Intermittent Versus Continuous Cerebrospinal Fluid Drainage Management in Adult Severe Traumatic Brain Injury: Assessment of Intracranial Pressure Burden

Nwachuku, Enyinna L.; Puccio, Ava M.; Fetzick, Anita; Scruggs, Bobby J.; Chang, Yue‐Fang; Shutter, Lori; Okonkwo, David O.

doi:10.1007/s12028-013-9885-3

Cited by 56 publications

(48 citation statements)

References 11 publications

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“…Moreover, hourly ICP measurements do not account for simultaneous exposures to other treatments that may temporarily elevate the recordings regardless of CE (such as painful procedures, or timing of tracheal suctioning). Although there is equipoise regarding the use of continuous CSF drainage for ICP management (50), it is our standard and may have underestimated the degree of brain swelling, (50) limiting our ability to detect associations between Sur1 levels/trajectories with ICP. Fortunately this reduces the likelihood of a falsely positive relationship.…”

Section: Discussionmentioning

confidence: 99%

Sulfonylurea Receptor-1: A Novel Biomarker for Cerebral Edema in Severe Traumatic Brain Injury

Jha

Puccio

Chou

et al. 2017

Critical Care Medicine

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Objective Cerebral edema(CE) is a key poor prognosticator in TBI. There are no biomarkers identifying patients at-risk, or guiding mechanistically-precise therapies. Sulfonylurea Receptor-1(Sur1) is upregulated only after brain injury, causing edema in animal studies. We hypothesized that Sur1 is measurable in human CSF after severe TBI (sTBI) and is an informative biomarker of edema and outcome. Methods 119 CSF samples were collected from 28 sTBI patients. Samples were retrieved at 12, 24, 48, 72h, and before EVD removal. 15 control samples were obtained from patients with normal pressure hydrocephalus. Sur1 was quantified by ELISA. Outcomes included CT edema, ICP measurements, therapies targeting edema and 3-month Glasgow Outcome Scale score. Results Sur1 was present in all sTBI patients (mean=3.54±3.39ng/ml, peak=7.13±6.09ng/ml) but undetectable in all controls (p<0.001). Mean and peak Sur1 was higher in patients with CT edema (4.96±1.13 ng/ml vs. 2.10±0.34 ng/ml, p=0.023). There was a temporal delay between peak Sur1 and peak ICP in 91.7% of patients with intracranial hypertension. There was no association between mean/peak Sur1 and mean/peak ICP, proportion of ICP > 20 mmHg, use of edema-directed therapies, decompressive craniotomy or 3 month Glasgow Outcome Score. However, decreasing Sur1 trajectories between 48–72h were significantly associated with improved CE and clinical outcome. Area under the multivariate model ROC curve was 0.881. Interpretation This is the first report quantifying human CSF Sur1. Sur1 was detected in sTBI, absent in controls, correlated with CT-edema and preceded peak ICP. Sur1 trajectories between 48–72h were associated with outcome. Since a therapy inhibiting Sur1 is available, assessing CSF Sur1 in larger studies is warranted to evaluate our exploratory findings regarding its diagnostic, and monitoring utility, as well as its potential to guide targeted therapies in TBI and other diseases involving CE.

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Section: Discussionmentioning

confidence: 99%

Sulfonylurea Receptor-1: A Novel Biomarker for Cerebral Edema in Severe Traumatic Brain Injury

Jha

Puccio

Chou

et al. 2017

Critical Care Medicine

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“…There are small retrospective studies demonstrating ICP reduction with continuous CSF drainage; however, the effect on mortality is unknown [46, 47]. The BTF level III recommendation is that continuous CSF drainage at the level of the midbrain may lower ICP more effectively than intermittent use [23].…”

Section: Cerebral Edema and Intracranial Pressurementioning

confidence: 99%

A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?

Jha

Kochanek

2018

Curr Neurol Neurosci Rep

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Purpose of Review Standard clinical protocols for treating cerebral edema and intracranial hypertension after severe TBI have remained remarkably similar over decades. Cerebral edema and intracranial hypertension are treated interchangeably when in fact intracranial pressure (ICP) is a proxy for cerebral edema but also other processes such as extent of mass lesions, hydrocephalus, or cerebral blood volume. A complex interplay of multiple molecular mechanisms results in cerebral edema after severe TBI, and these are not measured or targeted by current clinically available tools. Addressing these underpinnings may be key to preventing or treating cerebral edema and improving outcome after severe TBI. Recent Findings This review begins by outlining basic principles underlying the relationship between edema and ICP including the Monro-Kellie doctrine and concepts of intracranial compliance/elastance. There is a subsequent brief discussion of current guidelines for ICP monitoring/management. We then focus most of the review on an evolving precision medicine approach towards cerebral edema and intracranial hypertension after TBI. Personalization of invasive neuromonitoring parameters including ICP waveform analysis, pulse amplitude, pressure reactivity, and longitudinal trajectories are presented. This is followed by a discussion of cerebral edema subtypes (continuum of ionic/cytotoxic/vasogenic edema and progressive secondary hemorrhage). Mechanisms of potential molecular contributors to cerebral edema after TBI are reviewed. For each target, we present findings from preclinical models, and evaluate their clinical utility as biomarkers and therapeutic targets for cerebral edema reduction. This selection represents promising candidates with evidence from different research groups, overlap/inter-relatedness with other pathways, and clinical/translational potential. Summary We outline an evolving precision medicine and translational approach towards cerebral edema and intracranial hypertension after severe TBI.

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“…In a retrospective study, EVD use was associated with higher in-hospital mortality for those patients with GCS ≥6, but comatose patients with a lower GCS had a trend towards lower mortality with EVD use [45]. Furthermore, in a separate retrospective study of 62 patients, those patients managed with continual CSF drainage had more effective ICP control as compared to those sTBI patients with intermittent drainage [46]. Based on this evidence, the new guidelines recommend that CSF drainage to lower ICP could be used in patients with a low GCS (<6) within 12 hours of injury and that an EVD may be more effective at lowering ICP burden if it drains continually as opposed to intermittently.…”

Section: Neuromonitoring In the Intensive Care Unitmentioning

confidence: 99%

Medical Management of the Severe Traumatic Brain Injury Patient

et al. 2017

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Severe traumatic brain injury (sTBI) is a major contributor to long term disability and a leading cause of death worldwide. Medical management of the sTBI patient, beginning with pre-hospital triage, is aimed at preventing secondary brain injury. This review discusses prehospital and emergency department management of severe TBI, as well as aspects of TBI management in the intensive care unit where advances have been made in the past decade. Areas of emphasis include intracranial pressure management, neuromonitoring, management of paroxysmal sympathetic hyperactivity, neuroprotective strategies, prognostication, and communication with families about goals of care. Where appropriate, differences between the third and fourth editions of the Brain Trauma Foundation Guidelines for the Management of Severe Traumatic Brain Injury are highlighted.

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Intermittent Versus Continuous Cerebrospinal Fluid Drainage Management in Adult Severe Traumatic Brain Injury: Assessment of Intracranial Pressure Burden

Abstract: Continuous CSF drainage via an open EVD seemed to be associated with more effective ICP control in the management of adult severe TBI.

Cited by 56 publications

References 11 publications

Sulfonylurea Receptor-1: A Novel Biomarker for Cerebral Edema in Severe Traumatic Brain Injury

Sulfonylurea Receptor-1: A Novel Biomarker for Cerebral Edema in Severe Traumatic Brain Injury

A Precision Medicine Approach to Cerebral Edema and Intracranial Hypertension after Severe Traumatic Brain Injury: Quo Vadis?

Medical Management of the Severe Traumatic Brain Injury Patient

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