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Published on: May 21, 2019
Brain tissue oxygenation-guided management of diabetic ketoacidosis induced cerebral edema*
Nicole F O'Brien1, Cesar Mella
1Department of Pediatrics, Section of Critical Care Medicine, Nationwide Children's Hospital, The Ohio State University College of Medicine, Columbus, OH, USA. Nicole.OBrien@nationwidechildrens.org
Insights
Monitoring intracranial pressure and brain tissue oxygenation in children with diabetic ketoacidosis helped manage cerebral edema. This multimodal approach led to favorable neurologic outcomes in two pediatric patients.
Area of Science:
- Pediatric Intensive Care
- Neurology
- Endocrinology
Background:
- Diabetic ketoacidosis (DKA) is a serious complication of type 1 diabetes mellitus in children.
- DKA-associated cerebral edema can lead to severe, long-term neurologic disability and mortality.
- Limited treatment options exist for DKA-related cerebral edema.
Observation:
- Two pediatric patients with DKA presented with coma and cerebral edema.
- Intracranial pressure (ICP) and brain tissue oxygenation (BTO) monitoring were initiated to guide treatment.
- Episodes of brain tissue hypoxia were detected even when ICP was controlled.
Findings:
- ICP management with intubation, sedation, and hyperosmolar therapy improved BTO during intracranial hypertension.
- Augmenting cerebral perfusion pressure with fluids and inotropes increased BTO when ICP was controlled.
- Both patients, despite initial severe neurologic impairment, achieved favorable neurologic outcomes.
Implications:
- Multimodal neuromonitoring (ICP and BTO) is crucial for managing DKA-associated cerebral edema.
- This approach enables timely detection and treatment of critical ICP elevations and brain hypoxia.
- Optimizing neuromonitoring can improve neurologic outcomes in children with severe DKA complications.
Objective:
Type 1 diabetes mellitus is the most common chronic disease of childhood. Diabetic ketoacidosis is a well-known complication of diabetes mellitus and can be associated with devastating cerebral edema resulting in severe long-term neurologic disability. Despite the significant morbidity and mortality associated with this condition, relatively few treatments are recommended for these patients. The authors present two patients in which they used both intracranial pressure and brain tissue oxygenation monitoring to manage diabetic ketoacidosis-associated cerebral edema with favorable neurologic outcomes.
Setting:
Pediatric intensive care unit in a tertiary care teaching hospital.
Interventions:
Two children presented to the emergency room with vague complaints and were found to have diabetic ketoacidosis. During treatment, both patients became comatose with head computed tomography scans revealing diffuse cerebral edema and herniation syndrome. Intracranial pressure and brain tissue oxygenation monitors were placed to guide therapy.
Results:
Multiple episodes of brain tissue hypoxia were noted in both patients. Intracranial pressure control with intubation, sedation, and hyperosmolar therapy improved episodes of decreased brain tissue oxygenation associated with intracranial hypertension. Brain tissue oxygenation was also noted to be significantly less than the target value on several occasions even when intracranial pressure was controlled and an age-appropriate cerebral perfusion pressure goal was met. Augmentation of cerebral perfusion pressure above age-appropriate goal with fluid boluses and inotropic agents increased brain tissue oxygenation in these instances. Both children had very low Glasgow Coma Scale scores at admission, but ultimately had favorable neurologic outcomes.
Conclusions:
Multimodal neuromonitoring of both intracranial pressure and brain tissue oxygenation during episodes of clinically apparent diabetic ketoacidosis-associated cerebral edema allows for the detection and treatment of episodes of elevated intracranial pressure and/or brain tissue hypoxia that may be of clinical significance.
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