Pressure-derived versus pressure wave amplitude–derived indices of cerebrovascular pressure reactivity in relation to early clinical state and 12-month outcome following aneurysmal subarachnoid hemorrhage

Eide, Per Kristian; Sorteberg, Angelika; Bentsen, Gunnar; Marthinsen, Pål Bache; Stubhaug, Audun; Sorteberg, Wilhelm

doi:10.3171/2012.1.jns111313

Cited by 56 publications

(32 citation statements)

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“…Evaluation of cerebral autoregulation is being increasingly recognised as a factor requiring consideration in the management of patients with SAH 112 114 113 162–164. Three recent prospective studies have demonstrated that indirect indices of cerebral autoregulation can be used to prognosticate DCI as well as long-term outcome after SAH 112 113 163 164 165. Importantly, autoregulation was found to deteriorate before clinical symptoms as well as radiographically identifiable arterial narrowing 163.…”

Section: Cerebral Autoregulationmentioning

confidence: 99%

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

Budohoski

Guilfoyle

Helmy

et al. 2014

J Neurol Neurosurg Psychiatry

223

189

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Cerebral vasospasm has traditionally been regarded as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal subarachnoid haemorrhage, and often leads to cerebral infarction and poor neurological outcome. However, data from recent studies argue against a pure focus on vasospasm as the cause of delayed ischaemic complications. Findings that marked reduction in the incidence of vasospasm does not translate to a reduction in DCI, or better outcomes has intensified research into other possible mechanisms which may promote ischaemic complications. Early brain injury and cell death, blood-brain barrier disruption and initiation of an inflammatory cascade, microvascular spasm, microthrombosis, cortical spreading depolarisations and failure of cerebral autoregulation, have all been implicated in the pathophysiology of DCI. This review summarises the current knowledge about the mechanisms underlying the development of DCI. Furthermore, it aims to describe and categorise the known pharmacological treatment options with respect to the presumed mechanism of action and its role in DCI.

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Section: Cerebral Autoregulationmentioning

confidence: 99%

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

Budohoski

Guilfoyle

Helmy

et al. 2014

J Neurol Neurosurg Psychiatry

223

189

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“…PRx is an autoregulatory index that relies on the correlation between spontaneous fluctuations in mean arterial blood pressure (MAP) and intracranial pressure (ICP). PRx has been studied extensively in traumatic brain injury (TBI) and to some extent also in SAH [2, 14]. …”

Section: Introductionmentioning

confidence: 99%

Increased risk of critical CBF levels in SAH patients with actual CPP below calculated optimal CPP

et al. 2017

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BackgroundCerebral pressure autoregulation can be quantified with the pressure reactivity index (PRx), based on the correlation between blood pressure and intracranial pressure. Using PRx optimal cerebral perfusion pressure (CPPopt) can be calculated, i.e., the level of CPP where autoregulation functions best. The relation between cerebral blood flow (CBF) and CPPopt has not been examined. The objective was to assess to which extent CPPopt can be calculated in SAH patients and to investigate CPPopt in relation to CBF.MethodsRetrospective study of prospectively collected data. CBF was measured bedside with Xenon-enhanced CT (Xe-CT). The difference between actual CPP and CPPopt was calculated (CPP∆). Correlations between CPP∆ and CBF parameters were calculated with Spearman’s rank order correlation coefficient (rho). Separate calculations were done using all patients (day 0–14 after onset) as well as in two subgroups (day 0–3 and day 4–14).ResultsEighty-two patients with 145 Xe-CT scans were studied. Automated calculation of CPPopt was possible in adjunct to 60% of the Xe-CT scans. Actual CPP < CPPopt was associated with higher numbers of low-flow regions (CBF <10 ml/100 g/min) in both the early phase (day 0–3, n = 39, Spearman’s rho = −0.38, p = 0.02) and late acute phase of the disease (day 4–14, n = 35, Spearman’s rho = −0.39, p = 0.02). CPP level per se was not associated with CBF.ConclusionsCalculation of CPPopt is possible in a majority of patients with severe SAH. Actual CPP below CPPopt is associated with low CBF.

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“…The management goal is then to keep the mean ICP <20-25 mmHg [1,7], or the mean ICP wave amplitude (MWA) <5 mmHg [5]. In an attempt to characterize the intracranial pressure-volume compensatory reserve capacity some authors have in addition calculated ICP-derived indices [6,8,9]. An index measuring the correlation coefficient (R) between the ICP wave amplitude (A) and the mean ICP (P) level (referred to as RAP) has thus been applied in the surveillance of patient groups such as those suffering from traumatic brain injury (TBI), cerebral bleeds or hydrocephalus [8,10-12].…”

Section: Introductionmentioning

confidence: 99%

An intracranial pressure-derived index monitored simultaneously from two separate sensors in patients with cerebral bleeds: comparison of findings

Eide

Sorteberg

2013

BioMedical Engineering OnLine

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BackgroundIn an attempt to characterize the intracranial pressure-volume compensatory reserve capacity, the correlation coefficient (R) between the ICP wave amplitude (A) and the ICP (P) level (RAP) has been applied in the surveillance of neurosurgical patients. However, as the ICP level may become altered by electrostatic discharges, human factors, technical factors and technology issues related to the ICP sensors, erroneous ICP scores may become revealed to the physician, and also become incorporated into the calculated RAP index. To evaluate the problem with regard to the RAP, we compared simultaneous RAP values from two separate ICP signals in the same patient.Materials and MethodsWe retrieved our recordings in 20 patients with cerebral bleeds wherein the ICP had been recorded simultaneously from two different sensors. Sensor 1 was always a solid sensor while sensor 2 was a solid sensor (Category A), a fluid sensor (Category B), an air-pouch sensor (Category C), or a fibre-optic sensor (Category D). The simultaneous signals were analyzed with automatic identification of the cardiac induced ICP waves, with subsequent determination and comparison of the Pearson correlation coefficient between mean wave amplitude (MWA) and mean ICP (RAP) for 40 6-s time windows every 4-min period.ResultsA total of 23,056 4-min RAP observations were compared. A difference in RAP ≥0.4 between the two signals was seen in 4% of the observations in Category A-, in 44% of observations in Category B -, in 20% of observations in Category C -, and in 28% of observations in Category D patients, respectively. Moreover, the combination of a RAP of <0.6 in one signal and ≥0.6 in the other was seen in >20% of scores in 3/5 Category A -, in 3/5 Category B -, in 5/7 Category C - and 1/3 Category D patients.ConclusionsSimultaneous monitoring of the ICP-derived index RAP from two separate ICP sensors reveals marked differences in the index values. These differences in RAP may be explained by erroneous scoring of the ICP level. This will hamper the usefulness of RAP as a guide in the management of neurosurgical patients.

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Pressure-derived versus pressure wave amplitude–derived indices of cerebrovascular pressure reactivity in relation to early clinical state and 12-month outcome following aneurysmal subarachnoid hemorrhage

Cited by 56 publications

References 50 publications

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage

Increased risk of critical CBF levels in SAH patients with actual CPP below calculated optimal CPP

An intracranial pressure-derived index monitored simultaneously from two separate sensors in patients with cerebral bleeds: comparison of findings

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