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Insulin’s effect on lactate levels in extremely low birth weight neonates. a multi-center, observational study

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Insulin’s effect on lactate levels in extremely low birth weight neonates. a multi-center, observational study

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Content Insulin’s Effect on Lactate Levels in Extremely Low Birth Weight Neonates. A Multi-Center,
Observational Study

by

Thomas A Chavez

A Thesis Presented to the
FACULTY OF THE GRADUATE SCHOOL
UNIVERSITY OF SOUTHERN CALIFORNIA
In Partial Fulfillment of the
Requirements for the Degree
MASTER IN SCIENCE
APPLIED BIOSTATISTICS AND EPIDEMIOLOGY

August 2015
ii

Table of Contents

Page number

1) Acknowledgements iii
2) List of Tables iv
3) List of Figures v
4) Abbreviations vi
5) Abstract vii
6) Body 1-11

Background / Significance 1-2
Methods 2-3
Results 3-10
Discussion 10-11

7) References 12

iii

Acknowledgements

I would like to sincerely thank Dr. Philippe Friedlich, Dr. Wendy Mack and Dr. Christianne Joy Lane as
well as the Division of Neonatal Medicine for their unparalleled support and feedback during my
program in M.S. Applied Biostatistics and Epidemiology Program.

iv

List of Tables Page Number
Table 1 Demographics 4
Table 2 Differences in Group Predicted Means 9
Table 3 Assessment of Confounders 10

v

List of Figures
Figure 1 Study Flow Chart 5
Figure 2 Pre / Post-Insulin, Lactate Levels 6
Figure 3 Time Sequenced Results for Lactate Means 7
Figure 4 Insulin Use in Days by Patient 7
Figure 5 Differences in Group Predicted Means 8

vi

Abbreviations:

NICU: Neonatal Intensive Care Unit

ELBW: Extremely Low Birth Weight

HPMC: Hollywood Presbyterian Medical Center

GSH: Good Samaritan Hospital

LAC-USC: Los Angeles County – University of Southern California

NIS: Neonatal Information Systems

GA: Gestational Age

vii

ABSTRACT

BACKGROUND: Hyperglycemia (blood glucose level > 180 mg/dL) is observed in 40-80% of extremely low
birth weight (ELBW) (<1000 grams) infants. Previous studies showed that treatment with continuous
insulin infusion increased the risk of lactic acidosis. However, these results have not been replicated and
there have not been any other published studies evaluating the effect of continuous insulin infusion and
lactic acid levels in ELBW infants. The aim of this study is to assess the effects of insulin infusion on lactic
acid levels.
DESIGN/METHODS: This is a multi-center, non-randomized study conducted across 3-sites in Los Angeles
from 2007 - 2011. All infants less than 1000 grams at birth and admitted to the NICU were considered
eligible for study enrollment. Exclusions included genetic / congenital anomalies or who were born at an
outside hospital. Two study groups were defined as the need for insulin infusion and those not requiring
insulin. Wilcoxon signed rank test was used to assess the pre-insulin lactate level and post-insulin lactate
level’s population mean rank among the insulin group. A mixed effects linear model was used to model
daily lactate measurements between the insulin and non-insulin groups.
RESULTS: A total of 57 infants ([27 requiring insulin, 30 not requiring insulin], mean birth weight ± SD
773.70 ± 128.38 grams, mean gestational age 25 weeks 6/7 days ± 13 days) were enrolled. Median
lactate levels were lower post-insulin versus pre-insulin, 2.1 mMol/L (IQR 1.3, 2.8) versus 2.7 (IQR 2.3,
3.9) [p < 0.05]. Repeated measure models showed a decrease in lactate levels among the insulin group
vs. the non-insulin group (β = -0.15, p < 0.01). By day of life 9, the insulin group’s lactate did not differ
compared to the non-insulin’s group, and was even significantly lower by day of life 14.
CONCLUSION: These data show that insulin infusion was not associated with a higher lactic acid level in
hyperglycemic ELBW infants compared to non-hyperglycemic newborns. Lactate acid levels in the
hyperglycemic group were comparable to the non-insulin group by day of life 9 and were even lower
than the non-insulin group by the end of the study.
1

BACKGROUND & SIGNIFICANCE

The use of insulin therapy in preterm neonates experiencing prolonged hyperglycemia remains
controversial since the long-term effects of continuous insulin infusion remain unclear. Hyperglycemia
(blood glucose level > 180 mg%) is observed in 40-80% of extremely low birth weight (ELBW) infants (1).
The incidence of hyperglycemia has decreased with the prompt use of parenteral nutrition since early
amino acid administration increases insulin release (2). However, a very small study (n=4) showed that
treatment with continuous insulin infusion under “euglycemic hyperinsulinemic clamp” conditions
resulted in worsening lactic acidosis (from 2.1 ± 0.5 mMol/L pre-insulin to 5.7 ± 1.0 mMol/L post-insulin
infusion) (3). The authors did not give an explanation as to why this was seen. This observation was
likely due to the amount of glucose administered (6 mg/kg/min), which overwhelmed the glucose
oxidase activity, therefore forcing the glucose into anaerobic metabolism converting pyruvate into
lactate via lactate dehydrogenase activity. To our knowledge no other published studies have evaluated
the effect of continuous insulin infusion on lactic acid levels in ELBW infants.
Lactic acid can be converted into glucose and via the Cori Cycle can be used as an energy source
by red blood cells as well as brain cells (4). Preterm infants use lactate to generate glucose by this
method. Critically high levels of lactate were significantly correlated with mortality in a study of fifty
neonates (5). No studies have examined at the general course of lactate levels in preterm infants’ first
few weeks of life. It is therefore not known whether insulin infusion used as treatment of transient
hyperglycemia has an impact on lactate levels.
The cause of transient hyperglycemia in ELBW infants is not well understood. Causes may
include partially defective beta cell processing of pro-insulin to insulin (6), and relative insulin resistance
which may require a higher level of insulin to achieve euglycemia. This also may be due to the

inability to
down-regulate hepatic gluconeogenesis despite having an exogenous glucose infusion (7). In addition,
2

stress or infection produces a catecholamine surge which may further elevate glucose levels and inhibit
insulin release. This relative insulinopenia may lead to a state of transient extracellular hyperglycemia in
the face of intracellular hypoglycemia. Given the current lack of information surrounding insulin infusion
use and lactate acid levels, the aims of this study are to:
1) Assess the effects of insulin infusion on lactic acid level in ELBW infants
2) Evaluate lactate levels across the first 14 days of life between infants who received insulin
and those who did not receive insulin
METHODS

This is an Institutional Review Board approved, multi-center, observational study conducted at
Hollywood Presbyterian Medical Center (HPMC), Good Samaritan Hospital (GSH), and Los Angeles
County University of Southern California (LAC-USC) NICU’s. The study population consists of neonates, <
1000 grams at birth, inborn, admitted to the NICU from 2007 - 2011. Exclusions included infants with
congenital anomalies, metabolic disorders, genetic disorders, or born at an outside hospital.
Lactate levels were obtained daily for the first 14 days of life. Lactate levels were measured
using Lactate Pro
TM
Test Strip provided to each site to standardize lactate measurement levels and
minimize information bias. If the patient developed hyperglycemia, defined as a serum glucose level >
180 mg%, the patient’s glucose infusion rate was decreased. If hyperglycemia persisted during the first
14 days of life, insulin infusion was initiated and patient was placed in the insulin group. Infants
receiving continuous insulin infusion had their lactate levels measured immediately before and after
insulin infusion. If the patient did not develop hyperglycemia in the first 14 days of life, the patient was
placed in the non-insulin group.
Baseline demographics (race, sex, gestational age, birthweight, mode of delivery, prenatal
steroid use, small for gestational age status, presence of chorioamnionitis) were obtained through NIS in
3

2014. Independent t-tests were used to determine whether differences existed between the non-insulin
and insulin group’s continuous variables. Continuous variables are presented as mean ± SD and with
range. Fisher’s exact test was used to determine categorical associations between non-insulin and
insulin baseline demographics. Categorical variables are presented as frequency (%) of sample.
In the insulin group, Wilcoxon signed rank test was used to test whether the pre and post-insulin
lactate’s population mean rank levels differed. Cohen’s effect size index was used to estimate effect size
(small d=0.20, medium d=0.50, large d=0.80). A general linear mixed effects model was used to assess
the repeated continuous outcome variable (lactate levels) involving a combination of a continuous
predictor (time, days 1-14) and a binary categorical predictor (group, non-insulin and insulin). Post-hoc
test of orthogonal polynomial trends in lactate levels were examined for the non-insulin and insulin
groups. A priori covariates (sex, ethnicity, birthweight and GA) were assessed as potential confounders.
A 10% change in the unadjusted to adjusted slope was considered a confounder. Statistical significance
was set at a two-sided p < 0.05 for all tests. Data analysis was performed using STATA version 13
(StatCorp, College Stations, TX) and R (R Foundation for Statistical Computing).
RESULTS

Sixty parents consented to participate (32 from GSH, 22 from HPMC, 6 from LAC-USC) from Sept
2007 – July 2011, of which, 29 developed hyperglycemia requiring insulin within the first 10 days of life
and 31 did not require insulin. Three patients were excluded from analysis (one for genetic anomaly
[insulin group], one for parental withdrawal [non-insulin group], and one for death before any data was
collected [insulin group]). For additional information, see Figure 1 – Study Flow Chart. Neonates who
required insulin were more premature by birthweight [Insulin: 717.41 ± 121.96 (grams ± SD) compared
to non-insulin: 824.37 ± 113.52 (p < 0.01), Cohen’s d = 0.91], and gestational age: [Insulin: 24 weeks, 5/7
4

± 9 days compared to non-insulin: 26 weeks, 6/7 ± 12 days (p < 0.01), Cohen’s d = 1.46]. For additional
information see Table 1 – Demographics.

Table 1 - Demographics
Non-Insulin
n=30
Insulin
n=27
Effect Size
d
p-value Total
n=57
Male (%) 12 (40) 14 (51.85) -0.24 0.43 26 (45.61)
Race (%) -0.24 0.26
Asian 6 (20) 5 (18.5) 11 (19.3)
Black 1 (3.3) 3 (11.1) 4 (7)
Hispanic 22 (73.3) 15 (55.6) 37 (64.9)
White 1 (3.3) 1 (3.7) 2 (3.5)
Other 0 3 (11.1) 3 (5.3)
Birthweight in grams
[Range]
824.37 ± 113.52
[538 – 990]
717.41 ± 121.96
[486 – 960]
0.91 <0.01 773.70 ± 128.38
[486 – 990]
GA in weeks, days
[Range]
26 6/7 ± 12 days
[24 4/7 – 30 5/7]
24 5/7 ± 9 days
[23 0/7 – 27 0/7]
1.46 <0.01 25 6/7 ± 13 days
[23 0/7 – 30 5/7]
C-Section (%) 22 (75.9) 17 (68) 0.17 0.56 39 (72.2)
Prenatal Steroids (%) 21 (77.8) 16 (61.5) 0.35 0.24 37 (69.8)
Small for Gestational Age (%) 9 (32.1) 2 (7.7) 0.63 0.04 11 (20.4)
Chorioamnionitis (%) 3 (10.7) 2 (8.3) 0.79 0.58 5 (9.6)
Categorical variables presented as n (%)
Continuous variables presented as mean ± SD

5

Aim 1: Assess the effects of insulin infusion on lactic acid levels
The distribution of pre-insulin and post-insulin lactate levels was first ascertained through
density histograms to determine normality. Both pre and post lactate levels showed characteristics of
right skewed, non-normal distributions. Data transformation was attempted on the logarithm of pre and
post lactate levels, however, the right skews were still evident. Only 63% (n=17) of the patients requiring
insulin had both pre and post-lactate levels measured due to loss to follow up. Posteriori paired power
analysis was conducted to ensure power was still adequate. With a sample size of 17, pre-insulin lactate
mean ± SD of 3.47 ± 2.48, post-insulin lactate mean of 2.41 ± 1.79, correlation of 0.77, to detect one
standard deviation of change, the estimated power was 0.73.
The median of lactic acid pre-insulin was 2.7 (IQR 2.3, 3.9) while the median of lactic acid post-
insulin was 2.1 (IQR 1.3, 2.8). Wilcoxon signed-rank test indicated that the medians statistically
significantly differed (p = 0.03). See Figure 2 – Pre / Post-Insulin, Lactate Levels for visualization.

Figure 1 – Study Flow Chart
6

Aim 2: Evaluate lactate levels across the first 14 days of life between infants who received insulin and
those who did not receive insulin
The mean lactate of the insulin group in day 1 was 3.62 ± 2.29 and was 1.31 ± 0.25 by day 14.
The mean lactate of the non-insulin group in day 1 was 2.1 ± 0.89 and was 1.27 ± 0.36 by day 14.
Graphically (See Figure 3 – Time Sequenced Results for Lactate Mean), mean lactate levels of the insulin
group were higher in days 1-5, but by day 14, the insulin group’s lactate was approximately equivalent
to the non-insulin group’s lactate. The non-insulin group appears to have a slightly negative slope while
the insulin group appears to have a more drastically negative slope.
Figure 2 – Pre / Post-Insulin, Lactate Levels
7

The duration of insulin use varied from patient to patient. The average day of life for starting
insulin is 3.44±3.03 and the average day of life for discontinuing insulin is 6.35±3.48. See figure 4 –
Insulin Use in Days by Patient for visualization.

1 2 3 4
Daily Lactate Mean (mMol/L) with SE
1 2 3 4 5 6 7 8 9 10 11 12 13 14
Day of Life
Non-Insulin Insulin
SE
Figure 3 - Time-Sequenced Results for Lactate Mean
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14
Day of Life
27
26
25
24
23
22
21
20
19
18
17
16
15
14
13
12
11
10
9
8
7
6
5
4
3
2
1
Figure 4 - Insulin Use in Days by Patient
Insulin Start Date Insulin End Date
Patient
Mean Start: 3.44 days
Mean End: 6.35 days
8

The linear slope for the insulin group was β = -0.19 (95% CI -0.24, -0.13, Wald p-value < 0.01)
indicating that the insulin group’s slope was statistically different from zero. In other words, lactate
levels decreased by 0.19 mMol/L per day for neonates requiring insulin. The slope for the non-insulin
group was β = -0.03 (95% CI: -0.08, 0.02, Wald p-value = 0.20) indicating that the change in lactate mean
over 14 days in the non-insulin group was not statistically different from zero.
Comparison of linear trends across two weeks showed a statistically significantly difference in
lactate levels (χ
2
- 16.96, df - 1, p-value < 0.01). The difference in these slopes was β = -0.15 (95% CI -
0.23, -0.08, p-value < 0.01). In other words, for every additional day, the insulin group’s lactate level
decreased by an average of 0.15 mMol/L compared to the non-insulin group.
The predicted mean of lactate levels for the insulin group was then plotted against the non-
insulin group (See Figure 4, Table 2 – Differences in Group Predicted Means [Insulin – No Insulin]). For
days 1-8, the 95% confidence interval of the differences exclude zero. However, for days 9-13, the 95%
confidence interval includes the null, indicating that there were no differences between the mean
lactate levels of the insulin and non-insulin groups. In fact, by day of life 14, the insulin group’s lactate
level mean was significantly lower than the non-insulin group’s level (95% CI: -0.68, -0.03).

-1 0 1 2 3
1 2 3 4 5 6 7 8 9 10 11 12 13 14
group: Insulin vs No Insulin
Contrasts of Linear Prediction, Fixed Portion
Day of Life
Figure 5 - Differences in Group Predicted Means
9

Table 2 – Difference in Group Predicted Means
(Insulin – No Insulin)

Day of Life Sample Size per Group Contrast 95% CI
Insulin Non-Insulin
1 23 23 1.63 0.74, 2.52*
2 26 26 1.48 0.65, 2.30*
3 26 27 1.32 0.56, 2.08*
4 26 29 1.17 0.48, 1.86 *
5 22 28 1.02 0.39, 1.65 *
6 21 30 0.87 0.30, 1.43*
7 22 30 0.71 0.21, 1.22*
8 22 28 0.56 0.11, 1.01*
9 21 28 0.41 0.01, 0.81
10 21 25 0.26 -0.10, 0.61
11 19 26 0.10 -0.22, 0.43
12 18 24 -0.05 -0.36, 0.26
13 17 25 -0.20 -0.51, 0.10
14 15 25 -0.36 -0.68, -0.03*
Denotes Statistically significant value at α=0.05*

Coefficients of the orthogonal polynomials showed a significant negative linear trend (contrast
coefficient -0.14, Wald p-value < 0.01), and a significant positive quadratic trend (contrast coefficient
0.10, p = 0.01) for the non-insulin group. There was also a significant negative linear trend (-0.52, p <
0.01), and a significant positive quadratic trend (contrast coefficient (0.27, p < 0.01) for the insulin
group. These trends show that insulin’s group lactate acid significantly trended downwards.
Confounders and model assumptions were assessed prior to analysis. Sex, ethnicity, birthweight
and gestational age were assessed as potential confounders and were added to the model one at a time
to assess the change in slope. No covariate produced a slope change of 10% or more. See Table 3 –
Assessment of Confounders for full results. Distribution of residuals showed a slight right skewed
distribution but was assumed normal.

10

Table 3 – Assessment of Confounders

Variable Wald p-
value
LR Test p-
value
Slope Change %
from unadjusted
to adjusted
Sex 0.28 0.25 0.50
Ethnicity (Hispanic v
Non-Hispanic)
0.82 0.83 0.14
Birthweight in grams 0.14 0.15 1.51
GA in days 0.80 0.81 0.10

DISCUSSION

These results deviate from previous research which concluded that infants requiring insulin
showed worsening (higher) lactic acid levels (3). Post insulin lactate levels were lower compared to pre-
insulin lactate levels in this sample of hyperglycemic ELBW infants. Furthermore, the insulin group’s
repeated lactate measures are not statistically different to the non-insulin group’s repeated measures
by day of life 9. Finally, the post-hoc test showed a negative linear trend in lactate levels for the insulin
group.
There are several limitations to this study which will require further research. Patients requiring
insulin were more premature by mean birthweight 106.96 grams and were 2 weeks more premature by
gestational age compared to the non-insulin group. This may contribute to the higher lactate levels in
the first 3 days of life. There were a total of five deaths, all within the insulin group. Three patients died
within the first 7 days of life and the other two patients died after the 14 days of observation (1 and 3
months old, however, none of these deaths were attributed to insulin use.
Another limitation is the limited data available for analysis. There was no data collected on the
infant’s insulin infusion course during the first 14 days of life. Additional variables relating to insulin that
should be accounted for are: hours and dosage of insulin, concurrent nutritional support, number of
insulin boluses, number of insulin courses, and concurrent medications during insulin infusion. One
11

limitation of the NIS database is with the documentation of time. If a neonate was on insulin for one
hour, the NIS database will document this as one day or if the infant was on insulin for 25 hours, the NIS
database will document this as two days.
Missing data and loss to follow is very apparent in this vulnerable population. By day of life 14,
only 15 (55%) of the insulin group had daily measurements. Loss to follow up was mainly attributed to
transfers to an outside hospital or death. The posteriori paired power analysis is 0.73 due to loss to
follow up and small sample sizes. These results should be interpreted with caution. A general linear
mixed effects model was used over ANOVA repeated measures due to the unbalanced nature of
observed data between the group’s longitudinal data (daily lactate measurements). Additional modeling
should include a more complete dataset.
These data showed that insulin use was not associated with worsening lactic acid in the first 14
days of life for neonates < 1000 grams. The majority of patients completed their insulin course within
the first 7 days of life which also showed a downward trend in lactate levels. However, future studies
should model the course of insulin on hours versus days. Additional studies with a larger sample size,
more precise insulin data characteristics, and long term (>14 days) lactate levels are needed to
determine whether these associations persist.

12

References:
1. Meetze W, Bowsher R, Compton J, Moorehead H. Hyperglycemia in Extremely-Low-Birth-Weight
Infants. Biology of the Neonate. 1998; 74:214-221.
2. Micheli J, et al. Early postnatal intravenous amino acid administration to extremely low-birth-
weight preterm infants. Seminars in Neonatal nutrition and metabolism, Ross Products Division,
Abbott Lab, 1994, p1-3.
3. Poindexter B, Karn C, Denne S, Exogenous insulin reduces proteolysis and protein synthesis in
extremely low birth weight infants, The Journal of Pediatrics. June 1998; 132(6):948-953.
4. Kalhan, S.; Parimi, P. Gluconeogenesis in the fetus and neonate. Semin. Perinatol. 2000, 24, 94–
106.
5. Lekhwani S, Shanker V, Gathwala G, Vaswani ND. Acid-base disorders in critically ill neonates.
Indian Journal of Critical Care Medicine : Peer-reviewed, Official Publication of Indian Society of
Critical Care Medicine. 2010;14(2):65-69. doi:10.4103/0972-5229.68217.
6. Mitanchez-Mokhtari D., Lahlou N, Kieffer F, Magny J, Roger M, Voyer M, Both Relative Insulin
Resistance and Defective Islet B-Cell Processing of Proinsulin are responsible for Transient
Hyperglycemia in Extremely Preterm Infants, Pediatrics. March 2004; 113(3):537-541.
7. Ng S, May J, Emmerson A, Continuous insulin infusion in hyperglycaemic extremely-low-birth-
weight neonates, Biology of the Neonate, 2005; 87:269-272.

Abstract (if available)

Abstract BACKGROUND: Hyperglycemia (blood glucose level > 180 mg/dL) is observed in 40-80% of extremely low birth weight (ELBW) (<1000 grams) infants. Previous studies showed that treatment with continuous insulin infusion increased the risk of lactic acidosis. However, these results have not been replicated and there have not been any other published studies evaluating the effect of continuous insulin infusion and lactic acid levels in ELBW infants. The aim of this study is to assess the effects of insulin infusion on lactic acid levels. ❧ DESIGN/METHODS: This is a multi‐center, non‐randomized study conducted across 3-sites in Los Angeles from 2007-2011. All infants less than 1000 grams at birth and admitted to the NICU were considered eligible for study enrollment. Exclusions included genetic / congenital anomalies or who were born at an outside hospital. Two study groups were defined as the need for insulin infusion and those not requiring insulin. Wilcoxon signed rank test was used to assess the pre‐insulin lactate level and post‐insulin lactate level’s population mean rank among the insulin group. A mixed effects linear model was used to model daily lactate measurements between the insulin and non‐insulin groups. ❧ RESULTS: A total of 57 infants ([27 requiring insulin, 30 not requiring insulin], mean birth weight ± SD 773.70 ± 128.38 grams, mean gestational age 25 weeks 6/7 days ± 13 days) were enrolled. Median lactate levels were lower post‐insulin versus pre‐insulin, 2.1 mMol/L (IQR 1.3, 2.8) versus 2.7 (IQR 2.3, 3.9) [p < 0.05]. Repeated measure models showed a decrease in lactate levels among the insulin group vs. the non‐insulin group (β = -0.15, p < 0.01). By day of life 9, the insulin group’s lactate did not differ compared to the non‐insulin’s group, and was even significantly lower by day of life 14. ❧ CONCLUSION: These data show that insulin infusion was not associated with a higher lactic acid level in hyperglycemic ELBW infants compared to non‐hyperglycemic newborns. Lactate acid levels in the hyperglycemic group were comparable to the non‐insulin group by day of life 9 and were even lower than the non‐insulin group by the end of the study.

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Asset Metadata

Creator Chavez, Thomas A. (author)

Core Title Insulin’s effect on lactate levels in extremely low birth weight neonates. a multi-center, observational study

School Keck School of Medicine

Degree Master of Science

Degree Program Applied Biostatistics and Epidemiology

Publication Date 07/14/2015

Defense Date 07/12/2015

Publisher University of Southern California (original), University of Southern California. Libraries (digital)

Tag extremely low birth weight,insulin,lactate,Newborn,OAI-PMH Harvest,premature

Format application/pdf (imt)

Language English

Contributor Electronically uploaded by the author (provenance)

Advisor Friedlich, Philippe (committee chair), Lane, Christianne Joy (committee member), Mack, Wendy Jean (committee member)

Creator Email tachavez@usc.edu,thomaschavez@outlook.com

Permanent Link (DOI) https://doi.org/10.25549/usctheses-c3-592741

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