Neurocrit Care DOI 10.1007/s12028-014-0046-0

REVIEW ARTICLE

Monitoring of Cerebral Autoregulation Marek Czosnyka • Chad Miller • The Participants in the International Multidisciplinary Consensus Conference on Multimodality Monitoring

Ó Springer Science+Business Media New York 2014

Abstract Pressure autoregulation is an important hemodynamic mechanism that protects the brain against inappropriate fluctuations in cerebral blood flow in the face of changing cerebral perfusion pressure (CPP). Static autoregulation represents how far cerebrovascular resistance changes when CPP varies, and dynamic autoregulation represents how fast these changes happen. Both have been monitored in the setting of neurocritical care to aid prognostication and contribute to individualizing CPP targets in patients. Failure of autoregulation is associated with a worse outcome in various acute neurological diseases. Several studies have used transcranial Doppler ultrasound, intracranial pressure (ICP with vascular reactivity as surrogate measure of autoregulation), and nearinfrared spectroscopy to continuously monitor the impact of spontaneous fluctuations in CPP on cerebrovascular physiology and to calculate derived variables of autoregulatory efficiency. Many patients who undergo such monitoring demonstrate a range of CPP in which autoregulatory efficiency is optimal. Management of patients at or near this optimal level of CPP is associated with

The Participants in the International Multidisciplinary Consensus Conference on Multimodality Monitoring are listed in ‘‘Appendix’’. M. Czosnyka (&) Department of Clinical Neurosciences, Division of Neurosurgery, University of Cambridge, Addenbrooke’s Hospital, Box 167, Cambridge CB2 2QQ, UK e-mail: [email protected] C. Miller Department of Neurology and Neurosurgery, Wexner Medical Center at the Ohio State University, Columbus, OH, USA

better outcomes in traumatic brain injury. Many of these studies have utilized the concept of the pressure reactivity index, a correlation coefficient between ICP and mean arterial pressure. While further studies are needed, these data suggest that monitoring of autoregulation could aid prognostication and may help identify optimal CPP levels in individual patients. Keywords Autoregulation  Pressure reactivity  Cerebral perfusion pressure  Transcranial doppler ultrasound  Near-infrared spectroscopy  Cerebral blood flow

Introduction As long as autoregulation remains intact, the brain can protect itself against inappropriate blood flow, regardless of the level of cerebral perfusion pressure (CPP). Patients requiring neurocritical care may suffer from multifactorial insults, and abnormal vascular physiology is only a part of the overall scenario that leads to a cascade of possible complications [1]. Functionality of cerebral autoregulation governs multiple mechanisms of secondary injury including ischemia, hyperemia, intracranial hypertension, and hypoxia. Static and dynamic autoregulation both refer to regulation of brain vasculature to maintain constant CBF. Static autoregulation describes the extent to which the cerebrovascular bed can constrict or dilate when CPP varies. Dynamic autoregulation also incorporates information on the rate at which such adaptive changes in cerebrovascular resistance occur [2]. Both components are mutually correlated in most clinical scenarios [3]. Pressure reactivity can be derived from changes in cerebral blood volume as a surrogate for true autoregulation. In the patient

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with poor intracranial compliance, changes in vessel caliber (and hence cerebral blood volume) drive changes in intracranial pressure (ICP), and the dynamic relationship between ICP and MAP can serve as an indicator of cerebrovascular pressure reactivity (PRx) and hence provide information about autoregulation [4]. There is a general agreement that autoregulation is one of the most important intrinsic CNS auto-protective mechanisms. However, in management of neurocritically ill patients, autoregulation has never been widely included in independent monitoring protocols. Historically, a lack of dedicated autoregulation monitoring systems has contributed to this exclusion, but recent technological improvements merit reconsideration of the issue.

Methods This systematic review was performed according to the preferred reporting items for systematic reviews and metaanalyses (PRISMA) statement.

Search Criteria Using the PubMed database, we conducted a systematic review through September 2013. The search strategy used the following terms: autoregulation or vascular reactivity, monitoring, and intensive care or critical care. A total of 430 papers were identified, of which 67 were deemed by the authors as worthy of further screening. Finally, 56 were considered relevant for the consensus statement. We restricted the article language to English, and unpublished data or congressional presentations/abstracts were not considered, nor were animal experiments. Studies were considered eligible based on the PICO approach. After selection, the evidence was classified and practical recommendations developed according to the GRADE system.

Review End-Points The end-points of this review were to answer the following questions: 1.

2. 3.

Which neuromonitor and which methodology most reliably evaluates the state of autoregulation in neurocritical care? Does impairment of autoregulation complicate clinical course or lead to poor outcome? Does therapy that considers the state of autoregulation impact outcome?

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Summary of the Literature Technique Autoregulation following traumatic brain injury (TBI) may vary in a relatively short-time scale, therefore continuous or fast sequential monitoring is essential to capture these changes. The modalities which respond dynamically to spontaneous changes in arterial blood pressure or CPP and contain strong (direct or indirect) descriptors of cerebral blood flow/cerebral blood volume can be considered for use in this context. Examples of such monitors include ultrasound transcranial Doppler (TCD) that measures blood flow velocity [5], ICP [4, 6], and brain tissue oxygen content (direct—monitored with parenchymal probe (PbtO2) [7], or indirect—using near-infrared spectroscopy (NIRS)) [8]. Less frequently used are laser Doppler flowmetry (LDF) [9] and thermal dilution regional cerebral blood flow (td-rCBF) [10]. However, for many modalities, evidence for feasibility of clinical application is not yet fully documented. Continuous monitoring is preferred to intermittent assessments given the variability of autoregulation indices over time. Nevertheless, intermittent tests, like leg cuff deflation [11] and the transient hyperemic response test [12] are sufficiently documented as useful in the neurocritical management. Continuous methods describing the response of blood flow-related variables to spontaneous slow fluctuations in arterial blood pressure (preferred frequency range from 0.007 to 0.05 Hz) are based on the transfer function analysis and modeling of impulse response [13] or correlation methodology [5]. Difficulty in interpreting cerebral autoregulation data arises from the lack of standardized methods used for its assessment. Variability in monitoring modalities (ICP, TCD, PbtO2, NIRS, LDF, td-rCBF) and different calculation algorithms, modes of filtration of input/output signals, time windows used for signal processing, and artifact exclusion, have resulted in occasional conflicting results. Comparisons between the approaches and methods used in various centers are sparse, with significant, but only moderately strong correlations seen in the existing studies [14, 15]. The preponderance of data favors the correlation coefficient method, relying on monitoring ICP and ABP and calculating the pressure reactivity index (PRx) as a correlation coefficient between 10-s-averaged ICP and ABP over time window of 5 min. This approach has been validated using PET imaging, showing a good correlation with the static rate of autoregulation assessed using PET and oxygen extraction fraction (OEF), i.e., the de facto gold standard [16, 17]. It has also been validated by direct comparison to lower limit of autoregulation assessed with laser LDF in experimental arterial hypotension [15].

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Outcome There is observational evidence that impaired cerebral autoregulation is independently associated with worsened outcomes (Glasgow Outcome Score) in the early stages of treatment after TBI [9, 18–22]. In subarachnoid hemorrhage (SAH) patients, cerebral dysautoregulation which precedes vasospasm is predictive of observed delayed ischemic deficit [23, 24]. Autoregulation failure contributes independently to unfavorable outcome after SAH [25, 26]. In the largest observational cohort studies (>100 patients, these are restricted to TBI patients), a deranged pressure reactivity index correlated with fatal outcome, while an autoregulation index, derived from TCD blood flow velocity, differentiated between favorable and unfavorable clinical outcome [14, 22, 27]. Critical autoregulatory thresholds for survival and favorable neurological outcome may be different and may vary with age and gender [24]. Cerebrovascular reactivity deteriorates with age, potentially contributing to the overall worse outcomes observed in elderly patients [28]. Similarly, intermittent tests like the leg cuff release [11] or the transient hyperemic response test [12] have shown that dysautoregulation is associated with worse outcome. Continuous autoregulation indices can provide explanations for ICP elevation: e.g., plateau waves or refractory intracranial hypertension [29]. Cerebral autoregulation correlates with brain biochemistry findings determined with cerebral microdialysis [30, 31]. Changes in cerebral autoregulation have also been documented during therapeutic maneuvers: modulation of CPP [32], hypothermia and re-warming [33], change in ventilation [34], use of mannitol or hypertonic saline, barbiturates [35], and various anesthetic agents [36]. Furthermore, the average time course of autoregulation change has been described, suggesting that dysautoregulation is most commonly observed within the first days following injury. [4, 37].

Autoregulation guided management One management protocol has been derived with specific consideration of cerebral autoregulation. It relays on the concept of ‘optimal CPP’ [38] –identifying the value of CPP that maximizes the strength of cerebrovascular reactivity (or cerebral autoregulation). Retrospective analyses suggest that CPP below the ‘optimal’ level increases the incidence of fatal outcome, while too high CPP levels associate with the increased rate of severe disability [39]. Patients with CPP close to the optimal level are more likely to experience favorable outcome. Optimal CPP calculated based on PRx in TBI showed that the level of ‘optimal’ CPP varies from 65 to 95 mm Hg in 300 patients (with total mean value 75 mmHg). Furthermore, values of

optimal CPP were patient- and time- dependent, supporting the need for its continuous monitoring in the neurocritcal care setting. While these results provide a rational basis for targeting optimal CPP, there have been no prospective studies of CPP management using ‘autoregulation-optimal’ targets in head injury. In prospectively investigated patients requiring neurocritical care after SAH, CPP below the optimal level was associated with significantly worse outcome [40]. Optimization of CPP has been also documented using direct brain tissue oxygen monitoring [20]. Similar studies have been conducted using near-infrared spectroscopy indices in both adults [8] and neonates [41].

Discussion The state of autoregulation has an impact on prognosis and CPP management. Patients are able to tolerate fluctuations in CPP when they are on the autoregulatory plateau. The correlation of dysautoregulation with clinical outcome raises the issue of whether autoregulation can be therapeutically manipulated to improve recovery. This hypothesis has never been tested prospectively. The use of autoregulation-targeted management is not feasible without continuous assessment of the state of autoregulation as a part of multimodal brain monitoring. Elements of popular therapies used in neurocrital care units are also directed at disordered autoregulation. These include use of vasopressors to elevate inadequate CPP, reduction of raised ICP with optimized sedation and ventilation, use of hyperosmotic agents, and cerebral metabolic suppression. Other therapeutic interventions with the potential to modify autoregulation have been tested in SAH (e.g., statins [42] ) but not in TBI. Autoregulation and pressure reactivity can be measured episodically, but a continuous bedside monitoring may be more useful. Continuous TCD is limited by the lack of reliable long-term probe holders. NIRS is more promising, but still needs technical refinement, particularly in terms of maximizing signal-to-noise ratio [15]. Pressure reactivity index appears to be less difficult and consistently robust, making it suitable for long-term monitoring. PRx has been validated experimentally [43]. Lee and colleagues showed that breaching lower limits of autoregulation determined by laser LDF was associated with significant increase of PRx (AUC = 0.88) in a model of arterial hypotension. Positive correlation of PRx versus PET-derived static rate of autoregulation has been also demonstrated in TBI patients [16]. Monitoring of autoregulation through pressure reactivity and ICP relationships following decompressive craniectomy is also possible. In these conditions, PRx is clinically useful if it is clearly positive and indicates deranged vascular reactivity. PRx around zero may be less informative,

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especially in the patient with a generously compliant intracranial cavity after skull opening. The concept of optimal CPP seems to be well-founded, but its implementation as a therapeutic target is not (as yet) supported by prospective randomized studies. Pressure reactivity monitoring with continuous ICP/MAP analysis or NIRS—derived tissue oxygenation is easy to perform at the bedside. Examining the relationship of PRx monitoring during varying CPP provides a physiologically rational target for CPP optimization, which estimates CPP level equally distanced from the lower and upper limits of autoregulation. We believe that autoregulation assessment should have a place in clinical practice. We propose a tiered approach to monitoring, taking into account scientific, practical, and financial capabilities. Pressure reactivity can be properly estimated even with limited resources and low-cost instruments. We support the view that it can be used to extract more information, even from a standard monitoring algorithm. Future research in this area should focus on selective measures to manage disturbed cerebral autoregulation (drugs, pressure support, ventilation, etc.), prospective studies on optimal CPP/MAP-oriented therapies in various diseases and age groups, and the feasibility of non-invasive methodology (based on NIRS, TCD with more efficient probe holders) to follow optimal MAP.

Recommendations

No Recommendation

Strength

1

We suggest that monitoring and Weak recommendation, assessment of autoregulation Moderate quality of may be useful in broad targeting evidence of cerebral perfusion management goals and prognostication in acute brain injury

2

Continuous bedside monitoring of Weak recommendation, autoregulation is now feasible, Moderate quality of and we suggest that should be evidence considered as a part of multimodality monitoring. Measurement of pressure reactivity has been commonly used for this purpose, but many different approaches may be equally valid. Additional Conclusions



Given the absence of a proven Low level of evidence method to target CPP in individual patients, CPPopt (the CPP level or range at which PRx is minimal) may help in individualizing CPP therapy

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Conflict of interest Most of autoregulation monitoring methods is encapsulated in ICM+ software (www.neurosurg.cam.ac.uk/ icmplus), licensed by Cambridge Enterprise Ltd, UK. MC has a financial interest in a fraction (10%) of licensing fee.

Appendix: Participants in the International Multidisciplinary Consensus Conference on Multimodality Monitoring Peter Le Roux, MD, FACS, Brain and Spine Center, Lankenau Medical Center, Suite 370, Medical Science Building, 100 East Lancaster Avenue, Wynnewood, PA 19096, USA. Tel: +1 610 642 3005; Fax: 610 642 3057 [email protected] David K Menon MD PhD FRCP FRCA FFICM FMedSci Head, Division of Anaesthesia, University of Cambridge Consultant, Neurosciences Critical Care Unit Box 93, Addenbrooke’s Hospital, Cambridge CB2 2QQ, UK [email protected] Paul Vespa, MD, FCCM, FAAN, FNCS Professor of Neurology and Neurosurgery Director of Neurocritical Care David Geffen School of Medicine at UCLA Los Angeles, CA 90095, USA [email protected] Giuseppe Citerio, Director NeuroIntensive Care Unit, Department of Anesthesia and Critical Care Ospedale San Gerardo, Monza. Via Pergolesi 33, Monza 20900, Italy [email protected] Mary Kay Bader RN, MSN, CCNS, FAHA, FNCS Neuro/Critical Care CNS Mission Hospital Mission Viejo CA 92691, USA [email protected] Gretchen M. Brophy, PharmD, BCPS, FCCP, FCCM Professor of Pharmacotherapy & Outcomes Science and Neurosurgery Virginia Commonwealth University Medical College of Virginia Campus 410 N. 12th Street Richmond, Virginia 23298-0533 USA [email protected]

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Michael N. Diringer, MD Professor of Neurology, Neurosurgery & Anesthesiology Chief, Neurocritical Care Section Washington University Dept. of Neurology, Campus Box 8111 660 S Euclid Ave St Louis, MO 63110 USA [email protected] Nino Stocchetti, MD Professor of Anesthesia and Intensive Care Department of physiopathology and transplant, Milan University Director Neuro ICU Fondazione IRCCS Ca` Granda Ospedale Maggiore Policlinico Via F Sforza, 35 20122 Milan Italy e-mail [email protected] Walter Videtta, MD ICU Neurocritical Care Hospital Nacional ‘Prof. a. Posadas’ El Palomar - Pcia. de Buenos Aires Argentina [email protected] Rocco Armonda, MD Department of Neurosurgery MedStar Georgetown University Hospital Medstar Health, 3800 Reservoir Road NW Washington DC 20007 USA [email protected] Neeraj Badjatia, MD Department of Neurology University of Maryland Medical Center, 22 S Greene St Baltimore, MD, 21201 USA [email protected] Julian Boesel, MD Department of Neurology Ruprect-Karls University Hospital Heidelberg, Im Neuenheimer Feld 400, D-69120 Heidelberg, Germany [email protected] Randal Chesnut, MD, FCCM, FACS Harborview Medical Center, University of Washington Mailstop 359766 325 Ninth Ave, Seattle WA 98104-2499

USA [email protected] Sherry Chou, MD, MMSc Department of Neurology, Brigham and Women’s Hospital 75 Francis Street, Boston MA 02115 USA [email protected] Jan Claassen, MD, PhD, FNCS Assistant Professor of Neurology and Neurosurgery Head of Neurocritical Care and Medical Director of the Neurological Intensive Care Unit Columbia University College of Physicians & Surgeons 177 Fort Washington Avenue, Milstein 8 Center room 300, New York, NY 10032 USA [email protected] Marek Czosnyka, PhD Professor of Brain Physics Department of Clinical Neurosciences University of Cambridge, Addenbrooke’s Hospital, Box 167 Cambridge, CB20QQ United Kingdom [email protected] Michael De Georgia, MD Professor of Neurology Director, Neurocritical Care Center Co-Director, Cerebrovascular Center University Hospital Case Medical Center Case Western Reserve University School of Medicine 11100 Euclid Avenue Cleveland, Ohio 44106 [email protected] Anthony Figaji, MD, PhD Head of Pediatric Neurosurgery University of Cape Town 617 Institute for Child Health Red Cross Children’s Hospital Rondebosch, 7700 Cape Town, South Africa [email protected] Jennifer Fugate, DO Department of Neurology, Mayo Clinic, 200 First Street SW Rochester, MN 55905 [email protected]

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N Lake Shore Drive, 11th floor Chicago, IL 60611 [email protected]

Raimund Helbok, MD, PD Department of Neurology, Neurocritical Care Unit Innsbruck Medical University, Anichstr.35, 6020 Innsbruck, Austria [email protected]

Mauro Oddo, MD Department of Intensive Care Medicine CHUV University Hospital, BH 08-623 Faculty of Biology and Medicine University of Lausanne 1011 Lausanne, Switzerland [email protected]

David Horowitz, MD Associate Chief Medical Officer University of Pennsylvania Health System, 3701 Market Street Philadelphia, PA, 19104 USA [email protected]

DaiWai Olson, RN, PhD Associate Professor of Neurology, Neurotherapeutics and Neurosurgery University of Texas Southwestern 5323 Harry Hines Blvd. Dallas, TX 75390-8897 USA [email protected]

Peter Hutchinson, MD Professor of Neurosurgery NIHR Research Professor Department of Clinical Neurosciences University of Cambridge Box 167 Addenbrooke’s Hospital Cambridge CB2 2QQ United Kingdom [email protected] Monisha Kumar, MD Department of Neurology Perelman School of Medicine, Pennsylvania, 3 West Gates 3400 Spruce Street Philadelphia, PA, 19104 USA [email protected]

University

of

Molly McNett, RN, PhD Director, Nursing Research The MetroHealth System 2500 MetroHealth Drive, Cleveland, OH 44109 USA [email protected] Chad Miller, MD Division of Cerebrovascular Diseases and Neurocritical Care The Ohio State University 395 W. 12th Ave, 7th Floor Columbus, OH 43210 [email protected] Andrew Naidech, MD, MSPH Department of Neurology Northwestern University Feinberg SOM 710

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Kristine O’Phelan M.D. Director of Neurocritical Care Associate Professor, Department of Neurology University of Miami, Miller School of Medicine JMH, 1611 NW 12th Ave, Suite 405 Miami, FL, 33136 USA [email protected] Javier Provencio, MD Associate Professor of Medicine Cerebrovascular Center and Neuroinflammation Research Center Lerner College of Medicine Cleveland Clinic, 9500 Euclid Ave, NC30 Cleveland, OH 44195 USA [email protected] Corina Puppo, MD Assistant Professor, Intensive Care Unit, Hospital de Clinicas, Universidad de la Repu´blica, Montevideo Uruguay [email protected] Richard Riker, MD Critical Care Medicine Maine Medical Center, 22 Bramhall Street Portland, Maine 04102-3175 USA [email protected]

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Claudia Robertson, MD Department of Neurosurgery Medical Director of Center for Neurosurgical Intensive Care, Ben Taub Hospital Baylor College of Medicine, 1504 Taub Loop, Houston, TX 77030 USA [email protected]

9.

10.

11.

J. Michael Schmidt, PhD, MSc Director of Neuro-ICU Monitoring and Informatics Columbia University College of Physicians and Surgeons Milstein Hospital 8 Garden South, Suite 331 177 Fort Washington Avenue, New York, NY 10032 USA [email protected] Fabio Taccone, MD Department of Intensive Care, Laboratoire de Recherche Experimentale Erasme Hospital, Route de Lennik, 808 1070 Brussels Belgium [email protected]

12.

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Monitoring of cerebral autoregulation.

Pressure autoregulation is an important hemodynamic mechanism that protects the brain against inappropriate fluctuations in cerebral blood flow in the...
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