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Aspen 2002

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Guidelines for the Use of
Parenteral and Enteral
Nutrition in Adult and
Pediatric Patients
Guidelines for the Use of
Parenteral and Enteral
Nutrition in Adult and
Pediatric Patients

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Background

Metabolic bone disease (MBD) has been reported in
infants and premature neonates receiving PN.1,2

The
incidence of MBD is unknown, but it is common in
patients receiving long-term PN.3,4

Biochemical evi-
dence of MBD may include hypercalciuria, hypercalce-

mia, hyperphosphatemia, elevated serum alkaline
phosphatase, low-normal plasma parathyroid hor-
mone, and normal 25-hydroxyvitamin D and low 1,25
hydroxyvitamin D plasma concentrations.4,5

The etiol-
ogy of bone demineralization or inadequate bone
matrix mineralization is multifactorial and often asso-
ciated with calcium, phosphorus, and vitamin D defi-
ciencies.6,7

Aluminum accumulation in bones8

and

excessive vitamin D may also contribute.9

Evidence

Hypocalcemia in MBD patients may be due to
decreased calcium intake or increased urinary calcium
elimination. Because of solubility limitations, calcium
and phosphate in neonatal PN are generally inade-
quate to meet the needs for optimal bone growth. There
are few clinical trials investigating MBD in infants and
children and most data are derived from studies in
adult patients.
Investigators have shown that very low birth weight
infants who received high calcium (1.68 mM/dL) and
phosphate (2 mM/dL) in their daily PN had greater
calcium and phosphate retention and greater bone
mineral content.7,10,11

Hypocalcemia due to hypercal-
ciuria has been consistently reported in patients
receiving PN. Factors known to promote hypercalci-
uria include increased calcium intake, decreased phos-
phate supplementation, excessive amino acid infusion,
chronic metabolic acidosis, and cyclic PN infusion. A
reduction in calciuria and bone pain can be achieved by
reducing calcium intake and altering the calcium-to-
phosphate ratio from 1:1.5 to 1:2.12

Several studies
have correlated amino acid intake with hypercalci-
uria.5,13,14

Chronic metabolic acidosis from excessive
amounts of amino acids or from D-lactic acidosis can
lead to MBD by direct loss of bone involving buffering
bone systems or impaired vitamin D metabolism.15,16
Two studies comparing cycled versus noncycled
administration of PN showed that cycling increases
bone mineral loss.14,17

In one of these studies, mea-
surement of bone mass by photon absorbtiometry
showed reduced vertebral bone mass but not wrist
bone mass in long-term (55.2 8.7 months) PN
patients.

Small amounts of aluminum are present in calcium
and phosphate salts, vitamins, heparin, and trace ele-
ment solutions.18

Aluminum in PN solutions may
result in a decreased rate of bone formation.18,19

Koo et

al20

found that aluminum accumulated at the miner-
alization front of bones in premature infants. Measure-
ment of serum aluminum concentration can help deter-
mine the role of aluminum excess when MBD is
suspected in long-term PN patients. Aluminum toxic-
ity may be a particular problem in young infants whose
kidneys cannot adequately excrete aluminum com-
pared with older children. The FDA has recommended
restriction of aluminum contamination in large volume
parenterals to a maximum of 25 g/L. Patients who
have elevated aluminun levels should have parenteral
sources of aluminum investigated.21
Underlying conditions and concurrent medications
may also be responsible or predispose to MBD. These

JanuaryFebruary 2002

SECTION XII

109SA

are especially prevelant in patients with malabsorp-
tion, glucocorticoid administration, and antineoplastic
agents.19,21

Several reports of improvement of MBD after vita-
min D removal from PN suggest a possible role of
vitamin D in the development of MBD.9,22

If this is
attempted, it is advised that patients have their
plasma PTH and 25-hydroxyvitamin D and 1,25
hydroxyvitamin D concentrations measured. If PTH
and 1,25 hydroxyvitamin D concentrations are low and
25 hydroxyvitamin D concentrations are normal, then
vitamin D should be withdrawn from the PN solution.

Practice Guidelines

Complications Unique to Neonates:
Metabolic Bone Disease

1. Calcium and phosphate should be provided in
adequate amounts to assure optimal bone miner-
alization in long-term PN patients. (A)
2. Serum aluminum concentrations should be mea-
sured whenever unexplained MBD is present in
long-term PN patients. (B)
3. In patients with low PTH and 1,25 hydroxyvita-
min D concentrations and normal 25 hydroxyvi-
tamin D concentration with MBD, vitamin D
should be removed from the PN solution. (B)

REFERENCES

1. The TS, Kollee LA, Boon JM, et al: Rickets in a preterm infant
duringintravenousalimentation.ActaPediatrScand72:769–71,
1993

2. Kien CL, Browning C, Jona J, et al: Rickets in premature infants
receiving parenteral nutrition: A case report and review of the
literature. JPEN 6:152–156, 1982
3. Shike M, Harrison JE, Sturtridge WC, et al: Metabolic bone
disease in patients receiving long-term total parenteral nutri-
tion. Ann Intern Med 92:343–350, 1980
4. Shike M, Shils ME, Heller A. et al: Bone disease in prolonged
parenteral nutrition: Osteopenia without mineralization defect.
Am J Clin Nutr 44:89–98, 1986
5. De Vernejoul MC, Messing B, Modrowski D, et al: Multifactorial
low remodeling bone disease during cyclic total parenteral nutri-
tion. J Clin Endocrinol Metab 60:109, 1985

6. Leape LL, Valaes T: Rickets in low birth weight infants receiving
total parenteral nutrition. J Pediatr Surg 11:665–674, 1976
7. Prestridge LL, Schanler RJ, Shulman R, et al: Effect of paren-
teral calcium and phosphorus on mineral retention and bone
mineral content in very low birth weight infants. J Pediatr
122:761–768, 1993
8. Vargas JH, Klein GL, Ament ME, et al: Metabolic bone disease of
total parenteral nutrition: Course after changing from casein to
amino acids in parenteral solutions with reduced aluminum
content. Am J Clin Nutr 48:1070–1078, 1988
9. Shike M, Sturtridge WC, Tam CS, et al: A possible role for
vitamin D in the genesis of parenteral nutrition-induced meta-
bolic bone disease. Ann Intern Med 95:560–568, 1981
10. Wood RJ, Sitrin MD, Cusson GJ, et al: Reduction of total paren-
teral nutrition-induced urinary calcium loss by increasing the
phosphorus in the total parenteral nutrition prescription. JPEN
10:188–190, 1986
11. Sloan GM, White DE, Brennan MF: Calcium and phosphorus
metabolism during total parenteral nutrition. Ann Surg 197:
1–6, 1983
12. Larchet M, Garabedian M, Bourdeau A et al: Calcium metabo-
lism in children during long-term total parenteral nutrition: The
influence of calcium, phosphorus, and vitamin D intakes. J Pedi-
atr Gastroenterol Nutr 13:367–375, 1991
13. Bengoa JM, Sitrin MD, Wood RJ, et al: Amino acid-induced
hypercalciuria in patients on total parenteral nutrition. Am J
Clin Nutr 38:264–269, 1983
14. Lipkin EW, Ott SM, Chesnut CH, et al: Mineral loss in the
parenteral nutrition patient. Am J Clin Nutr 47:515–523, 1988
15. Cunningham J, Fraher LJ, Clemens TL, et al: Chronic acidosis
with metabolic bone disease. Am J Med 73:199–204, 1982
16. Karton MA, Rettmer R, Lipkin EW, et al: D-Lactate and meta-
bolic bone disease in patients receiving long-term parenteral
nutrition. JPEN 13:132–135, 1989
17. Wood RJ, Bengoa JM, Sitrin MD, et al: Calciuric effect of cyclic
versus continuous total parenteral nutrition. Am J Clin Nutr
41:614–619, 1985
18. Koo WWK, Kaplan LA, Horn J, et al: Aluminum on parenteral
nutrition solution-sources and possible alternatives. JPEN
10:591–595, 1986
19. Klein GL: Metabolic bone disease of total parenteral nutrition.
Nutrition 14:149–152, 1998
20. Koo WWK, Kaplan LA, Bendon R, et al: Response to aluminum
in parenteral nutrition during infancy. J Pediatr 109:883–887,
1986

21. Seidner DL, Licata A: Parenteral nutrition associated metabolic
bone disease: Pathophysiology, evaluation, and treatment. Nutr
Clin Pract 15:163–170, 2000
22. Verhage AH, Cheong WK, Allard JP, et al: Increase in lumbar
spine bone mineral content in patients on long-term parenteral
nutrition without vitamin D supplementation. JPEN 19:431–
436, 1995

110SA

A.S.P.E.N. BOARD OF DIRECTORS

Vol. 26, No. 1, Supplement

Section XIII: Specific Guidelines for Disease—Pediatrics

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