Intracranial Pressure/Cerebral Perfusion Pressure-Targeted Management of Life-Threatening Intracranial Hypertension Complicating Diabetic Ketoacidosis-Associated Cerebral Edema A Case Report

Department of Pediatrics, School of Medicine and Public Health, University of Wisconsin Madison, WI, USA.
Pediatric emergency care (Impact Factor: 1.05). 07/2012; 28(7):696-8. DOI: 10.1097/PEC.0b013e31825d2198
Source: PubMed


Symptomatic cerebral edema from diabetic ketoacidosis occurs infrequently but carries a high rate of mortality and morbidity owing to complications from intracranial hypertension. Treatment options are limited but include hyperosmolar therapy with mannitol or hypertonic saline, tracheal intubation for airway protection, and hyperventilation via mechanical ventilation. We describe here the successful use of an intracranial pressure/cerebral perfusion pressure-targeted management strategy through ventriculostomy catheter placement with intracranial pressure monitoring and cerebrospinal fluid drainage, hyperosmolar therapy with hypertonic saline, and controlled hyperventilation to treat life-threatening complications of cerebral edema in a pediatric patient with severe diabetic ketoacidosis.

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    ABSTRACT: The orbital cerebrospinal fluid pressure (CSFP) represents the true counter-pressure against the intraocular pressure (IOP) across the lamina cribrosa and is, therefore, one of the two determinants of the trans-lamina cribrosa pressure difference (TLPD). From this anatomic point of view, an elevated TLPD could be due to elevated IOP or abnormally low orbital CSFP. Both experimental and clinical studies have suggested that a low CSFP could be associated with glaucomatous optic neuropathy in normal-pressure glaucoma. These included monkey studies with an experimental long-term reduction in CSFP, and clinical retrospective and prospective studies on patients with normal-pressure glaucoma. Since the choroidal blood drains via the vortex veins through the superior ophthalmic vein into the intracranial cavernous sinus, anatomy suggests that the CSFP could influence choroidal thickness. A population-based study revealed that thicker subfoveal choroidal thickness was associated with higher CSFP. Since the central retinal vein passes through the orbital CSF space, anatomy suggests that the retinal venous pressure should be at least as high as the orbital CSFP. Other experimental, clinical or population-based studies suggested an association between higher CSFP and higher retinal venous pressure and wider retinal veins. Consequently, a higher estimated CSFP was associated with arterial hypertensive retinopathy (with respect to the dilated retinal vein diameter and higher arterial-to-venous diameter) and with the prevalence, severity and incidence of diabetic retinopathy. Physiologically, CSFP was related with higher IOP. The influence of the CSFP on the episcleral venous pressure and/or a regulation of both CSFP and IOP by a center in the dorsomedial/perifornical hypothalamus may be responsible for this. In summary, the CSFP may be an overlooked parameter in ocular physiology and pathology. Abnormal changes in the CSFP, in particular in relationship to the IOP, may have pathophysiologic importance. Copyright © 2015 Elsevier Ltd. All rights reserved.
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