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PEDIATRIC UROLOGY
doi: 10.1590/S1677-553820100002000031
Incidence
of new onset metabolic acidosis following enteroplasty for myelomeningocele
Adams RC, Vachha B, Samuelson ML, Keefover-Hicks A, Snodgrass WT
Department of Pediatrics, University of Texas Southwestern Medical Center
at Dallas, Dallas, Texas, USA
J Urol. 2010; 183: 302-5
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Purpose:
Extant literature is mixed regarding risk of metabolic acidosis after
enteroplasty for myelomeningocele. This study is the first known attempt
to describe the pattern of developing metabolic acidosis in a group
of children who underwent enteroplasty and served as their own controls.
Multiple preoperative and postoperative laboratory measures for each
child were obtained for comparison.
Materials and Methods: This retrospective cohort study allowed participants
to serve as their own controls for pre-intervention and post-intervention
analysis. The setting was a tertiary, university affiliated, interdisciplinary
spina bifida program. All patients followed in the spina bifida program
who had undergone ileal or colonic enteroplasty were included for
review (total 113). Strict exclusion criteria were preoperatively
diagnosed renal insufficiency, preexisting metabolic acidosis consistent
with renal tubular acidosis (pH less than 7.35, bicarbonate 20 mmol/l
or less) and history of augmentation using gastric or ureteral tissue.
Final analysis included 71 children who met inclusion criteria. Children
in our spina bifida program periodically undergo routine laboratory
evaluation of electrolytes, blood urea nitrogen, creatinine, blood
count, and venous blood gases including pH, bicarbonate and partial
pressure of carbon dioxide. Primary outcome measures were comparative
shifts in blood gases and electrolytes that would confirm the new
onset of metabolic acidosis after enteroplasty. Changes in electrolytes
and serum creatinine were secondary outcome measures to identify potential
markers for postoperative effects. With each child as his/her own
control, analysis included paired t tests.
Results: No statistically significant differences (p <0.05) were
found when comparing laboratory values before and after bladder augmentation,
including pH, bicarbonate, partial pressure of carbon dioxide and
electrolytes. No child had metabolic acidosis based on the aforementioned
criteria. Followup ranged from 1 to 138 months after enteroplasty
(mean 46.8). Respiratory compensation was considered in the analysis,
and no difference in partial pressure of carbon dioxide following
surgery was noted (p = 0.65).
Conclusions: To our knowledge no previous study has examined the matched
paired results of before and after development of metabolic acidosis
among children (serving as their own controls) with myelomeningocele
undergoing ileal or colonic enteroplasty. The negative statistical
results in this controlled cohort are clinically significant. If a
child with myelomeningocele has metabolic acidosis after enteroplasty,
other clinical reasons beyond the effects of surgery warrant careful
consideration.
- Editorial
Comment
The development of metabolic acidosis following enterocystoplasty
is a common concern particularly in the pediatric population where
such a procedure is intended to last a lifetime. The authors reviewed
data from their spina bifida program that had undergone bladder augmentation
using either ileum or colon. They excluded patients with preoperative
renal insufficiency or metabolic acidosis. Patients in their spina
bifida program routinely undergo serum evaluation of electrolytes,
BUN, creatinine blood count, and venous blood gases giving them a
unique opportunity to look at changes in serum values both before
and after enterocystoplasty. They identified 71 children who met the
inclusion criteria and had both preoperative and postoperative laboratory
values. Their primary outcome was a shift in blood gases and electrolytes
consistent with new onset of metabolic acidosis following bladder
augmentations. Secondary outcomes included changes in electrolytes
and serum creatinine. They found no evidence of new onset of metabolic
acidosis following surgery for a mean follow-up period of almost four
years.
Although concern for metabolic changes following enterocystoplasty
in the pediatric population must be considered over extremely long
time periods, it is interesting to note that these authors found no
significant changes even after following their patients for a mean
of four years. They also wisely point out that the spina bifida patient
population is at risk for metabolic acidosis for other reasons including
nutritional issues, chronic infection, pulmonary insufficiency, and/or
renal insufficiency. As the authors point out in their conclusion,
it may be just as important to consider other sources of metabolic
acidosis (some of which may be correctable) rather than assuming the
enterocystoplasty is to blame.
M.
Chad Wallis
Division of Pediatric Urology
University of Utah
Salt Lake City, Utah, USA
E-mail: chad.wallis@hsc.utah.edu
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