scholarly journals Heparin-Induced Fever in Neurointensive Care Unit: A Rarity Yet a Possibility

2021 ◽  
Author(s):  
Mathangi Krishnakumar ◽  
Shweta S. Naik ◽  
Venkatapura J. Ramesh ◽  
S Mouleeswaran
Keyword(s):  
Care Setting ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Protective Response ◽  
Inflammatory Cascade ◽  
Persistent Fever ◽  
Neurointensive Care Unit ◽  
Injured Tissue ◽  
Injured Brain ◽  
Resistance To Infection

AbstractFever is considered a protective response having multitude of benefits in terms of enhancing resistance to infection, recruiting cytokines to the injured tissue, and promoting healing. In terms of an injured brain, this becomes a double-edged sword triggering an inflammatory cascade resulting in secondary brain injury. It is important to identify the etiology so that corrective measures can be taken. Here we report a case of persistent fever in a patient with Guillain-Barré syndrome, which was probably due to heparin. This is the first report of heparin-induced fever in a neurocritical care setting and third report overall.

Severe Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Kee D. Kim ◽  
Marike Zwienenberg ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Brain Oxygenation ◽  
Barbiturate Coma ◽  
Blast Traumatic Brain Injury ◽  
Penetrating Traumatic Brain Injury

Traumatic brain injury remains a leading cause of death and disability worldwide. Patients with severe traumatic brain injury are best treated with a multidisciplinary, evidence-based, protocol-directed approach, which has been shown to decrease mortality and improve functional outcomes. Therapy is directed at the prevention of secondary brain injury through optimizing cerebral blood flow and the delivery of metabolic fuel (ie, oxygen and glucose). This is accomplished through the measurement and treatment of elevated intracranial pressure (ICP), the strict avoidance of hypotension and hypoxemia, and in some instances, surgical management. The treatment of elevated ICP is approached in a protocolized, tiered manner, with escalation of care occurring in the setting of refractory intracranial hypertension, culminating in either decompressive surgery or barbiturate coma. With such an approach, the rates of mortality secondary to traumatic brain injury are declining despite an increasing incidence of traumatic brain injury. This review contains 3 figures, 5 tables and 69 reference Key Words: blast traumatic brain injury, brain oxygenation, cerebral perfusion pressure, decompressive craniectomy, hyperosmolar therapy, intracranial pressure, neurocritical care, penetrating traumatic brain injury, severe traumatic brain injury

327 A Prospective Analysis of Hypovitaminosis D and Mortality in 400 Patients in the Neurocritical Care Setting

Neurosurgery ◽  
2016 ◽  
Vol 63 ◽  
pp. 195 ◽  
Author(s):  
Jian Guan ◽  
Michael Karsy ◽  
Andrea Archambault Brock ◽  
Ilyas Eli ◽  
Holly Ledyard ◽  
...  
Keyword(s):  
Care Setting ◽  
Neurocritical Care ◽  
Hypovitaminosis D ◽  
Prospective Analysis

scholarly journals HMGB1 a-Box Reverses Brain Edema and Deterioration of Neurological Function in a Traumatic Brain Injury Mouse Model

2018 ◽  
Vol 46 (6) ◽  
pp. 2532-2542 ◽  
Author(s):  
Lijun Yang ◽  
Feng Wang ◽  
Liang Yang ◽  
Yunchao Yuan ◽  
Yan Chen ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Therapeutic Potential ◽  
High Mobility ◽  
Neurological Injury ◽  
Secondary Brain Injury ◽  
Cell Degeneration ◽  
Injured Brain ◽  
Walking Tests

Background/Aims: Traumatic brain injury (TBI) is a complex neurological injury in young adults lacking effective treatment. Emerging evidences suggest that inflammation contributes to the secondary brain injury following TBI, including breakdown of the blood brain barrier (BBB), subsequent edema and neurological deterioration. High mobility group box-1 (HMGB1) has been identified as a key cytokine in the inflammation reaction following TBI. Here, we investigated the therapeutic efficacy of HMGB1 A-box fragment, an antagonist competing with full-length HMGB1 for receptor binding, against TBI. Methods: TBI was induced by controlled cortical impact (CCI) in adult male mice. HMGB1 A-box fragment was given intravenously at 2 mg/kg/day for 3 days after CCI. HMGB1 A-box-treated CCI mice were compared with saline-treated CCI mice and sham mice in terms of BBB disruption evaluated by Evan’s blue extravasation, brain edema by brain water content, cell death by propidium iodide staining, inflammation by Western blot and ELISA assay for cytokine productions, as well as neurological functions by the modified Neurological Severity Score, wire grip and beam walking tests. Results: HMGB1 A-box reversed brain damages in the mice following TBI. It significantly reduced brain edema by protecting integrity of the BBB, ameliorated cell degeneration, and decreased expression of pro-inflammatory cytokines released in injured brain after TBI. These cellular and molecular effects were accompanied by improved behavioral performance in TBI mice. Notably, HMGB1 A-box blocked IL-1β-induced HMGB1 release, and preferentially attenuated TLR4, Myd88 and P65 in astrocyte cultures. Conclusion: Our data suggest that HMGB1 is involved in CCI-induced TBI, which can be inhibited by HMGB1 A-box fragment. Therefore, HMGB1 A-box fragment may have therapeutic potential for the secondary brain damages in TBI.

Multimodality Monitoring in Neurocritical Care: Decision-Making Utilizing Direct And Indirect Surrogate Markers

2018 ◽  
Vol 34 (6) ◽  
pp. 449-463 ◽  
Author(s):  
Fawaz Al-Mufti ◽  
Megan Lander ◽  
Brendan Smith ◽  
Nicholas A. Morris ◽  
Rolla Nuoman ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neurocritical Care ◽  
Delayed Cerebral Ischemia ◽  
Neurological Injury ◽  
Innovative Technology ◽  
Secondary Brain Injury ◽  
Neurologic Injury ◽  
Irreversible Damage ◽  
Traumatic Intracranial Hemorrhage ◽  
Substantial Progress

Substantial progress has been made to create innovative technology that can monitor the different physiological characteristics that precede the onset of secondary brain injury, with the ultimate goal of intervening prior to the onset of irreversible neurological damage. One of the goals of neurocritical care is to recognize and preemptively manage secondary neurological injury by analyzing physiologic markers of ischemia and brain injury prior to the development of irreversible damage. This is helpful in a multitude of neurological conditions, whereby secondary neurological injury could present including but not limited to traumatic intracranial hemorrhage and, specifically, subarachnoid hemorrhage, which has the potential of progressing to delayed cerebral ischemia and monitoring postneurosurgical interventions. In this study, we examine the utilization of direct and indirect surrogate physiologic markers of ongoing neurologic injury, including intracranial pressure, cerebral blood flow, and brain metabolism.

Neurophysiologic Monitoring and Neuroprotection

2017 ◽  
Author(s):  
Aws Alawi ◽  
Michael Reznik ◽  
Jan Claassen
Keyword(s):  
Early Detection ◽  
Brain Injuries ◽  
Cerebral Injury ◽  
Secondary Brain Injury ◽  
Neurophysiologic Monitoring ◽  
Permanent Damage ◽  
Injured Brain ◽  
Physiological Assessment ◽  
Physiologic Parameters ◽  
Sedation Monitoring

One of the main goals of monitoring neurologically ill patients is detection of secondary brain injury early enough to intervene to prevent permanent damage. In some patients with impaired levels of consciousness and those who require sedation, monitoring various brain physiologic parameters by invasive and noninvasive means has become an essential tool in the care of critically ill patients. Integration of multiple physiological parameters provides a more comprehensive physiological assessment of the injured brain and allows real-time, early detection of secondary cerebral injury and intervention to prevent permanent damage. Importantly, these modalities should be interpreted collectively and not in isolation in order to manage acute brain injuries, which are often complex and dynamic at the same time.

scholarly journals Aspirin Exerts Neuroprotective Effects by Reversing Lipopolysaccharide-Induced Secondary Brain Injury and Inhibiting Matrix Metalloproteinase-3 Gene Expression

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Depeng Feng ◽  
Dezhe Chen ◽  
Tuanzhi Chen ◽  
Xiaoqian Sun
Keyword(s):  
Matrix Metalloproteinase ◽  
Test Scores ◽  
Neuroprotective Effect ◽  
Brain Area ◽  
Cerebral Injury ◽  
Control Group ◽  
Secondary Brain Injury ◽  
Walking Test ◽  
Matrix Metalloproteinase 3 ◽  
Injured Brain

Objective. This study is aimed at exploring the possible neuroprotective mechanism of aspirin and the effect of bacterial endotoxin lipopolysaccharide (LPS) during cerebral ischaemia-reperfusion (CIRP) injury. Methods. We established three animal models: the CIRP, LPS, and CIRP+LPS models. Mortality, the injured brain area, and the beam walking test were used to estimate the degree of cerebral injury among the rats. Immunohistochemistry and immunofluorescence were used to detect activated microglia, matrix metalloproteinase-3 (MMP-3), and osteopontin (OPN). Results. The injured brain area and mortality were dramatically reduced ( p < 0.01 ), and the beam walking test scores were elevated ( p < 0.01 ) in the acetylsalicylic acid (ASA) group compared to the control group. The number of microglia-, MMP-3-, and OPN-positive cells also increased. Furthermore, the number of GSI-B4, OPN, and MMP-3 cells decreased in the ASA group compared to the control group. After LPS stimulation, the number of microglia reached a peak at 24 h; at 7 d, these cells disappeared. In the ASA group, the number of microglia was significantly smaller ( p < 0.05 ), especially at 24 h ( p < 0.01 ), compared to the LPS group. Moreover, the injured brain area and the mortality were dramatically increased and the beam walking test scores were reduced ( p < 0.01 ) after LPS simulation following CIRP. The degree of injury in the ASA group resembled that in the control group. However, the number of MMP-3-immunoreactive neurons or microglia was significantly larger than that of the control group ( p < 0.05 ). In the ASA group, the MMP-3 expression was also considerably decreased ( p < 0.05 ). Conclusions. After CIRP, microglia were rapidly activated and the expression of MMP-3 and OPN significantly increased. For rats injected with LPS at reperfusion, the injured brain area and mortality also dramatically increased and the neurologic impairment worsened. However, ASA exhibited a neuroprotective effect during CIRP injury. Furthermore, ASA can reverse LPS-induced cerebral injury and inhibit the inflammatory reaction after CIRP injury.

Severe Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Kee D. Kim ◽  
Marike Zwienenberg ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Neurocritical Care ◽  
Secondary Brain Injury ◽  
Brain Oxygenation ◽  
Barbiturate Coma ◽  
Blast Traumatic Brain Injury ◽  
Penetrating Traumatic Brain Injury

Traumatic brain injury remains a leading cause of death and disability worldwide. Patients with severe traumatic brain injury are best treated with a multidisciplinary, evidence-based, protocol-directed approach, which has been shown to decrease mortality and improve functional outcomes. Therapy is directed at the prevention of secondary brain injury through optimizing cerebral blood flow and the delivery of metabolic fuel (ie, oxygen and glucose). This is accomplished through the measurement and treatment of elevated intracranial pressure (ICP), the strict avoidance of hypotension and hypoxemia, and in some instances, surgical management. The treatment of elevated ICP is approached in a protocolized, tiered manner, with escalation of care occurring in the setting of refractory intracranial hypertension, culminating in either decompressive surgery or barbiturate coma. With such an approach, the rates of mortality secondary to traumatic brain injury are declining despite an increasing incidence of traumatic brain injury. This review contains 3 figures, 5 tables and 69 reference Key Words: blast traumatic brain injury, brain oxygenation, cerebral perfusion pressure, decompressive craniectomy, hyperosmolar therapy, intracranial pressure, neurocritical care, penetrating traumatic brain injury, severe traumatic brain injury

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