical practice guidelines on the pharmacologic management of obesity
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 co-morbidities, such as hypertension, dyslipidemia, type 2 diabetes, or obstructive sleep apnea
There are 6 main anti-obesity medications: phentermine, phentermine/topiramate, orlistat, lorcaserin, bupropion/naltrexone, and liraglutide
161
Critical Illness
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.
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)
162
critical illness: 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.
163
In all ICU patients who require PN,
high protein hypocaloric PN should be considered initially over the first week, with pro- vision of 80% of energy requirements (20 kcal/kg actual body weight/day).
164
Complications PEG
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.
One common complication of PEG is peristomal wound infection.
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
165
Treatment PEG
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.
166
Other common complications PEG
include peristomal leakage, fever, ileus, cutaneous ulceration, and tube dislodgment.
Leakage around the gastrostomy site is a common and under recognized problem.
Risk factors for peristomal leakage include the use of glucocorticoids, chemotherapy, excessive cleaning with hydrogen peroxide or iodine, excessive tension and side-torsion of the tube, and absence of an external bumper.
Leakage of gastric acid or bile around the PEG tube can cause erythema and skin breakdown that is often mistaken for infection.
Treatment includes keeping the site dry with frequent dressing changes, 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.
167
after bariatric surgery
patients are sequentially advanced from a clear liquid diet to a solid diet, and postoperative nutritional guidance by a dedicated bariatric dietician is highly encouraged.
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.
Iron, folate, calcium, and vitamin B12 deficiencies can occur after Roux-en-Y gastric bypass.
168
Post-bariatric surgery nutritional deficiencies can be divided into 3 types
protein-calorie malnutrition, vitamin and mineral deficiencies, and dehydration.
169
According to the 2013 joint guidelines from the American College of Cardiology, the American Heart Association, and the Obesity Society for the management of over- weight and obesity in adults, and the Endocrine Society’s clinical practice guidelines on the pharmacologic management of obesity
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 co-morbidities, such as hypertension, dyslipidemia, type 2 diabetes, or obstructive sleep apnea
There are 6 main anti-obesity medications: phentermine, phentermine/topiramate, orlistat, lorcaserin, bupropion/naltrexone, and liraglutide
170
Critical Illness
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.
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)
171
critical illness: 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.
172
In all ICU patients who require PN,
high protein hypocaloric PN should be considered initially over the first week, with pro- vision of 80% of energy requirements (20 kcal/kg actual body weight/day).
173
Complications PEG
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.
One common complication of PEG is peristomal wound infection.
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
174
Treatment PEG
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.
175
Other common complications PEG
include peristomal leakage, fever, ileus, cutaneous ulceration, and tube dislodgement.
Leakage around the gastrostomy site is a common and under recognized problem.
Risk factors for peristomal leakage include the use of glucocorticoids, chemotherapy, excessive cleaning with hydrogen peroxide or iodine, excessive tension and side-torsion of the tube, and absence of an external bumper.
Leakage of gastric acid or bile around the PEG tube can cause erythema and skin breakdown that is often mistaken for infection.
Treatment includes keeping the site dry with frequent dressing changes, 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.
