What are we measuring? A refined look at the process of disrupted autoregulation and the limitations of cerebral perfusion pressure in preventing secondary injury after traumatic brain injury

Small, Coulter; Lucke‐Wold, Brandon; Patel, Chhaya; Abou‐Al‐Shaar, Hussam; Moor, Rachel; Mehkri, Yusuf; Still, Megan; Goldman, Matthew L.; Miller, Patricia E.; Robicsek, Steven A.

doi:10.1016/j.clineuro.2022.107389

Cited by 8 publications

(5 citation statements)

References 64 publications

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“…The decreased blood ow is often followed by delayed cerebral ischemia leading to catastrophic neurological outcomes or even death 52 . The use of CPP as therapy guidance after SAH is problematic because one can only roughly estimate CBF since it doesn't take vessel diameter, resistance, or blood viscosity into account 53 . But increased vascular resistance plays the key role in CBF after SAH.…”

Section: Discussionmentioning

confidence: 99%

Vasopressin increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Norepinephrine-Refractory Hypotension: A Preliminary Evaluation using the non-invasive Quantix ND in Comparison to the Literature

Bele,

Bründl,

Schmidt

et al. 2024

Preprint

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The maintenance of sufficient mean arterial pressure (MAP) to sustain perfusion and oxygen delivery to all major organs is important patients in intensive care but for neurosurgical patients after SAH or TBI it is essential to avoid secondary brain damage or delayed ischemia. So far most neurosurgical intensive care units use intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as therapy guidance for those patients. Use of fluid resuscitation and norepinephrine is standard to achieve CPP between 50–70 mmHg. But sometimes norepinephrine-refractory hypotension occurs. In those cases, arginin-vasopressin (AVP) is often the drug of choice. AVP and its synthetic analogies are widely used in modern medicine and gained interest in treatment of septic shock or refractory hypotension after cardiac surgery or hypovolemic shock. Recent papers also showed a significant impact of AVP in resuscitation of after traumatic brain injury (TBI) and influence on CPP in TBI patients during ICU treatment. But little is known about the effects of AVP on cerebral perfusion and oxygenation. The present preliminary study was carried out to examine the influence of vasopressin administration on cerebral blood flow by using the non-invasive QuantixND® device. We found significantly increased MAP and CPP but no concomitant elevation in CBF. In contrast, in most patients the CBF even decreased despite elevation of CPP. We conclude that AVP is an alternative drug to maintain MAP and CPP but must be used with care in patients with already compromised cerebral perfusion.

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Section: Discussionmentioning

confidence: 99%

Vasopressin increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Norepinephrine-Refractory Hypotension: A Preliminary Evaluation using the non-invasive Quantix ND in Comparison to the Literature

Bele,

Bründl,

Schmidt

et al. 2024

Preprint

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“…All this reinforces the idea that CA (or cerebral blood flow regulation) is not an all-or-nothing phenomenon, and the decomposition of CVR in two variables (CrCP and RAP) would give a more realistic bedside interpretation of the complex changes in cerebral hemodynamics of neurocritical patients. Likewise, these findings also emphasize the importance of not considering CPP strictly determined by the interaction between MAP and ICP in ABI [ 48 , 51 , 52 ] and advise for an individualized approach using parameters more representative of the real changes in brain hemodynamics, such as CrCP and RAP.…”

Section: Discussionmentioning

confidence: 99%

Critical Closing Pressure and Cerebrovascular Resistance Responses to Intracranial Pressure Variations in Neurocritical Patients

et al. 2023

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Background Critical closing pressure (CrCP) and resistance-area product (RAP) have been conceived as compasses to optimize cerebral perfusion pressure (CPP) and monitor cerebrovascular resistance, respectively. However, for patients with acute brain injury (ABI), the impact of intracranial pressure (ICP) variability on these variables is poorly understood. The present study evaluates the effects of a controlled ICP variation on CrCP and RAP among patients with ABI. Methods Consecutive neurocritical patients with ICP monitoring were included along with transcranial Doppler and invasive arterial blood pressure monitoring. Internal jugular veins compression was performed for 60 s for the elevation of intracranial blood volume and ICP. Patients were separated in groups according to previous intracranial hypertension severity, with either no skull opening (Sk1), neurosurgical mass lesions evacuation, or decompressive craniectomy (DC) (patients with DC [Sk3]). Results Among 98 included patients, the correlation between change (Δ) in ICP and the corresponding ΔCrCP was strong (group Sk1 r = 0.643 [p = 0.0007], group with neurosurgical mass lesions evacuation r = 0.732 [p < 0.0001], and group Sk3 r = 0.580 [p = 0.003], respectively). Patients from group Sk3 presented a significantly higher ΔRAP (p = 0.005); however, for this group, a higher response in mean arterial pressure (change in mean arterial pressure p = 0.034) was observed. Exclusively, group Sk1 disclosed reduction in ICP before internal jugular veins compression withholding. Conclusions This study elucidates that CrCP reliably changes in accordance with ICP, being useful to indicate ideal CPP in neurocritical settings. In the early days after DC, cerebrovascular resistance seems to remain elevated, despite exacerbated arterial blood pressure responses in efforts to maintain CPP stable. Patients with ABI with no need of surgical procedures appear to remain with more effective ICP compensatory mechanisms when compared with those who underwent neurosurgical interventions.

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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.…”

Section: Discussionmentioning

confidence: 99%

Secondary hyperperfusion injury following surgical evacuation for acute isolated epidural hematoma with concurrent cerebral herniation

Huang

Wang

et al. 2023

Front. Neurol.

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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.

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What are we measuring? A refined look at the process of disrupted autoregulation and the limitations of cerebral perfusion pressure in preventing secondary injury after traumatic brain injury

Cited by 8 publications

References 64 publications

Vasopressin increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Norepinephrine-Refractory Hypotension: A Preliminary Evaluation using the non-invasive Quantix ND in Comparison to the Literature

Vasopressin increases Cerebral Perfusion Pressure but not Cerebral Blood Flow in Neurosurgical Patients with Norepinephrine-Refractory Hypotension: A Preliminary Evaluation using the non-invasive Quantix ND in Comparison to the Literature

Critical Closing Pressure and Cerebrovascular Resistance Responses to Intracranial Pressure Variations in Neurocritical Patients

Secondary hyperperfusion injury following surgical evacuation for acute isolated epidural hematoma with concurrent cerebral herniation

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