Typical Phosphorus Lab Values for a Preterm Baby

Nutrients. 2015 April; 7(four): 2562–2573.

Serum Phosphorus Levels in Premature Infants Receiving a Donor Human Milk Derived Fortifier

Received 2014 Nov thirteen; Accepted 2015 Mar 30.

Abstract

An elevated serum phosphorus (P) has been anecdotally described in premature infants receiving homo milk fortified with donor human milk-derived fortifier (HMDF). No studies take prospectively investigated serum P in premature infants receiving this fortification strategy. In this single centre prospective observational cohort report, extremely premature infants ≤1250 grams (g) birth weight (BW) were fed an exclusive human milk-based diet receiving HMDF and serum P levels were obtained. Nosotros evaluated 93 infants with a mean gestational age of 27.5 ± 2.0 weeks (Mean ± SD) and BW of 904 ± 178 g. Seventeen infants (eighteen.iii%) had at least ane high serum P level with a mean serum P of 9.2 ± 1.1 mg/dL occurring at nineteen ± 11 days of life. For all infants, the highest serum P was inversely correlated to the twenty-four hour period of life of the infant (p < 0.001, R ² = 0.175) and positively correlated with energy density of HMDF (p = 0.035). Serum P was not significantly related to gender, BW, gestational age, or days to full feeds. We conclude that the incidence of hyperphosphatemia was mild and transient in this population. The risk decreased with baby age and was unrelated to gender, BW, or ethnicity.

Keywords: neonate, phosphorus, hyperphosphatemia, human milk, exclusive human milk-based diet, human milk-derived fortifier, prematurity, creatinine, donor milk, very low nascence weight

ane. Introduction

Human milk is the optimal source of nutrition for all infants, including preterm ones. The American Academy of Pediatrics (AAP) recommends that all infants <1500 g birth weight (BW) should receive human milk appropriately fortified [1]. An exclusive human being-milk based diet is divers equally female parent's ain milk (or pasteurized donor milk when mother'south own milk is unavailable) fortified with a donor human being milk-derived fortifier (HMDF), containing no preterm formula or cow milk protein-based fortifiers. This arroyo provides advantages over cow milk-containing products providing optimal growth rates, a lower rate of necrotizing enterocolitis, and decreased days of parenteral nutrition. Additionally, such an arroyo leads to lowered sepsis rates, decreased mortality, and shorter infirmary stays [ii,3,4,5,vi,7].

Extremely premature infants are susceptible to growth failure, metabolic growth abnormalities, and poor neurodevelopmental outcomes [5,viii,nine,10,11]. Common metabolic derangements of extremely premature infants including hypocalcemia, hyperphosphatemia, and hypomagnesemia are usually secondary to young hormone responses and renal dysfunction [8]. At that place are no published reports investigating the sequential early on postnatal mineral serum chemistries of very low birth weight infants receiving an sectional human milk-based diet with HMDF. This study aimed to evaluate how an exclusive man milk-based diet with HMDF can touch the adventure of electrolyte abnormalities, specifically serum phosphorus.

There have been anecdotal reports of hyperphosphatemia associated with HMDF in extremely low birth weight infants and some wellness intendance providers may exist limiting their use of this product because of this concern. Because of the potential benefits of using an exclusive human milk-based nutrition, but business nigh phosphorus metabolism, we chose to evaluate the incidence of hyperphosphatemia, hypophosphatemia and hypocalcemia in all infants <1250 g BW receiving this diet.

two. Experimental Section

Extremely premature infants were consecutively followed in this single-center prospective observational cohort written report from August 2010 to Dec 2011. Inclusion criteria were: premature infants <37 weeks gestation, BW <1250 g, admitted within 48 h of birth, receiving an exclusive man milk-based diet, and achievement of total enteral feedings by 4 weeks of age. Infants were excluded who died within the first calendar week of life and those who had major built anomalies. Infants were followed from birth until discharge and data were prospectively collected for growth and nutrition using pre-study divers variables and definitions [3].

Every bit canonical by the Institutional Review Lath of Baylor College of Medicine and Affiliated Hospitals, consent was waived for this observational written report. Our master effect of this written report was to evaluate the metabolic derangements in phosphorus levels for infants receiving an sectional human milk-based diet with HMDF. Specifically, study outcomes included the number of phosphorus levels, mean phosphorus level drawn per infant, mean peak phosphorus level, percentage of infants with hyperphosphatemia (serum phosphorus > eight.0 mg/dL), pct of infants with hypophosphatemia (serum phosphorus < 4.viii mg/dL), the incidence of hyperphosphatemia in relationship to serum creatinine, the incidence of hypocalcemia during hyperphosphatemia, and the twenty-four hours of life of peak phosphorus levels.

2.1. Standardized Feeding Protocol

Infants received a standardized feeding protocol which has been previously published past our group [3]. Human milk was fortified with HMDF Prolact +4, Prolact +6, Prolact +eight, or Prolact +10 (Prolacta Bioscience, Industry, CA, USA) with final energy concentrations of 24 kcal/oz, 26 kcal/oz, 28 kcal/oz, and 30 kcal/oz, respectively, based on expected homo milk free energy concentration of xx kcal/oz. Each fortifier adds 64 mg/dL of phosphorus and 122 mg/dL of calcium. This is comparable to most moo-cow milk protein-based homo milk fortifiers with phosphorus contents ranging from 26 mg/dL to 67 mg/dL and calcium contents ranging from 38 mg/dL to 138 mg/dL [2,12].

ii.two. Data Collection

Serum phosphorus levels were collected per unit protocol 3 days after stopping parenteral nutrition and repeated one week later if serum phosphorus was >eight.0 mg/dL. Further serum phosphorus values were collected at the discretion of the attending clinician. The superlative phosphorus level (or single highest phosphorus level for ane infant) was recorded along with the corresponding the twenty-four hour period of life, degree of calorie fortification (energy density), and the number of days after discontinuation of parenteral nutrition. All infants with serum phosphorus levels >8.0 mg/dL were assessed with a serum creatinine, serum calcium, and serum element of group i phosphatase level within three days if available. Normal and low serum phosphorus levels in all infants were collected with corresponding solar day of life. Serum phosphorus levels were treated as one value if separated by less than 2 days.

Only serum phosphorus levels drawn during the use of the HMDF were used in this written report. Of infants with multiple serum phosphorus levels on tape, the highest level was considered the acme serum phosphorus level. Of infants with only one serum phosphorus level on record, that level was used.

two.three. Statistical Analyses

Relationships amongst variables were evaluated using general linear modeling in which hyperphosphatemia was the primary outcome. Regression analysis was used to compare relationships between tiptop serum phosphorus and day of life, energy density of HMDF, and days to accomplish full feeds. Additionally, comparisons betwixt serum phosphorus and gender, BW, gestational age, race, and >750 g or below 750 thousand BW were completed with univariate regression assay. Statistical significance was defined as p < 0.05. A t-exam was performed to compare the serum phosphorus and serum creatinine between an babe grouping inside five days of discontinuation of parenteral nutrition and a group five days afterwards discontinuation of parenteral nutrition. Analyses were completed using SPSS 22.0 (SPSS Inc., Chicago, IL, USA). All information are mean ± standard deviation unless otherwise noted.

3. Results

Of 124 infants identified who initially met the inclusion criteria, 93 were included for the assay. (Effigy ane). The demographics and outcomes are shown in Table 1 and Table 2. In total, 356 serum phosphorus values were drawn amongst the 93 infants. On boilerplate, serum phosphorus levels were drawn 3.8 times per baby. 16 infants had only one serum phosphorus level checked, while 29 infants had serum phosphorus levels drawn over four times during their grade (Table 3). Of 356 discrete levels during the use of HMDF, 291 (81%) serum phosphorus levels were within normal limits. The mean peak serum phosphorus was 7.2 ± one.3 mg/dL. One infant was excluded for farthermost hyperphosphatemia (serum phosphorus 17.viii mg/dL) at 48 days of life and was considered an outlier secondary to developing an incarcerated hernia at that fourth dimension. Two infants also had hypocalcemia at the time of a high serum phosphorus level.

Infants receiving the exclusive human milk-based diet were prospectively followed.

Table 1

Babe demographics and characteristics.

Demographics and Characteristics	Cohort n = 93
Nascence weight, g	904 ± 178 *
Gestational age, weeks	27.5 ± 2.0
Male gender, due north (%)	47 (51)
Race, % Black/White/Hispanic/Other	36, 25, 22, 10
Number of days to full 140 mL/kg/mean solar day feeds	xvi.0 ± 4.0
Inborn, n (%)	53 (57)
Antenatal steroids, northward (%)	67 (72)

Table 2

Outcomes.

Outcomes	Accomplice northward = 93
Total serum phosphorus levels obtained	356
Mean number of serum phosphorus levels per infant	three.viii ± 2.5 *
Mean pinnacle serum phosphorus level of all infants (mg/dL)	7.two ± one.3 *
Infants with loftier serum phosphorus (>8 mg/dL), n (%)	17 (18.iii)
Total loftier serum phosphorus levels, northward (%)	23 (7)
Infants with multiple high serum phosphorus levels, n (%)	5 (v)
Average high serum phosphorus level (mg/dL)	9.two ± 1.1 *
Infants with depression serum phosphorus (<4.8 mg/dL), n (%)	19 (20)
Total low serum phosphorus values (<4.viii mg/dL), due north (%)	42 (13)
Infants with no serum phosphorus abnormalities, n (%)	64 (69)
Hypocalcemia occurring with loftier serum phosphorus level (serum calcium < seven.0 mg/dL or ionized calcium < 1.0 mmol/L), n	2

Table iii

Number of serum phosphorus levels recorded while on man milk-derived fortifier.

Number of Serum Phosphorus Levels Recorded Per Infant	n = 356
Only ane level	16
2–3 levels	36
>iv levels	29
>half dozen levels	xi

In the accomplice, 17 infants (eighteen.3%) had at least 1 laboratory effect indicating hyperphosphatemia. Of these, five (5%) infants had more than i loftier level. Additionally, xix (xx%) infants had at least one episode of hypophosphatemia. Sixty-four (69%) of infants had all normal serum phosphorus levels. Of the infants with multiple high serum phosphorus levels, 3 infants had a serum creatinine over 1.0 mg/dL. Four of these infants received interventions (Table 4).

Table four

Outcomes of infants with multiple high serum phosphorus levels.

Infant	Serum Phosphorus	Intervention	Outcome	Serum Creatinine within 3 Days	Calorie Fortification (kcal/oz)
ane	two high values on solar day of life (DOL) 18 and 24 (both 8.2 mg/dL)	None	Serum phosphorus normalized on DOL 31	None	DOL xviii: +4 DOL 24: +eight
ii	iii high values on DOL 13, fourteen, 19 (9.6, 8.one, and 9.3 mg/dL)	Treated for sepsis, found to take Klebsiella bacteremia	Serum phosphorus normalized on DOL 34	High creatinine one.1 and ii.ii mg/dL, lowered DOL 24 (0.89 mg/dL)	DOL 13: +vi DOL fourteen: +viii DOL 19: +x
3	2 high values on DOL 12, 19 (8.4 and 10 mg/dL)	Worked up for sepsis. Cultures negative	Serum phosphorus normalized in subsequent checks on DOL 31, 52, 80	Loftier creatinine 1.i mg/dL lowered DOL 33 (0.55 mg/dL).	DOL 12: +half dozen DOL nineteen: +8 DOL twenty: +10
4	2 high values on DOL 32, 45 (8.6 and 10.0 mg/dL)	Stopped HMDF for ane day, worked upwardly for sepsis	Serum phosphorus normalized in on DOL 50	High creatinine i.3 mg/dL, normalized 0.4 mg/dL on DOL 114 (on formula)	DOL 32: +10 DOL 45: +10
v	2 loftier values on DOL 15, 23 (11.viii and ten.5 mg/dL)	HMDF held i day, DOL sixteen. Infant received Four calcium for hypocalcemia	Serum phosphorus normalized on DOL 20 and was normal on DOL 30 afterwards resuming HDMF	Creatinine 0.74 and 0.91 mg/dL. Ionized calcium 0.84 mmol/50	DOL 15: +iv DOL 23: +ten

Ten (43%) of the high serum phosphorus levels were establish to be within 5 days of transitioning off of parenteral nutrition. Eleven (45%) of the high serum phosphorus levels were associated with normal creatinine levels of <1 mg/dL, and of these 9 (81%) were within five days of the transition off of parenteral diet. Of the loftier serum phosphorus levels plant v or more days subsequently the transition off parenteral diet (12, 52%), one-half were associated with creatinine levels >1 mg/dL (Effigy 2). Of the six high serum phosphorus levels associated with an elevated serum creatinine, the hateful number of days from the transition off parenteral nutrition was 10.5 ± five.0 days (Tabular array 5). This is significantly dissimilar than the 11 loftier serum phosphorus levels associated with a normal creatinine found to be 4.9 ± four.2 days from discontinuation of parenteral nutrition, p = 0.026.

Comparison of creatinine levels in early vs. belatedly hyperphosphatemia.

Table v

Comparison of serum creatinine and high serum phosphorus levels.

Serum Creatinine (± three Days of Loftier Serum Phosphorus Level)	Number of High Serum Phosphorus Levels (n = 17)	Mean Days afterward Parenteral Diet Discontinued
High (≥i mg/dL)	6	10.5 ± 5.0 *
Normal (<1 mg/dL)	11	four.9 ± four.ii *

The serum phosphorus levels were closely associated with the historic period (day of life) of the babe (p < 0.001, R ^two = 0.1746) (Figure 3a,b). The serum phosphorus levels were besides significantly correlated to energy density concentration of HMDF used (p = 0.035). The number of days the infant needed to achieve total feeds (140 mL/kg/day) and any intrinsic characteristics of the infant including gender, BW, gestational age, race, or ≥750 g or < 750 g BW were not significantly associated with the risk of hyperphosphatemia.

(a) Height phosphorus level declines with mean solar day of life; (b) All serum phosphorus levels in 93 infants.

Of 23 high serum phosphorus levels, 12 (52%) had serum calcium values drawn within three days. Ten of 12 levels were within normal limits. Two infants had laboratory prove of hypocalcemia defined as < 7.0 mg/dL. I baby had a serum calcium level of 5.4 mg/dL and required a calcium infusion with the calcium level subsequently normalizing the side by side twenty-four hour period. This baby had a creatinine level of 0.91 mg/dL and multiple loftier serum phosphorus levels. The other infant had a serum calcium level of half dozen.6 mg/dL which resolved three days subsequently without supplementation. Alkaline phosphatase activity inside 3 days was as well recorded in 14 of the infants with high serum phosphorus levels and was institute mildly elevated at 495 ± 215 mg/dL.

Very express interventions were used in the infants with high serum phosphorus. The infants with multiple high serum phosphorus levels were more than likely to receive interventions (Table four) and oftentimes associated with loftier energy fortification (+viii and +10 kcal/oz). In four of the 17 infants with hyperphosphatemia, a decrease in daily feeding book was made or the HMDF was stopped briefly (<three days). These interventions coincided with a patent ductus arteriosus ligation and a clinically identified ileus associated with proven bloodstream infection for two infants. Almost infants did not receive interventions, and all evidence of hyperphosphatemia resolved.

4. Discussion

Among 93 infants receiving an exclusive man milk-based diet, all serum phosphorus levels were analyzed with a focus on hyperphosphatemia. The average elevation serum phosphorus level of infants receiving HMDF was <8.0 mg/dL. All infants received rapid advancement of feedings and increasingly high enteral phosphate loads.

Infants are susceptible to hypocalcemia and hypophosphatemia during prolonged parenteral nutrition and are oftentimes weaned to oral feedings rapidly every bit treatment [12]. Preterm infants fed unfortified mother'southward milk early in life develop hypophosphatemia and elevated alkaline phosphatase levels leading to rickets [12,13,14,15,16]. Supplementation may protect against hypophosphatemia as premature infants have a limited body pool of phosphorus from their soft tissues risking demineralization leading to fractures [12]. Both hypophosphatemia and hyperphosphatemia occurred at similar rates in this study.

Seventeen (18%) infants in this study had hyperphosphatemia. The hyperphosphatemia was mild and transient occurring mostly early in life after the discontinuation of parenteral diet with few exceptions. In 17 infants with high serum phosphorus levels, 13 (76%) did not require intervention. The four interventions were minor dietary changes (slowing, stopping feeds or HMDF) for a brusque period of time. Ii infants also had a patent ductus arteriosus ligation and clinically identified ileus at the fourth dimension of intervention.

Hyperphosphatemia largely occurred within five days from the discontinuation of parenteral nutrition, at approximately 10–15 days of life. The take chances of hyperphosphatemia decreased as the infant anile. Several mechanisms could contribute to early on peak serum phosphorus levels including increasing feeding volumes, high absorption (bioavailability) of the phosphorus loads and suppression of parathyroid office by calcium in parenteral nutrition [12]. Parathyroid hormone surges are smaller in very low nativity weight infants but office improves with postnatal historic period as nephrogenesis continues through 34 weeks postal service-gestational age [eight,17].

Hyperphosphatemia occurring more than 5 days subsequently the discontinuation of parenteral nutrition (belatedly) was frequently associated with serum creatinine ≥1 mg/dL, possibly signifying renal dysfunction and an inability to excrete ingested phosphorus [17,18]. Our study also plant that the higher free energy density of HMDF was significantly associated with hyperphosphatemia (p = 0.025). Feeds were highly fortified (+8 kcal/oz or +10 kcal/oz) afterwards evidencing poor weight gain on full (140–150 mL/kg/day) feeds. Poor weight gain is an independent marker of underlying renal dysfunction [18]. Renal role should be investigated in infants with late hyperphosphatemia. Multiple high serum phosphorus levels were also a risk factor for intervention. One infant received a calcium infusion secondary to hypocalcemia during an episode of hyperphosphatemia. Alkaline phosphatase activeness was mildly high on boilerplate, however it is a not a highly specific marker for bone mineral defects in premature infants [12].

A limitation of this observational study was the non-randomized nature of this cohort. The prospective nature of this study was its strength, investigating a large accomplice of premature infants that were merely using an exclusive man milk-based diet, while analyzing serum phosphorus as an outcome.

5. Conclusions

An exclusive man milk-based diet provides phosphorus, supporting bone growth safely. Hyperphosphatemia was seen early in life with interventions being minor. Hypophosphatemia occurred with a like frequency in this cohort. The risk of high serum phosphorus decreased with infant age unrelated to gender, BW, or ethnicity. An interesting point of this study was the correlation of high creatinine and late hyperphosphatemia. A clinician should exist sensitive to serum phosphorus every bit a herald to renal dysfunction in these infants. When interpreting these interventions, recall that infants had comorbid renal dysfunction, sepsis, impending surgeries or a patent ductus arteriosus and had enteral feeds discontinued for those reasons rather than to treat hyperphosphatemia. Special consideration should be paid to electrolyte abnormalities when infants transition off of parenteral diet or demonstrate multiple high serum phosphorus levels as underlying renal dysfunction or rarely hypocalcemia may also be present. Monitoring serum phosphorus to assure a normalizing tendency for this subset of premature infants receiving HMDF is supported.

Acknowledgments

We would like to give thanks Pam Gordon RNC-NIC and Geneva Shores RNC-LRN for their dedication to the project. Funding source: This project has been funded in role with federal funds from the USDA/ARS under Cooperative Agreement 58-6250-half dozen-001 and National Center for Research Resources Full general Clinical Inquiry for Children Grant RR00188. This work is a publication of the Section of Pediatrics, Baylor Higher of Medicine, and Texas Children'south Hospital (Houston, TX, United states of america).

Writer Contributions

Katherine Due east. Chetta designed the written report, extracted the information, ran the statistics, authored and edited the newspaper. Amy B. Hair gained the IRB approval, mentored the blueprint, edited the paper, extracted and verified the data extraction. Keli M. Hawthorne extracted the data and edited the newspaper. Steven A. Abrams mentored the pattern and edited the newspaper.

Conflicts of Involvement

Katherine E. Chetta has no conflicts of involvement. Amy B. Hair receives research back up from Prolacta Bioscience for the Human Milk Foam Follow-upwardly Study. She receives speaker honoraria from Prolacta Bioscience and Mead Johnson Nutrition. Keli M. Hawthorne receives speaker honoraria from Mead Johnson Nutrition and Abbott Nutrition. Steven A. Abrams receives inquiry support from Mead Johnson Nutrition.

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Typical Phosphorus Lab Values for a Preterm Baby

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4425161/

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