2018
DOI: 10.1002/ccr3.1960
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Subclinical cerebral edema in diabetic ketoacidosis in children

Abstract: Key Clinical Message Subclinical cerebral edema in diabetic ketoacidosis tends to manifest with subtle neurological symptoms including headache, lethargy, or disorientation and a Glasgow Coma Scale of 14‐15. Treatment of subclinical cerebral edema with hyperosmolar therapy for persistent symptoms is associated with good outcomes.

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Cited by 7 publications
(6 citation statements)
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“…~ 5 ~ days (mean hospital stay of 5.6 days) which is comparable to the data from North India [2] . None of the participants in our study developed cerebral oedema and the reported incidence of cerebral edema in DKA patients in pediatric population is 0.5-1% in some studies [16,17] . Predicted mortality in DKA according to literature ranges from 0.15% to 0.35% in developed countries and 3.4% to 13.4% in developing countries including India [18,19] .…”
Section: Discussionmentioning
confidence: 52%
“…~ 5 ~ days (mean hospital stay of 5.6 days) which is comparable to the data from North India [2] . None of the participants in our study developed cerebral oedema and the reported incidence of cerebral edema in DKA patients in pediatric population is 0.5-1% in some studies [16,17] . Predicted mortality in DKA according to literature ranges from 0.15% to 0.35% in developed countries and 3.4% to 13.4% in developing countries including India [18,19] .…”
Section: Discussionmentioning
confidence: 52%
“…Also, the highest amount of ONSD was seen in children with moderate to severe DKA. ONSD, which indicates an increase in intracranial pressure, can be measured by bedside ultrasound, shows many changes during treatment of children with DKA, and reaches its highest values in the middle of treatment (47). In Hansen et al's study on ONSD sonography, it was found that subtle changes in ONSD may occur despite the absence of clinical signs of cerebral edema, but it is unclear to what extent these changes reflect actual changes in intracranial pressure (45).…”
Section: Discussionmentioning
confidence: 99%
“…Osmotic shifts and other therapy‐related factors during treatment may further exacerbate cerebral injury. However, both subclinical 12,13,154 and clinically apparent CE 4,14‐18 have been described before starting therapy, suggesting that reperfusion injury and treatment‐related factors are not necessary components of the pathophysiologic pathway leading to CE development, but may play a role in propagating cerebral injury in a subset of predisposed patients (i.e., those with more severe dehydration and acidosis at presentation). Figure 1 shows a proposed multifactorial pathway leading to the development of the different types of cerebral injury in patients with DKA.…”
Section: Discussionmentioning
confidence: 99%