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“…Compared with the aforementioned uncontrollable influencing factors, we first notice that the amplitude of instant change in CBF reperfusion is controllable to some extent. It is also an important factor affecting CBF reperfusion in patients with abnormal cerebral vascular autoregulation (27)(28)(29). Tamaki et al (30) found that the quick evacuation of the hematoma could decrease the intracranial pressure sharply and, at the same time, trigger a severe aggravation of hemodynamic change, thus worsening the overload injury to the decompensated cerebral vessels.…”
ObjectiveHemispherical cerebral swelling or even encephalocele after head trauma is a common complication and has been well elucidated previously. However, few studies have focused on the secondary brain hemorrhage or edema occurring regionally but not hemispherically in the cerebral parenchyma just underneath the surgically evacuated hematoma during or at a very early stage post-surgery.MethodsIn order to explore the characteristics, hemodynamic mechanisms, and optimized treatment of a novel peri-operative complication in patients with isolated acute epidural hematoma (EDH), clinical data of 157 patients with acute-isolated EDH who underwent surgical intervention were reviewed retrospectively. Risk factors including demographic characteristics, admission Glasgow Coma Score, preoperative hemorrhagic shock, anatomical location, and morphological parameters of epidural hematoma, as well as the extent and duration of cerebral herniation on physical examination and radiographic evaluation were considered.ResultsIt suggested that secondary intracerebral hemorrhage or edema was determined in 12 of 157 patients within 6 h after surgical hematoma evacuation. It was featured by remarkable, regional hyperperfusion on the computed tomography (CT) perfusion images and associated with a relatively poor neurological prognosis. In addition to concurrent cerebral herniation, which was found to be a prerequisite for the development of this novel complication, multivariate logistic regression further showed four independent risk factors contributing to this type of secondary hyperperfusion injury: cerebral herniation that lasted longer than 2 h, hematomas that were located in the non-temporal region, hematomas that were thicker than 40 mm, and hematomas occurring in pediatric and elderly patients.ConclusionSecondary brain hemorrhage or edema occurring within an early perioperative period of hematoma-evacuation craniotomy for acute-isolated EDH is a rarely described hyperperfusion injury. Because it plays an important prognostic influence on patients’ neurological recovery, optimized treatment should be given to block or reduce the consequent secondary brain injuries.
“…Compared with the aforementioned uncontrollable influencing factors, we first notice that the amplitude of instant change in CBF reperfusion is controllable to some extent. It is also an important factor affecting CBF reperfusion in patients with abnormal cerebral vascular autoregulation (27)(28)(29). Tamaki et al (30) found that the quick evacuation of the hematoma could decrease the intracranial pressure sharply and, at the same time, trigger a severe aggravation of hemodynamic change, thus worsening the overload injury to the decompensated cerebral vessels.…”
ObjectiveHemispherical cerebral swelling or even encephalocele after head trauma is a common complication and has been well elucidated previously. However, few studies have focused on the secondary brain hemorrhage or edema occurring regionally but not hemispherically in the cerebral parenchyma just underneath the surgically evacuated hematoma during or at a very early stage post-surgery.MethodsIn order to explore the characteristics, hemodynamic mechanisms, and optimized treatment of a novel peri-operative complication in patients with isolated acute epidural hematoma (EDH), clinical data of 157 patients with acute-isolated EDH who underwent surgical intervention were reviewed retrospectively. Risk factors including demographic characteristics, admission Glasgow Coma Score, preoperative hemorrhagic shock, anatomical location, and morphological parameters of epidural hematoma, as well as the extent and duration of cerebral herniation on physical examination and radiographic evaluation were considered.ResultsIt suggested that secondary intracerebral hemorrhage or edema was determined in 12 of 157 patients within 6 h after surgical hematoma evacuation. It was featured by remarkable, regional hyperperfusion on the computed tomography (CT) perfusion images and associated with a relatively poor neurological prognosis. In addition to concurrent cerebral herniation, which was found to be a prerequisite for the development of this novel complication, multivariate logistic regression further showed four independent risk factors contributing to this type of secondary hyperperfusion injury: cerebral herniation that lasted longer than 2 h, hematomas that were located in the non-temporal region, hematomas that were thicker than 40 mm, and hematomas occurring in pediatric and elderly patients.ConclusionSecondary brain hemorrhage or edema occurring within an early perioperative period of hematoma-evacuation craniotomy for acute-isolated EDH is a rarely described hyperperfusion injury. Because it plays an important prognostic influence on patients’ neurological recovery, optimized treatment should be given to block or reduce the consequent secondary brain injuries.
“…Early studies evaluating CA capacity in ABI focused on intermittent methods for CA determination including various neuroimaging modalities such as positron emission tomography (PET) and computed tomographic xenon (XE-CT) as well as indirect CBF estimation with transcranial doppler (TCD) in response to alterations in MAP either with vasopressors or non-invasively with techniques such as thigh-cuff deflation and orthostatic hypotension provocation ( 10 , 33 ). More recently, novel methods have been developed for continuous assessment of CA indices based on CBF responses to spontaneous changes in MAP or cerebral perfusion pressure CPP and are outlined in Table 1 ( 44 ).…”
Section: Cerebral Physiologymentioning
confidence: 99%
“…This multifaceted approach has begun to reshape the landscape of neurocritical care by moving away from standardized “one size fits all” treatment strategies to individualized precision medicine; however, questions still exist including how to best integrate and interpret the high dimensionality of signals and whether such an approach will result in improved patient outcomes ( 3 , 9 ). Furthermore, when interpreting monitoring data, it is important to recognize potential limitations of each modality and specific characteristics including whether it provides continuous or intermittent assessment as well as if the device is measuring focal or global cerebral parameters ( 10 , 11 ). Common neuromonitoring tools employed in the neurologic intensive care unit (ICU) are highlighted in Figure 1 .…”
Given the complexity of cerebral pathology in patients with acute brain injury, various neuromonitoring strategies have been developed to better appreciate physiologic relationships and potentially harmful derangements. There is ample evidence that bundling several neuromonitoring devices, termed “multimodal monitoring,” is more beneficial compared to monitoring individual parameters as each may capture different and complementary aspects of cerebral physiology to provide a comprehensive picture that can help guide management. Furthermore, each modality has specific strengths and limitations that depend largely on spatiotemporal characteristics and complexity of the signal acquired. In this review we focus on the common clinical neuromonitoring techniques including intracranial pressure, brain tissue oxygenation, transcranial doppler and near-infrared spectroscopy with a focus on how each modality can also provide useful information about cerebral autoregulation capacity. Finally, we discuss the current evidence in using these modalities to support clinical decision making as well as potential insights into the future of advanced cerebral homeostatic assessments including neurovascular coupling.
“…PRx has been demonstrated to be capable of adequately predicting the lower limit of cerebral autoregulation (LLA), but the upper limit of cerebral autoregulation (ULA) is not easily predictable [22,23]. Other tools also have had difficulties to predict the ULA, and it even might be that there is no strict ULA, and cerebral autoregulation is better in compensating for hypotension than for hypertension [24 ▪▪ ]. In retrospective series, it was found that when PRx is plotted against its corresponding CPP, in 60–70% of patients, this leads to a U-shaped curve, in which the lowest (i.e.…”
“…As they all measure a different parameter, they are not quite redeemable. Because the benefit of treatment protocols based on these metrics has not been unequivocally demonstrated in large prospective patient trials, their use cannot be recommended for clinical use so far [24 ▪▪ ,30].…”
Purpose of reviewSevere traumatic brain injury (TBI) remains the most prevalent neurological condition worldwide. Observational and interventional studies provide evidence to recommend monitoring of intracranial pressure (ICP) in all severe TBI patients. Existing guidelines focus on treating elevated ICP and optimizing cerebral perfusion pressure (CPP), according to fixed universal thresholds. However, both ICP and CPP, their target thresholds, and their interaction, need to be interpreted in a broader picture of cerebral autoregulation, the natural capacity to adjust cerebrovascular resistance to preserve cerebral blood flow in response to external stimuli.Recent findingsCerebral autoregulation is often impaired in TBI patients, and monitoring cerebral autoregulation might be useful to develop personalized therapy rather than treatment of one size fits all thresholds and guidelines based on unidimensional static relationships.SummaryToday, there is no gold standard available to estimate cerebral autoregulation. Cerebral autoregulation can be triggered by performing a mean arterial pressure (MAP) challenge, in which MAP is increased by 10% for 20 min. The response of ICP (increase or decrease) will estimate the status of cerebral autoregulation and can steer therapy mainly concerning optimizing patient-specific CPP. The role of cerebral metabolic changes and its relationship to cerebral autoregulation is still unclear and awaits further investigation.
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