Evidence map›Paper›PMID 40524982›Full record

ArticleCureus2025

Assessment of Pupillary Light Reflex Alterations in Pediatric Diabetic Ketoacidosis-Induced Encephalopathy: A Retrospective Analysis Using Quantitative Pupillometry.

Elber Y Aydin, Matthew Garber, Jose Irazuzta

Abstract read
In one paragraph

Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Elber Y AydinPediatrics, University of Florida College of Medicine - Jacksonville, Jacksonville, USA.
Matthew GarberHospital Medicine, University of Florida College of Medicine - Jacksonville, Jacksonville, USA.
Jose IrazuztaPediatric Critical Care, University of Florida College of Medicine - Jacksonville, Jacksonville, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic ketoacidosis (DKA) encephalopathy (DKAe) and its associated cerebral edema are serious complications of DKA. This study aimed to use quantitative pupillometry to determine whether changes in pupillary response are associated with alterations in neurological status in pediatric patients admitted to the pediatric intensive care unit (PICU) with DKA. Conducted as a retrospective electronic medical record review at Wolfson Children's Hospital in Jacksonville, Florida, the study included 21 pediatric patients, between 6 and 17 years of age, diagnosed with DKA. These patients were divided into two groups based on the presence or absence of encephalopathy at admission. Pupillometry readings were obtained at two time points: at admission (T0) and after the resolution of both DKA and DKAe (T1). At T0, the constriction velocity (CV) and maximum constriction velocity (MCV) were significantly lower in patients with encephalopathy compared to those without. By T1, there was no significant difference between the two groups, though the encephalopathic group demonstrated a significant improvement in pupillary velocities over time, while the non-encephalopathic group did not. The median time between measurements was 12.5 hours (IQR: 10-17) in the encephalopathic group and 10 hours (IQR: 10-11) in the non-encephalopathic group. The area under the curve for CV and MCV of the right eye at admission was 0.864 (95% CI: 0.709-1.0) and 0.845 (95% CI: 0.657-1.0), respectively. The receiver operating characteristic (ROC) curves were generated using SPSS (Statistical Package for the Social Sciences), with slower velocities considered evidence for encephalopathy. The best cutoff for CV was 3.26 mm/s, yielding a sensitivity of 100% and specificity of 54.5%, while the best cutoff for MCV was 4.545 mm/s, with a sensitivity of 90% and specificity of 81.8%. These findings suggest that DKAe leads to a transient slowing of CV and MCV, likely reflecting a temporary alteration in the parasympathetic component of the pupillary light reflex, which resolves as encephalopathy subsides. This raises important questions about the role of autonomic nervous system dysfunction in the pathophysiology of DKAe and highlights the potential utility of pupillometry as a noninvasive tool for monitoring neurological status in pediatric patients with DKA.

Indexed as

diabetic ketoacidosisdkamultimodal neuromonitoringneurocritical carepediatric encephalopathypupillometry

Identifiers

PMID40524982
PMCPMC12169357

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.