A Comparison of the Effects of Halothane, Isoflurane, and Pentobarbital Anesthesia on Intracranial Pressure and Cerebral Edema Formation Following Brain Injury in Rabbits

Abstract Background Our previous studies showed that topical application of mesenchymal stem cells (MSCs) improved functional recovery in rat traumatic brain injury (TBI) model, and hypoxic precondition further enhanced the therapeutic effects of MSCs. There was no previous study on the attenuation of cerebral edema by MSCs. We investigated whether topical application of normoxic and hypoxic MSCs could reduce cerebral edema in an experimental TBI model. Methods Two million normoxic (N = 24) and hypoxic (N = 24) MSCs were applied topically to exposed the cerebral cortex in a controlled cortical impact (CCI) model. The MSCs were fixed in position with fibrin glue. No treatment was given to control animals (TBI only: n = 24). After surgery, four animals in each group were sacrificed daily (day 1 to day 6) for edema evaluation. Normal animals without TBI were used as reference (n = 4). The expressions of GFAP, AQP4, and MMP9 were also investigated by immunofluorescence staining and RT-PCR at day 3. Results The edema peaked within 3 days after TBI. Compared with the control, hypoxic MSCs reduced brain water content significantly (p < 0.05). Both hypoxic and normoxic MSCs downregulated the expression of MMP9 and normalized AQP4 distribution to astrocyte end feet. Conclusion Our preliminary study showed that topical application of hypoxic MSCs suppressed both vasogenic and cytotoxic edema formation.

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EFFECT OF A HYPERTONIC LACTATED RINGERS SOLUTION ON CEREBRAL EDEMA AND INTRACRANIAL PRESSURE FOLLOWING CRYOGENIC BRAIN INJURY

Anesthesiology ◽

10.1097/00000542-198709001-00654 ◽

1987 ◽

Vol 67 (3) ◽

pp. A654-A654 ◽

Cited By ~ 1

Author(s):

M H Zornow ◽

M S Scheller ◽

S R Shackford ◽

S S Moore ◽

A E Bloom

Keyword(s):

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Edema

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TERAPI HIPEROSMOLAR SEBAGAI TATA LAKSANA EDEMA SEREBRI PASCACEDERA KEPALA: LAPORAN KASUS BERBASIS BUKTI

Majalah Kedokteran Neurosains Perhimpunan Dokter Spesialis Saraf Indonesia ◽

10.52386/neurona.v36i1.49 ◽

2018 ◽

Vol 36 (1) ◽

Author(s):

Ramdinal Aviesena Zairinal ◽

Irma Savitri Madjid ◽

Yetty Ramli ◽

Diatri Nari Lastri ◽

Adre Mayza

Keyword(s):

Systematic Review ◽

Traumatic Brain Injury ◽

Brain Injury ◽

Intracranial Pressure ◽

Hypertonic Saline ◽

Cerebral Edema ◽

Google Scholar ◽

Literature Searching ◽

Hyperosmolar Therapy ◽

Cochrane Database

HYPEROSMOLAR THERAPY FOR CEREBRAL EDEMA POST TRAUMATIC BRAIN INJURY: AN EVIDENCE-BASED CASE REPORTABSTRACTMannitol is an agent widely used to treat hyperosmolarity in cases of increased intracranial pressure after acute traumatic brain injury (TBI). Hypertonic saline is an alternative agent in such cases but is still not well-recognized in daily practice. Thus, a literature searching was conducted to see whether mannitol is more effective and safer than hypertonic saline in reducing intracranial pressure in patients with cerebral edema post TBI. The results of literature searching using PubMed, Google Scholar, and Cochrane Database of Systematic Review showed that there is no clear evidence suggesting mannitol is better than hypertonic saline, and vice versa. Therefore, hypertonic saline should be considered as an alternative treatment for hyperosmolarity besides mannitol.Keywords: Cerebral edema, hyperosmolar therapy, hypertonic saline, mannitol, traumatic brain injuryABSTRAKManitol sebagai agen terapi hiperosmolar untuk menurunkan tekanan intrakranial (TIK) pascacedera kepala telah digunakan secara luas. Sementara pilihan lainnya, yaitu larutan salin hipertonik, masih jarang diaplikasikan pada praktik sehari-hari. Oleh karena itu, dilakukan pencarian literatur untuk menilai efektivitas dan keamanan manitol dibandingkan larutan salin hipertonik dalam menurunkan tekanan intrakranial berdasarkan kasus pasien yang mengalami edema serebri pascacedera kepala. Hasil pencarian di PubMed, Google Scholar, dan Cochrane Database of Systematic Review menunjukkan belum ada bukti ilmiah yang secara tegas menyimpulkan manitol lebih efektif dan aman daripada larutan salin hipertonik maupun sebaliknya. Oleh karena itu, larutan salin hipertonik dapat dijadikan alternatif terapi hiperosmolar selain manitol.Kata kunci: Cedera kepala, edema serebri, manitol, salin hipertonik, terapi hiperosmolar

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Topical application of adipose tissue derived mesenchymal stem cells (ADMSCs) reduced cerebral edema in experimental traumatic brain injury (TBI)- a preliminary study

10.21203/rs.3.rs-27106/v2 ◽

2020 ◽

Author(s):

Hui MA ◽

Lian Xu Cui ◽

Ping Kuen Lam ◽

Cindy SW Tong ◽

Kin KY Lo ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Brain Injury ◽

Topical Application ◽

Cerebral Edema ◽

Therapeutic Effects ◽

Edema Formation ◽

Hypoxic Precondition ◽

Preliminary Study

Abstract Background: Our previous studies showed that topical application of mesenchymal stem cells (MSCs) improved functional recovery in rat traumatic brain injury (TBI) model, and hypoxic precondition further enhanced the therapeutic effects of MSCs. There was no previous study on the attenuation of cerebral edema by MSCs. Objective: We investigated whether topical application of normoxic and hypoxic MSCs could reduce cerebral edema in an experimental TBI model. Methods: 2 million normoxic (N=24) and hypoxic (N=24) MSCs were applied topically to exposed cerebral cortex in a controlled cortical impact (CCI) model. The MSCs were fixed in position with fibrin glue. No treatment was given to control animals (TBI only: n=24). After surgery, four animals in each group were sacrificed daily (day 1 to day 6) for edema evaluation. Normal animals without TBI were used as reference (n=4). The expressions of GFAP, AQP4 and MMP9 were also investigated by immunofluorescence staining and RT-PCR at day 3. Results: The edema peaked within 3 days after TBI. Compared with the control, hypoxic MSCs reduced brain water content significantly (p<0.05). Both hypoxic and normoxic MSCs downregulated the expression of MMP9 and normalized AQP4 distribution to astrocytes end feet. Conclusion: Our preliminary study showed that topical application of hypoxic MSCs suppressed both vasogenic and cytotoxic edema formation.

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Topical application of adipose tissue derived mesenchymal stem cells (ADMSCs) reduced cerebral edema in experimental traumatic brain injury (TBI)- a preliminary study

10.21203/rs.3.rs-27106/v1 ◽

2020 ◽

Author(s):

Hui MA ◽

Lian Xu Cui ◽

Ping Kuen Lam ◽

Cindy SW Tong ◽

Kin KY Lo ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Stem Cells ◽

Mesenchymal Stem Cells ◽

Brain Injury ◽

Topical Application ◽

Cerebral Edema ◽

Therapeutic Effects ◽

Edema Formation ◽

Hypoxic Precondition ◽

Preliminary Study

Abstract Background: Our previous studies showed that topical application of mesenchymal stem cells (MSCs) improved functional recovery in rat traumatic brain injury (TBI) model, and hypoxic precondition further enhanced the therapeutic effects of MSCs. There was no previous study on the attenuation of cerebral edema by MSCs. Objective: We investigated whether topical application of normoxic and hypoxic MSCs could reduce cerebral edema in an experimental TBI model. Methods: 2 million normoxic (N=24) and hypoxic (N=24) MSCs were applied topically to exposed cerebral cortex in a controlled cortical impact (CCI) model. The MSCs were fixed in position with fibrin glue. No treatment was given to control animals (TBI only: n=24). After surgery, four animals in each group were sacrificed daily (day 1 to day 6) for edema evaluation. Normal animals without TBI were used as reference (n=4). The expressions of GFAP, AQP4 and MMP9 were also investigated by immunofluorescence staining and RT-PCR at day 3. Results: The edema peaked within 3 days after TBI. Compared with the control, hypoxic MSCs reduced brain water content significantly (p<0.05). Both hypoxic and normoxic MSCs downregulated the expression of MMP9 and normalized AQP4 distribution to astrocytes end feet. Conclusion: Our preliminary study showed that topical application of hypoxic MSCs suppressed both vasogenic and cytotoxic edema formation. Keywords: topical, MSCs, cerebral edema, TBI

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Does Vasopressin Exacerbate Cerebral Edema in Patients with Severe Traumatic Brain Injury?

The American Surgeon ◽

10.1177/000313481808400121 ◽

2018 ◽

Vol 84 (1) ◽

pp. 43-50 ◽

Cited By ~ 4

Author(s):

Casey J. Allen ◽

Ty K. Subhawong ◽

Mena M. Hanna ◽

Lydia Chelala ◽

M. Ross Bullock ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Edema ◽

Perfusion Pressure ◽

Single Institution ◽

Lower Plasma ◽

Hyperosmolar Therapy ◽

Ct Attenuation ◽

Total Fluid

Arginine vasopressin (AVP) is often used as an alternative pressor to catecholamines (CATs). However, unlike CATs, AVP is a powerful antidiuretic that could promote edema. We tested the hypothesis that AVP promoted cerebral edema and/or increased requirements for osmotherapy, relative to those who received CATs, for cerebral perfusion pressure (CPP) management after traumatic brain injury (TBI). This is a retrospective review of 286 consecutive TBI patients with intracranial pressure monitoring at a single institution from September 2008 to January 2015. Cerebral edema was quantitated using CT attenuation in prespecified areas of gray and white matter. Results: To maintain CPP >60 mm Hg, 205 patients required no vasopressors, 41 received a single CAT, 12 received AVP, and 28 required both. Those who required no pressors were generally less injured; required less hyperosmolar therapy and less total fluid; and had lower plasma Na, lower intracranial pressure, less edema, and lower mortality (all P < 0.05). Edema; daily mean, minimum, and maximum Na levels; and mortality were similar with AVP versus CATs, but the daily requirement of mannitol and 3 per cent NaCl were reduced by 45 and 35 per cent (both P < 0.05). In patients with TBI who required CPP therapy, AVP reduced the requirements for hyperosmolar therapy and did not delay resolution or increase cerebral edema compared with CATs.

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Traumatic Epidural and Subdural Hematomas

Mayo Clinic Critical and Neurocritical Care Board Review ◽

10.1093/med/9780190862923.003.0088 ◽

2019 ◽

pp. 614-620

Author(s):

Patrick R. Maloney ◽

Michelle J. Clarke

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Intracranial Pressure ◽

Cerebral Edema ◽

Subdural Hematoma ◽

Epidural Hematoma ◽

Nonoperative Management ◽

Mass Effect ◽

Increased Intracranial Pressure ◽

Cerebral Herniation

Traumatic brain injury is a broad topic and encompasses a spectrum of pathophysiologic disorders that result in increased intracranial pressure (ICP), cerebral edema, bleeding, mass effect, cerebral herniation, and death. Traumatic epidural hematoma (EDH) and subdural hematoma (SDH) are the focus of this chapter. EDH and SDH are intracranial blood collections that have mass effect within the intracranial vault (Figure 88.1) for which operative and nonoperative management criteria are established.

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‘Hit & Run’ Model of Closed-Skull Traumatic Brain Injury (TBI) Reveals Complex Patterns of Post-Traumatic AQP4 Dysregulation

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2013.30 ◽

2013 ◽

Vol 33 (6) ◽

pp. 834-845 ◽

Cited By ~ 117

Author(s):

Zeguang Ren ◽

Jeffrey J Iliff ◽

Lijun Yang ◽

Jiankai Yang ◽

Xiaolin Chen ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Cerebral Edema ◽

Compensatory Mechanism ◽

Rodent Models ◽

Edema Formation ◽

Aqp4 Expression ◽

Head Fixation ◽

Skull Model ◽

Post Traumatic

Cerebral edema is a major contributor to morbidity associated with traumatic brain injury (TBI). The methods involved in most rodent models of TBI, including head fixation, opening of the skull, and prolonged anesthesia, likely alter TBI development and reduce secondary injury. We report the development of a closed-skull model of murine TBI, which minimizes time of anesthesia, allows the monitoring of intracranial pressure (ICP), and can be modulated to produce mild and moderate grade TBI. In this model, we characterized changes in aquaporin-4 (AQP4) expression and localization after mild and moderate TBI. We found that global AQP4 expression after TBI was generally increased; however, analysis of AQP4 localization revealed that the most prominent effect of TBI on AQP4 was the loss of polarized localization at endfoot processes of reactive astrocytes. This AQP4 dysregulation peaked at 7 days after injury and was largely indistinguishable between mild and moderate grade TBI for the first 2 weeks after injury. Within the same model, blood–brain barrieranalysis of variance permeability, cerebral edema, and ICP largely normalized within 7 days after moderate TBI. These findings suggest that changes in AQP4 expression and localization may not contribute to cerebral edema formation, but rather may represent a compensatory mechanism to facilitate its resolution.

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