scholarly journals Randomized Control Trial For Transcranial Doppler monitoring in patients with Traumatic Brain Injury.

2020 ◽  
Author(s):  
Nida Fatima
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Transcranial Doppler ◽  
Traumatic Event ◽  
Intervention Group ◽  
Control Group ◽  
Neurosurgical Intervention

Abstract Traumatic Brain Injury is the leading cause of disability and mortality throughout the world. It temporarily or permanently impairs the brain function. Primary injury is induced by mechanical forces and occurs at the moment of injury while secondary brain damage may occurs hours or even days after the traumatic event. This injury may result from impairment or local decline in the cerebral blood flow. Decreases in cerebral blood flow are the result of local edema, hemorrhage or increased intracranial pressure. Although major progress has been made in understanding of the pathophysiology of this injury, this has not yet led to substantial improvements in outcome. Traumatic Brain Injury is associated with various complications including raised intracranial pressure, midline shift due to worsening of the volume of intracranial hematoma, cerebral vasospasm in traumatic sub arachnoid hemorrhage. Transcranial Doppler (TCD) has been utilized as a monitoring tool in the neurocritical care unit since it is non-invasive tool and that can be brought to bedside.However, its utility in using as a protocol in management of traumatic brain injury patients has not been studied.We hypothesized that daily TCD followed by early performance of Neuroimaging (CT scan) and Neurosurgical intervention will lead to improvement in clinical outcome.Our study’s design is Randomized Controlled Trial with neurosurgical intervention based upon the Intervention Group as the TCD-Monitoring/Neuroimaging vs Control Group as the Clinical Imaging/Neurological status. Our study’s outcome is 90 days’ clinical outcome (modified rankin scale) and Glasgow Coma Outcome Scale.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

EFFECTS OF HYPERTONIC ARGININE ON CEREBRAL BLOOD FLOW AND INTRACRANIAL PRESSURE AFTER TRAUMATIC BRAIN INJURY COMBINED WITH HEMORRHAGIC HYPOTENSION

Shock ◽  
2006 ◽  
Vol 26 (3) ◽  
pp. 290-295 ◽  
Author(s):  
Donald S. Prough ◽  
George C. Kramer ◽  
Tatsuo Uchida ◽  
Rachael T. Stephenson ◽  
Helen L. Hellmich ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Hemorrhagic Hypotension

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

scholarly journals Facial Fractures: Independent Prediction of Neurosurgical Intervention

2021 ◽  
Author(s):  
Brandon Lucke-Wold ◽  
Kevin Pierre ◽  
Sina Aghili-Mehrizi ◽  
Gregory Murad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
External Ventricular Drain ◽  
Intervention Group ◽  
Facial Fracture ◽  
Pressure Monitor ◽  
Significant Difference ◽  
Neurosurgical Intervention

Abstract Background:Over half of patients with facial fractures have associated traumatic brain injury. Based on previous force dynamic cadaveric studies, Lefort type 2 and 3 fractures are more associated with severe injury. Whether this correlates to neurosurgical intervention have not been well characterized. The purpose of this retrospective data analysis is to characterize fracture pattern types in patients requiring neurosurgical intervention and to see if this is different from those not requiring intervention. Methods:Retrospective data was collected from the trauma registry from 2010-2019. Inclusion criteria: adults over 18, confirmed facial fracture with available neuroimaging, reported traumatic brain injury, and admission to ICU or floor bed. Exclusion criteria: patients less than 18 years old, patients with no neuroimaging, and patients that were deceased prior to initiation of neurosurgical intervention. Data included: basic demographic data, presenting Glasgow Coma Scale (GCS) score, mechanism of injury, type of traumatic brain injury, neurosurgical intervention, and facial fracture type. Retrospective Contingency Analysis with Fraction of Total Comparison was used with Chi-Square analysis for demographic and injury characteristic data.Results:1172 patients met inclusion criteria. 1001 required no neurosurgical intervention and 171 required intervention. No significant difference was seen between the non-intervention group and intervention group in terms of demographic data or baseline injury characteristics except for presenting GCS. A significant difference was seen between groups for presenting Glasgow Coma Scale (c2=67.71, p<0.001). The intervention group had greater number of patients with GCS<8 compared to the non-intervention group. Fracture patterns were overall similar between the non-intervention group compared to intervention group (c2=4.518, p=0.92), however subset analysis did reveal a 2 fold increase in Lefort type 2 fractures and notable increase in Lefort type 3 and panfacial fractures in the intervention group. The intervention group was further divided into those requiring external ventricular drain or intracranial pressure monitor only vs. patients requiring craniectomy, craniotomy, or burr holes with or with external ventricular drain or intracranial pressure monitor. A significant difference was seen between groups (c2=20.02, p=0.03). The craniectomy, craniotomy, or burr hole group was much more likely to have Lefort type 2 or 3 fractures compared to the external ventricular drain or intracranial pressure monitor group only. Conclusions:Lefort type 2 and type 3 fractures are significantly associated with requiring neurosurgical intervention. An improved algorithm for managing these patients has been proposed in the discussion. Ongoing work will focus on validating and refining the algorithm in order to improve patient care for trauma patients with facial fracture and traumatic brain injury.

A prospective, randomized clinical trial to compare the effect of hyperbaric to normobaric hyperoxia on cerebral metabolism, intracranial pressure, and oxygen toxicity in severe traumatic brain injury

2010 ◽  
Vol 112 (5) ◽  
pp. 1080-1094 ◽  
Author(s):  
Sarah B. Rockswold ◽  
Gaylan L. Rockswold ◽  
David A. Zaun ◽  
Xuewei Zhang ◽  
Carla E. Cerra ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Brain Tissue ◽  
Cerebral Metabolism ◽  
Treatment Session ◽  
Control Group ◽  
Normobaric Hyperoxia ◽  
The Brain

Object Oxygen delivered in supraphysiological amounts is currently under investigation as a therapy for severe traumatic brain injury (TBI). Hyperoxia can be delivered to the brain under normobaric as well as hyperbaric conditions. In this study the authors directly compare hyperbaric oxygen (HBO2) and normobaric hyperoxia (NBH) treatment effects. Methods Sixty-nine patients who had sustained severe TBIs (mean Glasgow Coma Scale Score 5.8) were prospectively randomized to 1 of 3 groups within 24 hours of injury: 1) HBO2, 60 minutes of HBO2 at 1.5 ATA; 2) NBH, 3 hours of 100% fraction of inspired oxygen at 1 ATA; and 3) control, standard care. Treatments occurred once every 24 hours for 3 consecutive days. Brain tissue PO2, microdialysis, and intracranial pressure were continuously monitored. Cerebral blood flow (CBF), arteriovenous differences in oxygen, cerebral metabolic rate of oxygen (CMRO2), CSF lactate and F2-isoprostane concentrations, and bronchial alveolar lavage (BAL) fluid interleukin (IL)–8 and IL-6 assays were obtained pretreatment and 1 and 6 hours posttreatment. Mixed-effects linear modeling was used to statistically test differences among the treatment arms as well as changes from pretreatment to posttreatment. Results In comparison with values in the control group, the brain tissue PO2 levels were significantly increased during treatment in both the HBO2 (mean ± SEM, 223 ± 29 mm Hg) and NBH (86 ± 12 mm Hg) groups (p < 0.0001) and following HBO2 until the next treatment session (p = 0.003). Hyperbaric O2 significantly increased CBF and CMRO2 for 6 hours (p ≤ 0.01). Cerebrospinal fluid lactate concentrations decreased posttreatment in both the HBO2 and NBH groups (p < 0.05). The dialysate lactate levels in patients who had received HBO2 decreased for 5 hours posttreatment (p = 0.017). Microdialysis lactate/pyruvate (L/P) ratios were significantly decreased posttreatment in both HBO2 and NBH groups (p < 0.05). Cerebral blood flow, CMRO2, microdialysate lactate, and the L/P ratio had significantly greater improvement when a brain tissue PO2 ≥ 200 mm Hg was achieved during treatment (p < 0.01). Intracranial pressure was significantly lower after HBO2 until the next treatment session (p < 0.001) in comparison with levels in the control group. The treatment effect persisted over all 3 days. No increase was seen in the CSF F2-isoprostane levels, microdialysate glycerol, and BAL inflammatory markers, which were used to monitor potential O2 toxicity. Conclusions Hyperbaric O2 has a more robust posttreatment effect than NBH on oxidative cerebral metabolism related to its ability to produce a brain tissue PO2 ≥ 200 mm Hg. However, it appears that O2 treatment for severe TBI is not an all or nothing phenomenon but represents a graduated effect. No signs of pulmonary or cerebral O2 toxicity were present.

Transcranial Doppler to measure cerebral blood flow in management of traumatic brain injury

Injury ◽  
2014 ◽  
Vol 45 (11) ◽  
pp. 1801-1802
Author(s):  
A. Salvadori ◽  
P. Pasquier ◽  
A. Jarrassier ◽  
J.V. Schaal ◽  
S. Mérat
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Transcranial Doppler

From redefined hypotension to optimal cerebral blood flow in traumatic brain injury: Let's use transcranial Doppler

Injury ◽  
2013 ◽  
Vol 44 (11) ◽  
pp. 1666 ◽  
Author(s):  
A. Salvadori ◽  
P. Pasquier ◽  
J.V. Schaal ◽  
A. Jarrassier ◽  
J. Renner ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Transcranial Doppler
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