The Prognostic Value of Intracranial Pressure Monitoring After Severe Head Injuries

Feldmann, H.J.; Klages, G; Gärtner, Fania R.; Scharfenberg, John C.

doi:10.1007/978-3-7091-4088-8_15

Cited by 15 publications

(11 citation statements)

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“…It is widely known that edema causes a rise in intracranial pressure, which contributes significantly to neuronal cell damage, [19] as well as increases in morbidity and mortality of TBI patients [2][3][4]. The present study provides insight into the development of brain edema from dysfunctional AQPs via an HIF mediated mechanism which could lead both to neuronal damage and functional deficits following TBI.…”

Section: Discussionmentioning

confidence: 85%

“…Cerebral edema, a common pathology in TBI, develops within hours of impact and remains a critical problem in the emergency room. Edema brings about an elevated intracranial pressure (ICP) and may lead to brain herniation, which increases morbidity and carries a poor prognosis among survivors [2][3][4]. Edema develops as a consequence of breakdown of the blood brain barrier (BBB), and is thought to be mediated by specific water channels in certain cell membranes called aquaporins (AQPs) [5].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Neuronal damage and functional deficits are ameliorated by inhibition of aquaporin and HIF1α after traumatic brain injury (TBI)

Shenaq

Kassem

Peng

et al. 2012

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Neuronal damage and functional deficits are ameliorated by inhibition of aquaporin and HIF1α after traumatic brain injury (TBI)

Shenaq

Kassem

Peng

et al. 2012

Journal of the Neurological Sciences

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“…In humans, the amount of post-injury brain edema (as is measured here by NIVD and changes in ADC values) is an important predictor of acute mortality after TBI. In those patients who survive, TBI-related brain edema is also a poor prognostic indicator for later recovery (27, 37–38) . In addition, blood-brain barrier disruption (measured here as BBBD) has been increasingly indentified as a prominent contributor to epileptogenesis in both in vitro and in vivo models of experimental epilepsy (39) .…”

Section: Discussionmentioning

confidence: 99%

ADC mapping and T1-weighted signal changes on post-injury MRI predict seizure susceptibility after experimental traumatic brain injury

Frey

Lepkin²,

Schickedanz³

et al. 2013

Neurological Research

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“…Cerebral Edema (CE) is strongly associated with death and unfavorable outcome in Traumatic Brain Injury (TBI) (1–5). It is a significant cause of in-hospital death occurring in >60% of TBI patients with mass lesions and even occurs in 15% of those with normal initial CT scans(6).…”

Section: Introductionmentioning

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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The Prognostic Value of Intracranial Pressure Monitoring After Severe Head Injuries

Cited by 15 publications

References 0 publications

Neuronal damage and functional deficits are ameliorated by inhibition of aquaporin and HIF1α after traumatic brain injury (TBI)

Neuronal damage and functional deficits are ameliorated by inhibition of aquaporin and HIF1α after traumatic brain injury (TBI)

ADC mapping and T1-weighted signal changes on post-injury MRI predict seizure susceptibility after experimental traumatic brain injury

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

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