Minimizing the risk of brain herniation during treatment of diabetic ketoacidemia: A retrospective and prospective study

doi:10.1016/S0022-3476(05)82439-4

The Journal of Pediatrics

Volume 117, Issue 1, Part 1, July 1990, Pages 22-31

https://doi.org/10.1016/S0022-3476(05)82439-4 Get rights and content

We studied retrospectively, 219 episodes of diabetic ketoacidemia in 119 patients aged 13 months to 30 years, to determine the trend of the concentration of sodium in serum as glucose declined during treatment of uncomplicated episodes and of episodes with complications attributable to brain swelling. Of 20 complications, 13 were minor (headache only) and 7 major (death or near death). The concentration of sodium in serum failed to rise as that of glucose declined in 82 (54%) of 164 uncomplicated episodes and in 18 (95%) of 20 complicated episodes (p<0.01). Hence complications were more likely to occur among patients with a failure of the concentration of sodium to rise as glucose declined. Fifty-eight episodes of diabetic ketoacidemia in 40 patients aged 1 1/2 to 20 years were then studied prospectively on a 48-hour treatment plan to provide the volume of deficit evenly, with half the deficit of sodium in the first 12 hours. Sodium concentration in serum rose in 55 (95%) of 58 episodes as that of glucose declined. No patient had a major complication. We conclude that failure of the sodium concentration measured in serum to rise as glucose concentration declines is a marker for excessive administration of free water. An expanded repair period, with repair fluid containing an average of 125 mmol/L Na⁺ early in therapy, will usually protect against a downward trend in the concentration of sodium in serum and therefore against a rapid decline in effective serum osmolality. This regimen may be protective against near-death episodes and brain herniation during treatment.

References (15)

RosenbloomAL et al.
Cerebral edema complicating diabetic ketoacidosis in childhood
J Pediatr
(1980)
ClementsRS et al.
Increased cerebrospinal-fluid pressure during treatment of diabetic ketosis
Lancet
(1971)
DuckSC et al.
Factors associated with brain herination in the treatment of diabetic ketoacidosis
J Pediatr
(1988)
FitzGeraldMG et al.
Fatal diabetic ketosis
Br Med J
(1961)
YoungE et al.
Cerebral edema with irreversible coma in severe diabetic ketoacidosis
N engl J Med
(1967)
TaubinH et al.
Cerebral edema, diabetes insipidus, and sudden death during the treatment of diabetic ketoacidosis
Diabetes
(1968)
HayesTM et al.
Unexpected death during treatment of uncomplicated diabetic ketoacidosis
Br Med J
(1968)

There are more references available in the full text version of this article.

Cited by (166)

Updates in pediatric emergency medicine for 2021
2022, American Journal of Emergency Medicine
Physicians routinely treat sick children in the emergency department (ED). Many relevant articles on pediatric medicine are published in journals that are not typically read by many general emergency medicine physicians. We reviewed salient pediatric emergency medicine literature from the past year and identified ten impactful articles for general emergency physicians. This review includes studies of pediatric pneumonia, brief resolved unexplained events, covid-19, hemorrhage control, retropharyngeal abscess, infant fever, diabetic ketoacidosis, mastitis, buckle fractures, and invasive herpes simplex virus infection.
Diabetes Mellitus
2020, Sperling Pediatric Endocrinology: Expert Consult - Online and Print
Diabetes mellitus (DM) is a syndrome of disturbed energy metabolism, conveniently defined by the degree of hyperglycemia, resulting from an absolute or relative deficiency of insulin action. These concepts are the basis of the current classification as type 1 DM (T1DM), type 2 DM (T2DM), and other predominantly genetic forms. T1DM is a disease of insulin deficiency associated with autoimmune destruction of functional beta cells, a process begun by environmental insults in genetically determined susceptible hosts; it is the most common form of DM in childhood. In this chapter, we discuss the advances in understanding the genetics, pathophysiology, evolution, and treatment of all forms of DM, increasingly driven by technologic advances in glucose sensing, continuous glucose monitoring, and algorithmically regulated pumps that constitute an “artificial pancreas,” together with newer insulin preparations that facilitate simulating normal basal and bolus patterns in normal persons. T2DM is increasing in adolescents, particularly with obesity and prevalence in minority populations; obesity with insulin resistance has unmasked genetic defects in the regulation of insulin synthesis and secretion. For these individuals, lifestyle modification and weight loss remain the cornerstone of prevention and treatment. However, if this approach fails, newer modalities of treatment, such as a variety of incretin hormones, inhibitors of its destruction, agents that promote glucose excretion, and rarely bariatric surgery are revolutionizing treatment. Several of the genes involved in T2DM cause specific syndromes of monogenic diabetes at birth (neonatal DM) and during adolescence (maturity onset-diabetes of youth [MODY]), often misdiagnosed as T1- or T2DM and for which oral treatments rather than insulin injections are available and effective. Together, these advances are associated with better quality of life, less complications, and the promise of potential prevention of diabetes in childhood.
Type 1 Diabetes in Children and Adolescents
2018, Canadian Journal of Diabetes
Emergency Medicine Myths: Cerebral Edema in Pediatric Diabetic Ketoacidosis and Intravenous Fluids
2017, Journal of Emergency Medicine
Citation Excerpt :
One major complication is cerebral edema. Cerebral edema (CE) is clinically apparent and life threatening in 0.5–1% of patients with DKA (2,14–17). Though the mortality of DKA is < 1%, CE accounts for a significant proportion of these deaths due to brain herniation, which can occur prior to initiation of treatment (15,17).
Pediatric diabetic ketoacidosis (DKA) is a disease associated with several complications that can be severe. One complication includes cerebral edema (CE), and patients may experience significant morbidity with this disease.
This review evaluates the myths concerning CE in pediatric DKA including mechanism, presentation of edema, clinical assessment of dehydration, and association with intravenous (i.v.) fluids.
Multiple complications may occur in pediatric DKA. CE occurs in < 1% of pediatric DKA cases, though morbidity and mortality are severe without treatment. Several myths surround this disease. Subclinical CE is likely present in many patients with pediatric DKA, though severe disease is rare. A multitude of mechanisms likely account for development of CE, including vasogenic and cytotoxic causes. Clinical dehydration is difficult to assess. Literature has evaluated the association of fluid infusion with the development of CE, but most studies are retrospective, with no comparator groups. The few studies with comparisons suggest fluid infusion is not associated with DKA. Rather, the severity of DKA with higher blood urea nitrogen and greater acidosis contribute to CE. Multiple strategies for fluid replacement exist. A bolus of 10 mL/kg of i.v. fluid is likely safe, which can be repeated if hemodynamic status does not improve.
Pediatric CE in DKA is rare but severe. Multiple mechanisms result in this disease, and many patients experience subclinical CE. Intravenous fluids are likely not associated with development of CE, and 10-mL/kg or 20-mL/kg i.v. bolus is safe.
Optic Nerve Sheath Diameter Ultrasonography in Pediatric Patients with Diabetic Ketoacidosis
2016, Canadian Journal of Diabetes
Subclinical cerebral edema has been reported in pediatric patients with type 1 diabetes and diabetic ketoacidosis (DKA) through magnetic resonance imaging. Ultrasonography of the optic nerve sheath diameter (ONSD) has been used to evaluate intracranial pressure. The objective of this study was to examine the utility of ONSD ultrasonography to evaluate intracranial pressures in children with DKA.
This prospective cohort evaluated pediatric patients who presented to the emergency department of the Children's Hospital at the University of Manitoba with DKA within 3 hours of initial treatment. A pediatric bedside neurologic evaluation tool for cerebral edema was utilized 1) within the first hour of the intravenous fluid initiation (t=0 hr); 2) 8 hours after initiation of treatment (t=8 hr); and 3) at hours after presentation (t=24 hr). At each time interval, 3 images of the patients' ONSDs were scanned by an 11 MHz linear array transducer. Increased intracranial pressure was considered in all patients whose mean ONSDs were >4.5 mm.
We evaluated 7 patients, aged 4 to 17 years. No patients were clinically assessed as having cerebral edema. Overall, no significant differences emerged among the 3 time points (t=0 vs. t=8 hr; t=0 vs. t=24 hr; t=8 vs. t=24 hr) (all p>.216). Effect sizes were small at 0.14 (t=0 vs. t=8 hr); 0.27 (t=8 vs. t=24 hr); and 0.07 (t=0 vs. t=24).
Although not statistically significant, subtle changes in intracranial pressure may have been detected with ONSD ultrasonography in pediatric patients with DKA.
L'œdème cérébral subclinique a été rapporté chez les patients de pédiatrie souffrant du diabète de type 1 et d'acidocétose diabétique (ACD) par l'imagerie par résonance magnétique. L'ultrasonographie du diamètre de la gaine du nerf optique (DGNO) a été utilisée pour évaluer la pression intracrânienne. L'objectif de cette étude était d'examiner l'utilité de l'ultrasonographie du DGNO pour évaluer les pressions intracrâniennes chez les enfants souffrant d'ACD.
Cette cohorte prospective évaluait les patients de pédiatrie qui se présentaient au service des urgences de l'Hôpital pour enfants de l'Université du Manitoba en raison d'une ACD au cours des 3 heures suivant le traitement initial. Un outil d'évaluation neuropédiatrique de l'œdème cérébral au chevet du patient était utilisé 1) au cours de la première heure après l'administration d'un liquide par voie intraveineuse (t=0 h); 2) 8 heures après le début du traitement (t=8 h); 3) dans les heures après l'arrivée (t=24 h). À chaque intervalle de temps, 3 images des DGNO des patients étaient balayées par une sonde linéaire de 11 MHz. L'augmentation de la pression intracrânienne était considérée chez tous les patients dont la moyenne du DGNO était>4.5 mm.
Nous avons évalué 7 patients âgés de 4 à 17 ans. Aucun patient n'était cliniquement évalué comme souffrant d'un œdème cérébral. Dans l'ensemble, aucune différence significative n'est apparue entre les 3 moments temporels (t=0 vs t=8 h; t=0 vs t=24 h; t=8 vs t=24 h) (tous p>0.216). Les petites tailles de l'effet se situaient à 0.14 (t=0 vs t=8 h); 0,27 (t=8 vs t=24 h); 0,07 (t=0 vs t=24).
Bien que non significatifs sur le plan statistique, les changements subtils de la pression intracrânienne pouvaient être détectés à l'ultrasonographie du DGNO chez les patients de pédiatrie souffrant d'ACD.
Le diabète de type 1 chez les enfants et les adolescents
2013, Canadian Journal of Diabetes

View all citing articles on Scopus

View full text

Original articleMinimizing the risk of brain herniation during treatment of diabetic ketoacidemia: A retrospective and prospective study

J Pediatr

Lancet

J Pediatr

Fatal diabetic ketosis

Br Med J

Cerebral edema with irreversible coma in severe diabetic ketoacidosis

N engl J Med

Cerebral edema, diabetes insipidus, and sudden death during the treatment of diabetic ketoacidosis

Diabetes

Unexpected death during treatment of uncomplicated diabetic ketoacidosis

Br Med J

Original article
Minimizing the risk of brain herniation during treatment of diabetic ketoacidemia: A retrospective and prospective study