Brain tissue oxygenation-guided management of diabetic ketoacidosis induced cerebral edema*.
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.


METHODS
Pediatric intensive care unit in a tertiary care teaching hospital.


METHODS
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.
Department 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
Nicole F
NF
O'Brien
Cesar
C
Mella
D000293:Adolescent; D058665:Adrenergic beta-1 Receptor Agonists / Q000627:therapeutic use; D001921:Brain / Q000378:metabolism*; D001929:Brain Edema / Q000209:etiology / Q000378:metabolism* / Q000628:therapy*; D002648:Child; D016883:Diabetic Ketoacidosis / Q000150:complications / Q000188:drug therapy; D004280:Dobutamine / Q000627:therapeutic use; D004837:Epinephrine / Q000627:therapeutic use; D005260:Female; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D002534:Hypoxia, Brain / Q000209:etiology / Q000628:therapy; D007328:Insulin / Q000627:therapeutic use; D007427:Intracranial Pressure; D008297:Male; D008991:Monitoring, Physiologic / Q000379:methods; D010100:Oxygen / Q000378:metabolism* / Q000627:therapeutic use; D012121:Respiration, Artificial; D012462:Saline Solution, Hypertonic / Q000627:therapeutic use; D014662:Vasoconstrictor Agents / Q000627:therapeutic use
D058665:Adrenergic beta-1 Receptor Agonists; D007004:Hypoglycemic Agents; D007328:Insulin; D012462:Saline Solution, Hypertonic; D014662:Vasoconstrictor Agents; D004280:Dobutamine; D010100:Oxygen; D004837:Epinephrine