Neuromonitoring Techniques: Quick Guide for Clinicians and Residents

Neuromonitoring Techniques

Quick Guide for Clinicians and Residents

Editor

Hemanshu Prabhakar

Department of Neuroanaesthesiology and Critical Care, All India Institute of Medical Sciences (AIIMS), Ansari Nagar, New Delhi, Delhi, India

Table of Contents

Cover image

Title page

Copyright

Dedication

Contributors

Foreword

Preface

Acknowledgment

Introduction to Monitoring Techniques

Chapter 1. Intracranial Pressure Monitoring

Introduction

Pathophysiology

Invasive ICP

Noninvasive ICP

Invasive Readings and Interpretation

Effect of Anesthetics on Intracranial Pressure

Current Evidence, Applications, and Discussion

Suggested Readings

Chapter 2. Cerebral Blood Flow Monitoring

Introduction

Cerebral Metabolic Parameters

Autoregulation

Importance of CBF Monitoring

CBF Monitoring

Future Directions

Chapter 3. Jugular Venous Oximetry

Introduction

Basic Principles

Understanding the Equipment

Indications and Contraindications

Readings and Interpretation

Effect of Anesthetics

Advantages and Disadvantages

Summary

Suggested Readings

Chapter 4. Electroencephalography-Based Monitors

Introduction

Basic Principles

Understanding the Equipment

Indications and Contraindications

Readings and Interpretation

Effect of Anesthetics

Advantages and Disadvantages

Current Opinion

Suggested Readings

Chapter 5. Transcranial Doppler Ultrasonography

Introduction

Basic Principles

Understanding the Equipment

Performing TCD Examination

Readings and Interpretation

Clinical Applications of TCD Ultrasonography

Effect of Anesthetics

Advantages and Disadvantages

Current Opinion

Chapter 6. Evoked Response Monitoring

Introduction

Basic Principles

Understanding the Equipment

Indications and Contraindications

Effect of Anesthetics

Readings and Interpretation

Advantages and Disadvantages

Current Evidence

Conclusion

Suggested Readings

Chapter 7. Near-Infrared Spectroscopy

Introduction

Physical Principles

Types of Near-Infrared Spectroscopy Systems

Near-Infrared Spectroscopy Devices

Quantitative and Nonquantitative Near-Infrared Spectroscopy

Indications

Reading and Interpretation: The Montreal Heart Institute Algorithm

Effects of Anesthetics

Advantages of Near-Infrared Spectroscopy

Limitations of Near-Infrared Spectroscopy

Current Opinion: Role in Various Situations

Conclusion and Future Developments

Suggested Readings

Abbreviations

Chapter 8. Brain Microdialysis

Introduction

Basic Principles

Understanding the Equipment

Indications and Contraindications

Neurocritical Care

Effects on Anesthetics

Advantages and Disadvantages

Current Opinion

Suggested Reading

Appendix

Chapter 9. Brain Tissue Oxygenation

Introduction

Basic Principles

Understanding the Equipment

Indications and Contraindications

Readings and Interpretation

Effect of Anesthetics

Advantages and Disadvantages

Current Evidence

Suggested Readings

Chapter 10. Cognitive Function Monitoring

Timing, or When to Start?

Diagnostic Tools

Tools to Assess in the Early Postoperative Period

Riker Agitation–Sedation Scale

Perioperative Neuropsychological Testing

Conclusion

Chapter 11. Functional MR Imaging

History of Functional Magnetic Resonance Imaging

What Is Functional Magnetic Resonance Imaging?

Practical Aspects of Functional Magnetic Resonance Imaging: How Is the Data Collected

How Is an Functional Magnetic Resonance Imaging Carried Out?

Other Signals Studied in Functional Magnetic Resonance Imaging

Functional Magnetic Resonance Imaging Studies

Functional Magnetic Resonance Imaging Data Analysis

Functional Magnetic Resonance Imaging Anesthesia Studies

Cortical Effects of Anesthesia

Connectivity

Functional Magnetic Resonance Imaging in Clinical Practice

Index

Copyright

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Notices

Knowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility.

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Dedication

Dedicated to my parents and the ones with whom I have always shared childhood memories and dreams of my future, Hemant and Sunil Saraswat.

Contributors

Aymen Benkreira

Montreal Heart Institute, Montreal, QC, Canada

Sherbrooke University, Sherbrooke, QC, Canada

Federico Bilotta,     Sapienza University of Rome, Rome, Italy

Vincent Bonhomme

CHU University Hospital of Liege, Liege, Belgium

GIGA - Consciousness, Anesthesia and Intensive Care Laboratory, University and CHU University Hospital of Liege, Belgium

CHR Citadelle, Liege, Belgium

Anastasia Borozdina,     First Moscow Medical University named after I.M. Sechenov.Petrovsky National Research Center of Surgery, Moscow, Russia

Nophanan Chaikittisilpa,     University of Washington, Seattle, WA, United States

Alexis Cournoyer

Université de Montréal, Montreal, QC, Canada

Hôpital du Sacré-Coeur de Montreal, Montreal, QC, Canada

Montreal Heart Institute, Montreal, QC, Canada

Nadine Cueni,     University Hospital Basel, Basel, Switzerland

Aline Defresne

CHU University Hospital of Liege, Liege, Belgium

GIGA - Consciousness, Anesthesia and Intensive Care Laboratory, University and CHU University Hospital of Liege, Belgium

CHR Citadelle, Liege, Belgium

André Y. Denault,     Université de Montréal, Montreal, QC, Canada

Lis Evered,     University of Melbourne, Melbourne, VIC, Australia

Colette Franssen,     CHU University Hospital of Liege, Liege, Belgium

Alexa Hollinger,     University Hospital Basel, Basel, Switzerland

Michael L. James,     Duke University, Durham, NC, United States

Antoun Koht,     Northwestern University Feinberg School of Medicine, Chicago, IL, United States

Abhijit V. Lele,     University of Washington, Seattle, WA, United States

Tanya Mailhot,     Université de Montréal, Montreal, QC, Canada

Basil Matta,     Cambridge University Hospitals NHS Foundation, Cambridge, United Kingdom

Marc McLawhorn,     Duke University, Durham, NC, United States

Hemanshu Prabhakar,     AIIMS, New Delhi, India

Ramachandran Ramani,     University of Florida College of Medicine, Gainesville, FL, United States

Frank Rasulo,     University of Brescia at Spedali Civili Hospital, Brescia, Italy

Chiara Robba,     Addenbrooke's Hospital, Cambridge, United Kingdom

Mohamed Shaaban-Ali,     Assiut University, Assiut, Egypt

Deepak Sharma,     University of Washington, Seattle, WA, United States

Martin Siegemund,     University Hospital Basel, Basel, Switzerland

Tod B. Sloan,     University of Colorado School of Medicine, Aurora, CO, United States

Luzius A. Steiner,     University Hospital Basel, Basel, Switzerland

Gabriel Tran

CHU University Hospital of Liege, Liege, Belgium

GIGA - Consciousness, Anesthesia and Intensive Care Laboratory, University and CHU University Hospital of Liege, Belgium

Niccoló Varanini,     University of Brescia at Spedali Civili Hospital, Brescia, Italy

Monica S. Vavilala,     University of Washington, Seattle, WA, United States

Foreword

I first became interested in neuroanesthesia during my residency at New York Hospital during the 1960s. Thus, I can recount the state of monitoring those 6  decades ago, within living memory, that is, my memory. The department, which had only very recently become independent, and no longer a division of the much larger department of surgery, owned about six bullets: cylindrical, free-standing devices that continuously recorded the ECG on a screen about eight inches across through three leads with needles that pierced the patient's skin. As a resident, one had to get to the operating room early to lay claim to such a monitor. Most rooms had a separate, nonautomatic blood pressure machine. For the rest, we counted respirations, felt the hands to estimate temperature, and looked at the pupils (if accessible) to gauge depth of anesthesia. The chair of neurosurgery, Professor Bronson Ray, preferred the use of ether, which he claimed allowed the maintenance of spontaneous respiration during craniotomies. All well and good, but he also used cautery, which meant we had to drape the anesthetic machine and ourselves, especially our feet, in wet towels. His anesthesiologist, Professor Alan Van Poznack, distracted himself from these harsh conditions by making whistles out of syringes.

Now, as I look at Dr. Prabhakar's compendium of neuromonitoring techniques, I cannot but marvel at the enormous advances that have been made in a relatively short time. Although, scientists had developed large, cumbersome means to measure intracranial pressure, the machines were far too cumbersome to even be considered for practical use. The same could be said for assessing cerebral blood flow and brain electrical activity. Who would have thought that at a flick of a switch, we can realize brain tissue oxygenation? Or monitor cognitive function in a sedated patient? Now, what existed only in drawings and the imagination of early pioneers has become reality and within the grasp of today's neuroanesthesiologist, making it ever easier to successfully undertake increasingly complex procedures.

Dr. Prabhakar has gathered together an impressive cadre of experts from across Europe, India, and the United States. He is to be congratulated on producing and editing a comprehensive volume that outlines and even simplifies the state of the art in neuromonitoring today.

Elizabeth A.M. Frost, MD,     Icahn Medical Center at Mount Sinai, New York, NY

January 2017

Preface

Over the years, neuromonitoring systems have evolved from the basic intracranial pressure monitoring to more sophisticated ones such as brain microdialysis and neuroimaging techniques. The progression has been from neurological assessment at bedside to advanced monitoring systems that assess various functions of the brain. Specialized neuromonitoring is now routinely done for most of the neurosurgical cases. In many instances, specialists such as neurophysiologists and neurologists also get involved. For anesthesiologists, it is imperative that we understand the basics of each neuromonitor as anesthetics can greatly influence the readings and so the interpretations.

This book will be useful for practitioners associated with neurosurgical and allied branches such as neurology and neuroradiology. It will provide a quick and easy access to understand various neuromonitoring equipment. Neuromonitoring is now an integral part of neurosciences, and residents are expected to have knowledge about it (theoretical and clinical). The book has examples, images, reference values, and their interpretations for each of the monitoring system. It will also help readers to get acquainted with various neuromonitoring systems and ways to use them.

I am thankful to all my authors who believed in me and my proposed format of this book. All contributors are renowned researchers and experts in their field. They have vast experience with various neuromonitoring systems. I am sure the readers will be benefitted from the cognizance of these distinguished authors.

Hemanshu Prabhakar

Acknowledgment

I wish to acknowledge the support of the administration of the All India Institute of Medical Sciences (AIIMS), New Delhi, in allowing me to conduct this academic task.

I will always remain indebted to Prof. P.K. Bithal (Ex Head, Neuroanaesthesiology and Critical Care, AIIMS, New Delhi) for his unconditional support and constant encouragement in all academic endeavors. I thank the faculty and staff of the department of Neuroanaesthesiology and Critical Care, for their support.

Special thanks are due to the production team of Elsevier.

Introduction to Monitoring Techniques

Neuromonitoring helps maintain the functional integrity of the central nervous system and also decreases the iatrogenic risk to neural structures. In neurologically compromised patients who have a rapidly fluctuating neurologic status, neuromonitoring provides guidance to both the neurosurgeon and anesthesiologists. It timely detects the sudden change in the neurologic function during the intraoperative period as well as in the intensive care unit, which may prove catastrophic to the patient. Neuromonitoring is also helpful in prognostication in critically ill patients. It is a rapidly growing field that involves the monitoring of both central and peripheral nervous systems and is considered to be a part of standard practice worldwide. However, due to the lack of facilities, many centers continue to perform neurosurgical procedures without specific intraoperative neuromonitoring. Apart from neurosurgeons and neurophysiologists, neuroanesthesiologists play a key role in patient management tailored according to the results of these monitoring devices. Thus, it is important for us to understand the basics of these devices, their correct usage, and interpretation of results. In this book, we will be discussing various modalities of neuromonitoring from intracranial pressure (ICP) monitoring to the most advanced ones such as functional neuroimaging and brain microdialysis.

Reviewing some of the recent literature on various monitoring systems in neurosciences, we came across interesting work by authors across the world. In a neurocritical care unit where neurological status may be difficult to assess in a sedated patient, ICP monitoring may help to guide therapy. But clear consensus on whether it improves outcome or not is still unclear. Kirkness and colleagues demonstrated the importance of ICP monitoring in their study on patients with traumatic brain injury (TBI).¹ They suggested that a continuous and visible display of the cerebral perfusion pressure (CPP) was associated with better survival and overall condition at discharge. The BEST TRIP trial assessed the effect of ICP monitoring on outcome in patients who had severe TBI.² One group was managed according to a protocol based on ICP monitoring, and in other group, treatment was based on imaging and clinical examination. The authors found that outcome was similar in both groups. However, the study lacks external validity, and results need to be carefully interpreted as two different protocols were compared and not ICP per se.³ Moreover, the authors suggest that this should not change the practice of those currently monitoring ICP. Cossu et al. recently conducted a systematic review to examine whether elevated intracranial pressure and ICP-derived variables predict mortality and functional outcomes after aneurysmal subarachnoid hemorrhage (SAH). The authors found that variables derived from ICP monitoring like pressure reactivity index, ICP pulse wave amplitude, ICP-arterial blood pressure wave amplitude correlation, and ICP variability are more accurate than ICP absolute values in predicting outcome.⁴

One group of researchers went on to compare the modified Lund concept with the CPP targeted therapy in patients with SAH and severe TBI with the aim of preventing secondary brain injury.⁵ They found that brain biochemistry using brain microdialysis was better maintained with the modified Lund concept method of management. The use of albumin for resuscitation in patients with severe TBI has been shown to be associated with increased ICP during the first week.⁶ This was believed to be the most likely mechanism of increased mortality in these patients.

Several electroencephalography (EEG)-based monitors have now been used in clinical practice, with varying degree of success to monitor the depth of anesthesia. Bispectral index (BIS) monitoring has stood the test of time and is very popular. The collaborators and the B-Unaware Study group found that there was an association between cumulative duration of low BIS and mortality in the setting of cardiac surgery.⁷ Results have been encouraging with use of the Cerebral State Monitor (CSM), where the authors have found that the ability of CSM for separation of consciousness and unconsciousness is comparable to other commercially available EEG-based indices.⁸ Recently, some researchers evaluated the alternative auditory evoked potential (AEP)-based index (aepEX) for the measurement of hypnotic depth in patients undergoing general anesthesia with xenon.⁹ They found that this monitor provided index in the range of adequate depth of xenon anesthesia.

Various clinical trials demonstrating the effect of drugs on vasospasm have been conducted over the past few years. Transcranial Doppler (TCD) has played an essential role in this regard, and drugs such as the statins,¹⁰ intensive insulin therapy,¹¹ clazosenton,¹² erythropoietin,¹³ methylprednisolone,¹⁴ cilostazol,¹⁵ magnesium sulfate,¹⁶ and many others have been investigated.

Evoked potential (EP) monitoring has gained popularity as its use has reduced the incidence of neurologic injuries following spine surgeries. Its anesthetic considerations have been comprehensively dealt with in an article by Bithal PK.¹⁷ In search of an ideal anesthetic technique during EP monitoring, researchers have investigated anesthetic agents such as desflurane, sevoflurane, esmolol, dexmedetomidine, and presence or absence of neuromuscular block.¹⁸–²⁰

The subjects of brain tissue oxygenation, cerebral oximetry, and brain microdialysis have always intrigued researchers, and a lot of research has been done in an attempt to unfold the mysteries of the brain. Researchers have tried to assess the effects of volatile and intravenous anesthetics on cerebral oxygenation.²¹,²² It has been observed that cerebral oxygen saturation is better maintained under sevoflurane anesthesia than total intravenous anesthetic technique. Using brain microdialysis techniques, researchers have also found that there is no difference in the sedation with propofol, midazolam, or dexmedetomidine when administered in patients with severe TBI.²³,²⁴

Despite tremendous advances in research in neurosciences, work related to cognitive function monitoring is comparatively limited. Studies have been conducted to identify the best anesthetic technique to prevent postoperative cognitive dysfunction (POCD) or cognitive decline.²⁵,²⁶ It has been found that intraoperative monitoring is associated with a lesser incidence of delirium. BIS monitoring reduces the anesthetic exposure, and it decreases the risk of POCD.²⁵,²⁶

Intraoperative neuromonitoring has become an important integral part of many types of neurosurgical procedures. A neurosurgical procedure with a high risk of neural injury will undoubtedly benefit from intraoperative neuromonitoring, whereas a procedure with low risk of nerve injury will almost not benefit from intraoperative neuromonitoring.

Various modalities used for neuromonitoring in patients with acute brain injury are expanding. However the answer to the best neuromonitor available to date remains unanswered. A multimodal approach toward neuromonitoring is the plausible choice in the near future.²⁷,²⁸ It integrates clinical examination, hemodynamic parameters, and variables derived from various neuromonitors to derive a management strategy for brain-injured patients. Updated consensus guidelines regarding multimodality monitoring need to be followed to optimize patient management.

Hemanshu Prabhakar

Indu Kapoor

Charu Mahajan

References

1. Kirkness C.J, Burr R.L, Cain K.C, et al. Effect of continuous display of cerebral perfusion pressure on outcomes in patients with traumatic brain injury. Am J Crit Care. 2006;15:600–609.

2. Chesnut R.M, Temkin N, Carney N, et al. Global neurotrauma research group. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367:2471–2481.

3. Chesnut R.M, Bleck T.P, Citerio G, et al. A consensus-based interpretation of the benchmark evidence from South American trials: treatment of intracranial pressure trial. J Neurotrauma. 2015;32:1722–1724.

4. Cossu G, Messerer M, Stocchetti N, et al. Intracranial pressure and outcome in critically ill patients with aneurysmal subarachnoid hemorrhage: a systematic review. Minerva Anestesiol. 2016;82:684–696.

5. Dizdarevic K, Hamdan A, Omerhodzic I, et al. Modified Lund concept versus cerebral perfusion pressure-targeted therapy: a randomised controlled study in patients with secondary brain ischaemia. Clin Neurol Neurosurg. 2012;114:142–148.

6. Cooper D.J, Myburgh J, Heritier S, SAFE-TBI Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group, et al. Albumin resuscitation for traumatic brain injury: is intracranial hypertension the cause of increased mortality? J Neurotrauma. 2013;30:512–518.

7. Kertai M.D, Pal N, Palanca B.J, B-Unaware Study Group, et al. Association of perioperative risk factors and cumulative duration of low bispectral index with intermediate-term mortality after cardiac surgery in the B-unaware trial. Anesthesiology. 2010;112:1116–1127.

8. Pilge S, Blum J, Kochs E.F, et al. Does the cerebral state index separate consciousness from unconsciousness? Anesth Analg. 2011;113:1403–1410.

9. Stoppe C, Peters D, Fahlenkamp A.V, et al. aepEX monitor for the measurement of hypnotic depth in patients undergoing balanced xenon anaesthesia. Br J Anaesth. 2012;108:80–88.

10. Lynch J.R, Wang H, McGirt M.J, et al. Simvastatin reduces vasospasm after aneurysmal subarachnoid hemorrhage: results of a pilot randomized clinical trial. Stroke. 2005;36:2024–2026.

11. Bilotta F, Spinelli A, Giovannini F, et al. The effect of intensive insulin therapy on infection rate, vasospasm, neurologic outcome, and mortality in neurointensive care unit after intracranial aneurysm clipping in patients with acute subarachnoid hemorrhage: a randomized prospective pilot trial. J Neurosurg Anesthesiol. 2007;19:156–160.

12. Barth M, Capelle H.H, Münch E, et al. Effects of the selective endothelin A (ET(A)) receptor antagonist Clazosentan on cerebral perfusion and cerebral oxygenation following severe subarachnoid hemorrhage – preliminary results from a randomized clinical series. Acta Neurochir (Wien). 2007;149:911–918. .

13. Springborg J.B, Møller C, Gideon P, et al. Erythropoietin in patients with aneurysmal subarachnoid haemorrhage: a double blind randomised clinical trial. Acta Neurochir (Wien). 2007;149:1089–1101.

14. Gomis P, Graftieaux J.P, Sercombe R, et al. Randomized, double-blind, placebo-controlled, pilot trial of high-dose methylprednisolone in aneurysmal subarachnoid hemorrhage. J Neurosurg. 2010;112:681–688.

15. Han S.W, Lee S.S, Kim S.H, et al. Effect of cilostazol in acute lacunar infarction based on pulsatility index of transcranial Doppler(ECLIPse): a multicenter, randomized, double-blind, placebo-controlled trial. Eur Neurol. 2013;69:33–40.

16. Wong G.K, Chan M.T, Boet R, et al. Intravenous magnesium sulfate after aneurysmal subarachnoid hemorrhage: a prospective randomized pilot study. J Neurosurg Anesthesiol. 2006;18:142–148.

17. Bithal P.K. Anaesthetic considerations for evoked potential monitoring. J Anaesthesiol Crit Care. 2014;1:2–12.

18. Chong C.T, Manninen P, Sivanaser V, et al. Direct comparison of the effect of desflurane and sevoflurane on intraoperative motor-evoked potentials monitoring. J Neurosurg Anesthesiol. 2014;26:306–312.

19. Ibraheim O.A, Abdulmonem A, Baaj J, et al. Esmolol versus dexmedetomidine in scoliosis surgery: study on intraoperative blood loss and hemodynamic changes. Middle East J Anaesthesiol. 2013;22:27–33.

20. Kim W.H, Lee J.J, Lee S.M, et al. Comparison of motor-evoked potentials monitoring in response to transcranial electrical stimulation in subjects undergoing neurosurgery with partial vs no neuromuscular block. Br J Anaesth. 2013;110:567–576.

21. Valencia L, Rodríguez-Pérez A, Kühlmorgen B, et al. Does sevoflurane preserve regional cerebral oxygen saturation measured by near-infrared spectroscopy better than propofol? Ann Fr Anesth Reanim. 2014;33:e59–65.

22. Güçlü Ç.Y, Ünver S, Aydınlı B, et al. The effect of sevoflurane vs. TIVA on cerebral oxygen saturation during cardiopulmonary bypass–randomized trial. Adv Clin Exp Med. 2014;23:919–924.

23. Tanguy M, Seguin P, Laviolle B, et al. Cerebral microdialysis effects of propofol versus midazolam in severe traumatic brain injury. J Neurotrauma. 2012;29:1105–1111.

24. James M.L, Olson D.M, Graffagnino C. A pilot study of cerebral and haemodynamic physiological changes during sedation with dexmedetomidine or propofol in patients with acute brain injury. Anaesth Intensive Care. 2012;40:949–957.

25. Chan M.T, Cheng B.C, Lee T.M, et al. CODA trial group. BIS-guided anesthesia decreases postoperative delirium and cognitive decline. J Neurosurg Anesthesiol. 2013;25:33–42.

26. Radtke F.M, Franck M, Lendner J, et al. Monitoring depth of anaesthesia in a randomized trial decreases the rate of postoperative delirium but not postoperative cognitive dysfunction. Br J Anaesth. 2013;110(Suppl. 1):i98–105.

27. Le Roux P, Menon D.K, Citerio G, et al. Consensus summary statement of the international multidisciplinary consensus conference on multimodality monitoring in neurocritical care: a statement for healthcare professionals from the Neurocritical Care Society and the European Society of Intensive Care Medicine. Neurocrit Care. 2014;21(Suppl. 2):S1–S26.

28. Roh D, Park S. Brain multimodality monitoring: updated perspectives. Curr Neurol Neurosci Rep. 2016;16(6):56.

Chapter 1

Intracranial Pressure Monitoring

Chiara Robba     Addenbrooke's Hospital, Cambridge, United Kingdom

Abstract

Despite recent research that has been equivocal, intracranial pressure (ICP) monitoring is invaluable in the management of neurocritical care patients, including head injury, poor grade subarachnoid hemorrhage, stroke, intracerebral hematoma, meningitis, acute liver failure, hydrocephalus, benign intracranial hypertension, etc. Monitoring of ICP requires an invasive transducer, and an intraventricular drain connected to an external pressure transducer is still considered to be the ‘‘gold standard’’ method.

However, some attempts have been made to measure ICP noninvasively, with promising results.

Information can be derived from ICP and its waveforms, including cerebral perfusion pressure, brain compensatory reserve, regulation of cerebral blood flow and volume, and content of vasogenic events. There are many possible conditions that can lead to elevated intracranial pressure, for acute, chronic, and both intracranial or extracranial causes. Since increased intracranial pressure is associated with increased morbidity and mortality, it should be promptly detected, and treatment must be immediately started with appropriate intensive care.

Keywords

Cerebral perfusion pressure; Intracranial pressure; Microtransducer; Neuromonitoring

Contents

Introduction

Pathophysiology

Invasive ICP

External Ventricular Drainage

Microtransducer Devices

Epidural and Subdural Devices

Intraparenchymal Microtransducers

Noninvasive ICP

Invasive Readings and Interpretation

Waveform Analysis

Index of Pressure–Volume Compensatory Reserve (RAP)

Effect of Anesthetics on Intracranial Pressure

Propofol

Barbiturates

Etomidate

Benzodiazepines

Opioids

Ketamine

Dexmedetomidine

Current Evidence, Applications, and Discussion

Suggested Readings

References

Introduction

Increased intracranial pressure (ICP) is an important cause of secondary brain injury, and it is associated with poor outcome.¹ Several conditions are associated with intracranial hypertension (ICH), including extracranial (fever, increased abdominal and intrathoracic pressure, hypercarbia, hypoxia) and intracranial causes (cerebral edema, hematoma, contusion, cerebrospinal fluid (CSF) disturbance).² In this setting, ICP monitoring is crucial in the management of neurocritical care patients, as clinical signs of ICH are tardive and poor predictors of elevated ICP.³

Invasive monitoring through an intraventricular or intraparenchymal catheter is indicated in all severe traumatic brain injured (TBI) patients with positive brain computed tomography (CT) findings, or normal brain CT if the patient is older than 40  years or in the presence of systolic blood pressure below 90  mm Hg or in the case of abnormal flexion or extension in response to pain⁴; however, invasive techniques are associated with certain risks, including infections and hemorrhage (Fig. 1.1).⁵

Pathophysiology

Pathologic ICH is defined when ICP raises persistently above 20  mm Hg. The intracranial volume, consisting of brain parenchyma, blood, and CSF, is enveloped by the rigid skull bone.⁶,⁷ Under physiological conditions the total intracranial volume remains constant because of compensatory mechanisms, which operate to maintain a constant and adequate cerebral blood flow (CBF), and ICP. According to the Monro-Kellie doctrine,⁶,⁷ ICP is the result of the volume and compliance of each intracranial component (brain parenchyma, arterious blood, venous blood, CSF) within the intracranial compartment. The relationship between ICP variations and the volume of intracranial contents defines the compliance characteristics of the intracranial compartment. The intracranial compliance can be defined as the change in volume over the change in pressure (dV/dP).

Figure 1.1  Examples of hemorrhagic complication associated with invasive ICP monitoring. (A) Brain CT showing an extradural hemorrhage after ICP bolt insertion, which required surgical evacuation. (B) Follow-up brain MRI in a patient previously monitored with an intraparenchymal device, showing a contusion on its trajectory.

In the presence of an intracranial mass (e.g., brain swelling, hydrocephalus, hematomas, or abscesses), compensatory mechanisms operate to maintain ICP and CBF constant by displacing CSF into the thecal sac and by compressing the cerebral venous compartment via venoconstriction and extracranial drainage.

The relationship between ICP and volume is not linear. Initially, pressure increases only slightly with increasing volume. There, compensatory mechanisms allow ICP to elevate only slightly with increase of volume. When these compensatory mechanisms have been exhausted or when autoregulation is impaired, small volume increases develop significant increases in pressure, leading to a dramatic rise in ICP (Fig. 1.2).

CBF is maintained relatively constant within a well-known range of mean arterial pressure (MAP) due to the modulation of cerebrovascular resistances. The relationship between ICP and MAP has been defined as the Pressure Reactivity index (PRx), considered the main marker of autoregulatory reserve. Low PRx values indicate a poor association between ICP and MAP and thus a good autoregulation capacity, whereas values approaching 1.0 indicate a strong positive association between the two parameters, thus a poor autoregulation⁸ (Fig. 1.3).

Cerebral perfusion pressure (CPP), defined as the difference between MAP and ICP, is the driving force responsible for adequate brain perfusion and oxygenation. Following a significant ICP increase, CPP decreases, resulting in an inadequate brain tissue perfusion and oxygenation. The consequent ischemia will induce further cytotoxic edema resulting in even higher ICP.

Figure 1.2  The relationship between intracranial volume and pressure is exponential. Thus, initially, increases of volume determinate only slightly pressure increases, but when the buffering capabilities of the system are exceeded, ICP dramatically rises.

Figure 1.3  Autoregulation.

(A) Screenshots showing cerebral perfusion pressure (CPP) and mean arterial pressure (MAP) trend (upper), ICP trend (middle), and pressure reactivity index (PRx, lower panel). (B) An automated curve fitting method was applied to determine CPP at the minimum value for pressure reactivity index (CPPopt). A time trend of CPPopt was created using a moving 4-hr window, updated every minute. For each bin the corresponding values of PRx were assembled. The mean value and SD of each bin were then plotted against the bins' mean CPP values to create the error bar chart representing the relationship between PRx and CPP. Autoregulation is preserved when PRx has low values and MAP and ICP are negatively correlated. When autoregulation is impaired, MAP increase is followed by ICP increases as well. Thus, there is a positive correlation between the two parameters. In this example, this relationship forms a smooth U-shaped curve, and the CPP plot indicates an optimal CPP (CPPopt) at approximately 73  mm Hg. (C) Schematic representation of autoregulation of cerebral blood flow in normotensive and hypertensive subjects. The relationship between CBF and CPP is regulated by Ohm's law and depends on cerebrovascular resistances (CVR) according to the following formula: CBF  =  CPP  ÷  CVR. Thus, within certain ranges of MAP, CVR changes to maintain an appropriate CBF, and initial increases or decreases in MAP are associated with maintenance of CBF due to appropriate changes in arteriolar resistance. More marked changes in pressure are eventually associated with loss of autoregulation, leading to a reduction (with hypotension) or an elevation (with marked hypertension) in cerebral blood flow. These changes occur at higher pressures in patients with hypertension, presumably due to arteriolar thickening.

In this perspective, an ICP increase is followed by an impairment of CBF, which is responsible for subsequent metabolic and functional alterations. On the other hand, a primary flow impairment or metabolic disfunction (such as hypoxia and hypoglycemia) with a consequent cytotoxic edema determines a very quick ICP increase.

Invasive ICP

External Ventricular Drainage

External ventricular drainage (EVD) is widely considered the gold standard for ICP monitoring (Table 1.1, Fig. 1.4).

The EVD system is also useful to drain CSF for ICP control, further to manage acute hydrocephalus, intraventricular hemorrhage, and for direct intraventricular drug delivery. The main complications associated with EVD are malfunctioning due to malpositioning or obstruction, infections, and hemorrhage.⁹ Malpositionings occur with a rate of 1.5%–20% and can also damage crucial brain structures (internal capsule basal ganglia or thalamus, for example).¹⁰,¹¹

The risk of infection is higher with ventricular catheters than with parenchymal probes¹² and may vary between 0 and 22% (averaging 10%) (revised in Ref. 13). The coagulase-negative staphylococcus seems to be the most common infecting organism, responsible for nearly half of the cases, followed by Staphylococcus aureus (15%), and Klebsiella (6.6%).¹⁴–¹⁶ The risk of infection is significantly dependent on the time of permanence of the catheter (cut off over 5  days), the presence of cranial fracture with CSF leak or an extracranial infection site, and the insertion of more than one invasive ICP monitoring device. Catheter infection rate can be reduced by a strict adherence to a sterile practice during EVD positioning, generous subcutaneous catheter tunnelization, and by the minimization of catheter manipulation.¹⁷ Neither preventive catheter change nor antibiotics prophylaxis prior to EVD insertion seem to reduce the risk of EVD infections.

EVD positioning can further harbor risks of hemorrhagic complications, especially in patients with coagulopathy or low platelets (below 100,000).¹⁸ Postoperative CT positive for blood after EVD positioning was found in 41% in a consecutive series of 188 patients, though only in one out of four the hematoma was larger than 15  mL, and other authors found a cumulative rate of hemorrhagic complications ranging from 5.7% to 7%.¹⁹

Table 1.1

Methods to assess ICP

CT, computed tomography; EEG, electroencephalography; EOAEs, evoked otoacoustic emission; MR, magnetic resonance; NIRS, near infrared spectroscopy; ONSD, optic nerve sheath diameter; TCD, transcranial Doppler; TCD CrCp, critical closing pressure formula; TCD FVdICP, flow velocity diastolic formula; TCD nPI, pulsatility index TCD-derived formula; TMD, tympanic membrane displacement; TOF, time of flight; VEP, visual evoked potential.

Reproduced from Robba et al. Non invasive assessment of intracranial pressure. Acta Neurol Scand. July 2016;134(1):4–21.

Figure 1.4  External ventricular drainage (EVD) device.

In general, the rate of clinically significant hemorrhagic complications after EVD insertion is relatively