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

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          Abstract

          Background

          Cerebral 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.

          Methods

          Retrospective 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).

          Results

          Eighty-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.

          Conclusions

          Calculation 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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          Most cited references26

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          Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury.

          To define optimal cerebral perfusion pressure (CPPOPT) in individual head-injured patients using continuous monitoring of cerebrovascular pressure reactivity. To test the hypothesis that patients with poor outcome were managed at a cerebral perfusion pressure (CPP) differing more from their CPPOPT than were patients with good outcome. Retrospective analysis of prospectively collected data. Neurosciences critical care unit of a university hospital. A total of 114 head-injured patients admitted between January 1997 and August 2000 with continuous monitoring of mean arterial blood pressure (MAP) and intracranial pressure (ICP). MAP, ICP, and CPP were continuously recorded and a pressure reactivity index (PRx) was calculated online. PRx is the moving correlation coefficient recorded over 4-min periods between averaged values (6-sec periods) of MAP and ICP representing cerebrovascular pressure reactivity. When cerebrovascular reactivity is intact, PRx has negative or zero values, otherwise PRx is positive. Outcome was assessed at 6 months using the Glasgow Outcome Scale. A total of 13,633 hrs of data were recorded. CPPOPT was defined as the CPP where PRx reaches its minimum value when plotted against CPP. Identification of CPPOPT was possible in 68 patients (60%). In 22 patients (27%), CPPOPT was not found because it presumably lay outside the studied range of CPP. Patients' outcome correlated with the difference between CPP and CPPOPT for patients who were managed on average below CPPOPT (r =.53, p <.001) and for patients whose mean CPP was above CPPOPT (r = -.40, p <.05). CPPOPT could be identified in a majority of patients. Patients with a mean CPP close to CPPOPT were more likely to have a favorable outcome than those whose mean CPP was more different from CPPOPT. We propose use of the criterion of minimal achievable PRx to guide future trials of CPP oriented treatment in head injured patients.
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            Impairment of cerebral autoregulation predicts delayed cerebral ischemia after subarachnoid hemorrhage: a prospective observational study.

            Delayed cerebral ischemia (DCI) is a recognized contributor to unfavorable outcome after subarachnoid hemorrhage (SAH). Recent data challenge the concept of vasospasm as the sole cause of ischemia and suggest a multifactorial process with dysfunctional cerebral autoregulation as a component. We tested the hypothesis that early autoregulatory failure, detected using near-infrared spectroscopy-based index, TOxa and transcranial Doppler-based index, Sxa, can predict DCI. In this prospective observational study we enrolled consecutive patients with aneurysmal SAH that occurred <5 days from admission. The primary end point was the occurrence of DCI within 21 days of ictus. The predictive value of autoregulatory disturbances detected in the first 5 days was assessed using univarate proportional hazards model and a multivariate model. Ninety-eight patients were included. Univariate analysis demonstrated increased odds of developing DCI when early autoregulation failure was detected (odds ratio [OR], 7.46; 95% confidence interval [CI], 3.03-18.40 and OR, 4.52; 95% CI, 1.84-11.07 for Sxa and TOxa, respectively) but not TCD-vasospasm (OR, 1.36; 95% CI, 0.56-3.33). In a multivariate model Sxa and TOxa remained independent predictors of DCI (OR, 12.66; 95% CI, 2.97-54.07 and OR, 5.34; 95% CI, 1.25-22.84 for Sxa and TOxa, respectively). Disturbed autoregulation in the first 5 days after SAH significantly increases the risk of DCI. Autoregulatory disturbances can be detected using near-infrared spectroscopy and transcranial Doppler technologies.
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              Predictors of cerebral infarction in aneurysmal subarachnoid hemorrhage.

              Clinical and radiologic predictors of cerebral infarction occurrence and location after aneurysmal subarachnoid hemorrhage have been seldom studied. We evaluated all patients admitted to our hospital with aneurysmal subarachnoid hemorrhage between 1998 and 2000. Cerebral infarction was defined as a new hypodensity located in a vascular distribution on computed tomography (CT) scan. Fifty-seven of 143 patients (40%) developed a cerebral infarction. On univariate analysis, occurrence of cerebral infarction was associated with a worse World Federation of Neurological Surgeons grade (P=0.01), use of ventriculostomy catheter (P=0.01), preoperative vasospasm (P=0.03), surgical clipping (P=0.02), symptomatic vasospasm (P<0.01), and vasospasm on transcranial Doppler ultrasonography (TCD) or repeat angiogram (P<0.01). On multivariable analysis, only presence of symptoms ascribed to vasospasm (P<0.01) and evidence of vasospasm on TCD or angiogram predicted cerebral infarction (P<0.01). TCD and angiogram agreed on the diagnosis of vasospasm in 73% of cases (95% CI, 63% to 81%), but the diagnostic accuracy of this combination of tests was suboptimal for the prediction of cerebral infarction occurrence (sensitivity, 0.72; specificity, 0.68; positive predictive value, 0.67; negative predictive value, 0.72). Location of the cerebral infarction on delayed CT was predicted by neurological symptoms in 74%, by aneurysm location in 77%, and by angiographic vasospasm in 67%. Evidence of vasospasm on TCD and angiogram is predictive of cerebral infarction on CT scan but sensitivity and specificity are suboptimal. Cerebral infarction location cannot be predicted in one quarter to one third of patients by any of the studied clinical or radiological variables.
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                Author and article information

                Contributors
                +46(0)186110000 , Ulf.johnson@neuro.uu.se
                Journal
                Acta Neurochir (Wien)
                Acta Neurochir (Wien)
                Acta Neurochirurgica
                Springer Vienna (Vienna )
                0001-6268
                0942-0940
                30 March 2017
                30 March 2017
                2017
                : 159
                : 6
                : 1065-1071
                Affiliations
                [1 ]ISNI 0000 0004 1936 9457, GRID grid.8993.b, Department of Neuroscience/Neurosurgery, , Uppsala University, ; S-75185 Uppsala, Sweden
                [2 ]ISNI 0000 0004 1936 9457, GRID grid.8993.b, Department of Surgical sciences/Radiology, , Uppsala University, ; Uppsala, Sweden
                [3 ]ISNI 0000 0004 1936 9457, GRID grid.8993.b, Department of Surgical sciences/Anaesthesia and Intensive care, , Uppsala University, ; Uppsala, Sweden
                Article
                3139
                10.1007/s00701-017-3139-7
                5425502
                28361248
                a439d7eb-4327-4abf-a403-c8324aed65c4
                © The Author(s) 2017

                Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

                History
                : 4 December 2016
                : 27 February 2017
                Funding
                Funded by: Uppsala University
                Categories
                Original Article - Vascular
                Custom metadata
                © Springer-Verlag Wien 2017

                Surgery
                subarachnoid hemorrhage,sah,cerebral blood flow,cbf,autoregulation,optimal,cerebral perfusion pressure,cppopt,neurointensive care

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